=== Generating (published_papers) ===
=== Generating (teaching_experience) ===
=== Generating (misc) ===
=== Generating (research_projects) ===
=== Generating (presentations) ===
==== begin registerFile(/WWW/pub2/data/ERD/person/323761/researchmap/published_papers.jsonl) ====
line:1, {"insert":{"user_id":"B000344297","type":"published_papers","id":"43540147"},"force":{"see_also":[{"@id":"https://search.jamas.or.jp/link/ui/W615480014","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050010997647006592/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=392267","label":"url"}],"paper_title":{"en":"徳島県民が知っておくべき予防医学∼病気にならないための秘訣∼ 肥満から読み解く高齢者の栄養の問題点と管理","ja":"徳島県民が知っておくべき予防医学∼病気にならないための秘訣∼ 肥満から読み解く高齢者の栄養の問題点と管理"},"authors":{"en":[{"name":"Sakaue Hiroshi"},{"name":"Kuroda Masashi"},{"name":"Tsutsumi Rie"}],"ja":[{"name":"阪上 浩"},{"name":"黒田 雅士"},{"name":"堤 理恵"}]},"description":{"en":"The shift of Japanese eating habits from salty and grain-based consumption with low animal protein to a diet with a variety of lipids and animal products after Second World War has significantly reduced the rate of infections and cerebral bleeding. On the other hand, the increase in life-style related diseases such as cancer, heart disease, stroke, diabetes has become a serious problem in our country. However, it is difficult to discuss the nutrition of the elderly in a stereotype because of the diversity in physical and psychological feature. Although there are many important issues that require discussions encompassing broad aspects in taking high protein diet as a main topic, it may be possible to consider a question in the aspects of body weight or body composition in the elderly. In this section, we discuss the `secret key' in nutrition to health for the aged.","ja":"The shift of Japanese eating habits from salty and grain-based consumption with low animal protein to a diet with a variety of lipids and animal products after Second World War has significantly reduced the rate of infections and cerebral bleeding. On the other hand, the increase in life-style related diseases such as cancer, heart disease, stroke, diabetes has become a serious problem in our country. However, it is difficult to discuss the nutrition of the elderly in a stereotype because of the diversity in physical and psychological feature. Although there are many important issues that require discussions encompassing broad aspects in taking high protein diet as a main topic, it may be possible to consider a question in the aspects of body weight or body composition in the elderly. In this section, we discuss the `secret key' in nutrition to health for the aged."},"publication_date":"2022-04-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.78","number":"No.1-2","starting_page":"3","ending_page":"8","languages":["jpn"],"referee":true,"identifiers":{"issn":["0037-3699"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116998","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35228123","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=388474","label":"url"}],"paper_title":{"en":"Development of a screening system for agents that modulate taste receptor expression with the CRISPR-Cas9 system in medaka.","ja":"Development of a screening system for agents that modulate taste receptor expression with the CRISPR-Cas9 system in medaka."},"authors":{"en":[{"name":"Beppu Kana"},{"name":"Tsutsumi Rie"},{"name":"Ansai Satoshi"},{"name":"Ochiai Nana"},{"name":"Terakawa Mai"},{"name":"Mori Marie"},{"name":"Kuroda Masashi"},{"name":"Horikawa Kazuki"},{"name":"Tomoi Takumi"},{"name":"Sakamoto Joe"},{"name":"Kamei Yasuhiro"},{"name":"Naruse Kiyoshi"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"Beppu Kana"},{"name":"堤 理恵"},{"name":"Ansai Satoshi"},{"name":"Ochiai Nana"},{"name":"Terakawa Mai"},{"name":"Mori Marie"},{"name":"黒田 雅士"},{"name":"堀川 一樹"},{"name":"Tomoi Takumi"},{"name":"Sakamoto Joe"},{"name":"Kamei Yasuhiro"},{"name":"Naruse Kiyoshi"},{"name":"阪上 浩"}]},"description":{"en":"Taste recognition mediated by taste receptors is critical for the survival of animals in nature and is an important determinant of nutritional status and quality of life in humans. However, many factors including aging, diabetes, zinc deficiency, infection with influenza or cold viruses, and chemotherapy can trigger dysgeusia, for which a standard treatment has not been established. We here established an engineered strain of medaka (Oryzias latipes) that expresses green fluorescent protein (GFP) from the endogenous taste 1 receptor 3 (T1R3) gene locus with the use of the CRISPR-Cas9 system. This T1R3-GFP knock-in (KI) strain allows direct visualization of expression from this locus by monitoring of GFP fluorescence. The pattern of GFP expression in the T1R3-GFP KI fish thus mimicked that of endogenous T1R3 gene expression. Furthermore, exposure of T1R3-GFP KI medaka to water containing monosodium glutamate or the anticancer agent 5-fluorouracil resulted in an increase or decrease, respectively, in GFP fluorescence intensity, effects that also recapitulated those on T1R3 mRNA abundance. Finally, screening for agents that affect GFP fluorescence intensity in T1R3-GFP KI medaka identified tryptophan as an amino acid that increases T1R3 gene expression. The establishment of this screening system for taste receptor expression in medaka provides a new tool for the development of potential therapeutic agents for dysgeusia.","ja":"Taste recognition mediated by taste receptors is critical for the survival of animals in nature and is an important determinant of nutritional status and quality of life in humans. However, many factors including aging, diabetes, zinc deficiency, infection with influenza or cold viruses, and chemotherapy can trigger dysgeusia, for which a standard treatment has not been established. We here established an engineered strain of medaka (Oryzias latipes) that expresses green fluorescent protein (GFP) from the endogenous taste 1 receptor 3 (T1R3) gene locus with the use of the CRISPR-Cas9 system. This T1R3-GFP knock-in (KI) strain allows direct visualization of expression from this locus by monitoring of GFP fluorescence. The pattern of GFP expression in the T1R3-GFP KI fish thus mimicked that of endogenous T1R3 gene expression. Furthermore, exposure of T1R3-GFP KI medaka to water containing monosodium glutamate or the anticancer agent 5-fluorouracil resulted in an increase or decrease, respectively, in GFP fluorescence intensity, effects that also recapitulated those on T1R3 mRNA abundance. Finally, screening for agents that affect GFP fluorescence intensity in T1R3-GFP KI medaka identified tryptophan as an amino acid that increases T1R3 gene expression. The establishment of this screening system for taste receptor expression in medaka provides a new tool for the development of potential therapeutic agents for dysgeusia."},"publication_date":"2022-02-23","publication_name":{"en":"Biochemical and Biophysical Research Communications","ja":"Biochemical and Biophysical Research Communications"},"volume":"Vol.601","starting_page":"65","ending_page":"72","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbrc.2022.02.082"],"issn":["1090-2104"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://repo.lib.tokushima-u.ac.jp/117128","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050292251404941184/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=402617","label":"url"}],"paper_title":{"en":"生活習慣病と栄養学 : 最近のトピックスを交えて","ja":"生活習慣病と栄養学 : 最近のトピックスを交えて"},"authors":{"en":[{"name":"Tsutsumi Rie"},{"name":"三島 優奈"},{"name":"川上 歩花"},{"name":"Kuroda Masashi"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"堤 理恵"},{"name":"三島 優奈"},{"name":"川上 歩花"},{"name":"黒田 雅士"},{"name":"阪上 浩"}]},"description":{"en":"Metabolic syndrome is a pathological condition with hyperglycemia, dyslipidemia, or hypertension resulting in cardiovascular and cerebrovascular disease. Factors that affect visceral fat accumulation and weight gain include not only physiological factors such as heredity, constitution, and age, but also behavioral factors and environmental factors. Eating behavior and eating environment are critical for the prevention and treatment of metabolic syndrome. In this report, we will discuss about recent topics of nutrition in metabolic syndrome, especially association with macronutrients such as carbohydrate, fatty acids and protein. In recent years, several publications have determined the benefit of low carbohydrate diet on obesity and diabetes, and the American Diabetes Association has also recommended low carbohydrate diet, Mediterranean diet, and a diet mainly consistent with vegetables and plants. There have been many reports that the effect of carbohydrate restriction has not only the weight loss effect but also reduces risk factors such as cardiovascular disease and cerebrovascular disease. Fanelli et al . recently have shown that half of US adults with diabetes have less than the recommended daily intake of protein, which may lead to poor dietary quality. Diabetic patients with low protein intake had significantly lower dietary nutrient density and 12．5% higher carbohydrate intake, whereas diabetic patients with daily protein intake meeting the recommended amount have shown that the overall quality of the diet was high and almost met the recommended daily amount of vegetables, whole grains, dairy products and added sugars. Therefore, in addition to the prevention of metabolic syndrome, protein is important for treatment of metabolic syndrome and higher QOL. Nutritional research needs further development to deal with metabolic syndrome.","ja":"Metabolic syndrome is a pathological condition with hyperglycemia, dyslipidemia, or hypertension resulting in cardiovascular and cerebrovascular disease. Factors that affect visceral fat accumulation and weight gain include not only physiological factors such as heredity, constitution, and age, but also behavioral factors and environmental factors. Eating behavior and eating environment are critical for the prevention and treatment of metabolic syndrome. In this report, we will discuss about recent topics of nutrition in metabolic syndrome, especially association with macronutrients such as carbohydrate, fatty acids and protein. In recent years, several publications have determined the benefit of low carbohydrate diet on obesity and diabetes, and the American Diabetes Association has also recommended low carbohydrate diet, Mediterranean diet, and a diet mainly consistent with vegetables and plants. There have been many reports that the effect of carbohydrate restriction has not only the weight loss effect but also reduces risk factors such as cardiovascular disease and cerebrovascular disease. Fanelli et al . recently have shown that half of US adults with diabetes have less than the recommended daily intake of protein, which may lead to poor dietary quality. Diabetic patients with low protein intake had significantly lower dietary nutrient density and 12．5% higher carbohydrate intake, whereas diabetic patients with daily protein intake meeting the recommended amount have shown that the overall quality of the diet was high and almost met the recommended daily amount of vegetables, whole grains, dairy products and added sugars. Therefore, in addition to the prevention of metabolic syndrome, protein is important for treatment of metabolic syndrome and higher QOL. Nutritional research needs further development to deal with metabolic syndrome."},"publication_date":"2021-12-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.77","number":"No.5-6","starting_page":"187","ending_page":"192","languages":["jpn"],"referee":true,"identifiers":{"issn":["0037-3699"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117442","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34801078","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=389315","label":"url"}],"paper_title":{"en":"Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model.","ja":"Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model."},"authors":{"en":[{"name":"Morio Atsushi"},{"name":"Tsutsumi Rie"},{"name":"Satomi Shiho"},{"name":"Kondo Takashi"},{"name":"Miyoshi Hirotsugu"},{"name":"Kato Takahiro"},{"name":"Kuroda Masashi"},{"name":"Kitamura Tadahiro"},{"name":"Hara Kenta"},{"name":"Saeki Noboru"},{"name":"Sakaue Hiroshi"},{"name":"Yasuo M. Tsutsumi ."}],"ja":[{"name":"Morio Atsushi"},{"name":"堤 理恵"},{"name":"里見 志帆"},{"name":"Kondo Takashi"},{"name":"Miyoshi Hirotsugu"},{"name":"Kato Takahiro"},{"name":"黒田 雅士"},{"name":"Kitamura Tadahiro"},{"name":"Hara Kenta"},{"name":"Saeki Noboru"},{"name":"阪上 浩"},{"name":"Yasuo M. Tsutsumi ."}]},"description":{"en":"Leu treatment improved the damage caused by myocardial I/R injury by promoting mTOR activity and mitochondrial fusion on prediabetic hearts in mice.","ja":"mice. Additionally, Leu increased the percentage of fused mitochondria and the mitochondrial volume, and decreased the number of mitochondria per cell in isolated cardiomyocytes. In HFD-induced obese mice, Leu treatment significantly reduced infarct size (41.0% ± 1.1% vs. 51.0% ± 1.4%, n = 7, p < 0.05), which was not induced by ischemic preconditioning, and this effect was inhibited by Rap. Furthermore, we observed enhanced mTOR protein expression and mitochondrial fusion with decreased reactive oxygen species production with Leu treatment in HFD-induced obese mice, but not in mTOR"},"publication_date":"2021-11-20","publication_name":{"en":"Diabetology & Metabolic Syndrome","ja":"Diabetology & Metabolic Syndrome"},"volume":"Vol.13","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1186/s13098-021-00755-z"],"issn":["1758-5996"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"B000344297","type":"published_papers","id":"33869511"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116689","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33775867","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85114290883&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=382161","label":"url"}],"paper_title":{"en":"Long-chain monounsaturated fatty acids improve endothelial function with altering microbial flora","ja":"Long-chain monounsaturated fatty acids improve endothelial function with altering microbial flora"},"authors":{"en":[{"name":"Tsutsumi Rie"},{"name":"Yamasaki Yuki"},{"name":"Takeo Jiro"},{"name":"Miyahara Hiroko"},{"name":"Sebe Mayu"},{"name":"Bando Masahiro"},{"name":"Tanba Yousuke"},{"name":"Mishima Yuna"},{"name":"Takeji Kana"},{"name":"Ueshima Nanako"},{"name":"Kuroda Masashi"},{"name":"Masumoto Saeko"},{"name":"Harada Nagakatsu"},{"name":"Fukuda Daiju"},{"name":"Yoshimoto Ryoko"},{"name":"Yasuo M. Tsutsumi ."},{"name":"Aihara Ken-ichi"},{"name":"Sata Masataka"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"堤 理恵"},{"name":"山﨑 幸"},{"name":"Takeo Jiro"},{"name":"Miyahara Hiroko"},{"name":"瀬部 真由"},{"name":"板東 正浩"},{"name":"Tanba Yousuke"},{"name":"Mishima Yuna"},{"name":"Takeji Kana"},{"name":"Ueshima Nanako"},{"name":"黒田 雅士"},{"name":"升本 早枝子"},{"name":"原田 永勝"},{"name":"福田 大受"},{"name":"Yoshimoto Ryoko"},{"name":"Yasuo M. Tsutsumi ."},{"name":"粟飯原 賢一"},{"name":"佐田 政隆"},{"name":"阪上 浩"}]},"description":{"en":"Fish oil-derived long-chain monounsaturated fatty acids (LCMUFAs) with a carbon chain length longer than 18 units ameliorate cardiovascular risk in mice. In this study, we investigated whether LCMUFAs could improve endothelial functions in mice and humans. In a double-blind, randomized, placebo-controlled, parallel-group, multi-center study, healthy subjects were randomly assigned to either an LCMUFA oil (saury oil) or a control oil (olive and tuna oils) group. Sixty subjects were enrolled and administrated each oil for 4 weeks. For the animal study, ApoE mice were fed a Western diet supplemented with 3% of either gadoleic acid (C20:1) or cetoleic acid (C22:1) for 12 weeks. Participants from the LCMUFA group showed improvements in endothelial function and a lower trimethylamine-N-oxide level, which is a predictor of coronary artery disease. C20:1 and C22:1 oils significantly improved atherosclerotic lesions and plasma levels of several inflammatory cytokines, including IL-6 and TNF-α. These beneficial effects were consistent with an improvement in the gut microbiota environment, as evident from the decreased ratio of Firmicutes and/ or Bacteroidetes, increase in the abundance of Akkermansia, and upregulation of short-chain fatty acid (SCFA)-induced glucagon-like peptide-1 (GLP-1) expression and serum GLP-1 level. These data suggest that LCMUFAs alter the microbiota environment that stimulate the production of SCFAs, resulting in the induction of GLP-1 secretion. Fish oil-derived long-chain monounsaturated fatty acids might thus help to protect against cardiovascular disease.","ja":"Fish oil-derived long-chain monounsaturated fatty acids (LCMUFAs) with a carbon chain length longer than 18 units ameliorate cardiovascular risk in mice. In this study, we investigated whether LCMUFAs could improve endothelial functions in mice and humans. In a double-blind, randomized, placebo-controlled, parallel-group, multi-center study, healthy subjects were randomly assigned to either an LCMUFA oil (saury oil) or a control oil (olive and tuna oils) group. Sixty subjects were enrolled and administrated each oil for 4 weeks. For the animal study, ApoE mice were fed a Western diet supplemented with 3% of either gadoleic acid (C20:1) or cetoleic acid (C22:1) for 12 weeks. Participants from the LCMUFA group showed improvements in endothelial function and a lower trimethylamine-N-oxide level, which is a predictor of coronary artery disease. C20:1 and C22:1 oils significantly improved atherosclerotic lesions and plasma levels of several inflammatory cytokines, including IL-6 and TNF-α. These beneficial effects were consistent with an improvement in the gut microbiota environment, as evident from the decreased ratio of Firmicutes and/ or Bacteroidetes, increase in the abundance of Akkermansia, and upregulation of short-chain fatty acid (SCFA)-induced glucagon-like peptide-1 (GLP-1) expression and serum GLP-1 level. These data suggest that LCMUFAs alter the microbiota environment that stimulate the production of SCFAs, resulting in the induction of GLP-1 secretion. Fish oil-derived long-chain monounsaturated fatty acids might thus help to protect against cardiovascular disease."},"publication_date":"2021-11","publication_name":{"en":"Translational Research : The Journal of Laboratory and Clinical Medicine","ja":"Translational Research : The Journal of Laboratory and Clinical Medicine"},"volume":"Vol.237","starting_page":"16","ending_page":"30","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.trsl.2021.03.016"],"issn":["1878-1810"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34362635","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=381339","label":"url"}],"paper_title":{"en":"Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling.","ja":"Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling."},"authors":{"en":[{"name":"Morio Atsushi"},{"name":"Tsutsumi Rie"},{"name":"Kondo Takashi"},{"name":"Miyoshi Hirotsugu"},{"name":"Kato Takahiro"},{"name":"Narasaki Soshi"},{"name":"Satomi Shiho"},{"name":"Nakaya Erika"},{"name":"Kuroda Masashi"},{"name":"Sakaue Hiroshi"},{"name":"Kitamura Tadahiro"},{"name":"Yasuo M. Tsutsumi ."}],"ja":[{"name":"Morio Atsushi"},{"name":"堤 理恵"},{"name":"Kondo Takashi"},{"name":"Miyoshi Hirotsugu"},{"name":"Kato Takahiro"},{"name":"Narasaki Soshi"},{"name":"里見 志帆"},{"name":"Nakaya Erika"},{"name":"黒田 雅士"},{"name":"阪上 浩"},{"name":"Kitamura Tadahiro"},{"name":"Yasuo M. Tsutsumi ."}]},"description":{"en":"Leu treatment is critical in rendering a cardioprotective effect exhibited by BCAAs via mTOR signaling. Furthermore, Leu improved mitochondrial function.","ja":"Cardiac myocytes isolated from adult male Wistar rats were incubated and exposed to simulated I/R (SI/R) injury by replacing the air content. Cardiac myocytes were treated with Leu and subsequently, their survival rate was calculated. To elucidate the signaling pathway and mitochondrial function, immunoblots and mitochondrial permeability transition pore were examined. Cell survival rate was decreased with SI/R but improved by 160 μM Leu (38.5 ± 3.6% vs. 64.5 ± 4.2%, respectively, p < 0.001). Although rapamycin (mTOR inhibitor) prevented this cardioprotective effect induced by Leu, wortmannin (PI3K inhibitor) did not interfere with this effect. In addition, we indicated that overexpression of Opa-1 and mitochondrial function are ameliorated via Leu-induced mitochondrial biogenesis. In contrast, knockdown of Opa-1 suppressed Leu-induced cardioprotection."},"publication_date":"2021-07-10","publication_name":{"en":"Nutrition, Metabolism, and Cardiovascular Diseases : NMCD","ja":"Nutrition, Metabolism, and Cardiovascular Diseases : NMCD"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.numecd.2021.06.025"],"issn":["1590-3729"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:7, {"insert":{"user_id":"B000344297","type":"published_papers","id":"33414383"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116598","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33065161","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=380324","label":"url"}],"paper_title":{"en":"UCP1-dependent and UCP1-independent metabolic changes induced by acute cold exposure in brown adipose tissue of mice.","ja":"UCP1-dependent and UCP1-independent metabolic changes induced by acute cold exposure in brown adipose tissue of mice."},"authors":{"en":[{"name":"Okamatsu-Ogura Yuko"},{"name":"Kuroda Masashi"},{"name":"Tsutsumi Rie"},{"name":"Tsubota Ayumi"},{"name":"Saito Masayuki"},{"name":"Kimura Kazuhiro"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"Okamatsu-Ogura Yuko"},{"name":"黒田 雅士"},{"name":"堤 理恵"},{"name":"Tsubota Ayumi"},{"name":"Saito Masayuki"},{"name":"Kimura Kazuhiro"},{"name":"阪上 浩"}]},"description":{"en":"These results revealed that cold exposure induces UCP1-mediated thermogenesis-dependent glucose utilization and UCP1-independent active lipid metabolism in BAT. In addition, cold exposure largely affects amino acid metabolism in BAT, especially UCP1-dependently enhances glutamine utilization. These results contribute a comprehensive understanding of UCP1-mediated thermogenesis-dependent and thermogenesis-independent metabolism in BAT.","ja":"These results revealed that cold exposure induces UCP1-mediated thermogenesis-dependent glucose utilization and UCP1-independent active lipid metabolism in BAT. In addition, cold exposure largely affects amino acid metabolism in BAT, especially UCP1-dependently enhances glutamine utilization. These results contribute a comprehensive understanding of UCP1-mediated thermogenesis-dependent and thermogenesis-independent metabolism in BAT."},"publication_date":"2020-10-14","publication_name":{"en":"Metabolism: Clinical and Experimental","ja":"Metabolism: Clinical and Experimental"},"volume":"Vol.113","starting_page":"154396","ending_page":"154396","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.metabol.2020.154396"],"issn":["1532-8600"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:8, {"insert":{"user_id":"B000344297","type":"published_papers","id":"33414384"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118304","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32513534","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367805","label":"url"}],"paper_title":{"en":"Assessment of insulin resistance in the skeletal muscle of mice using positron emission tomography/computed tomography imaging.","ja":"Assessment of insulin resistance in the skeletal muscle of mice using positron emission tomography/computed tomography imaging."},"authors":{"en":[{"name":"Miyatake Yumiko"},{"name":"Mishima Yuna"},{"name":"Tsutsumi Rie"},{"name":"Otani Tamaki"},{"name":"Suemasa Naoya"},{"name":"Masumoto Saeko"},{"name":"Kuroda Masashi"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"宮武 由実子"},{"name":"三島 優奈"},{"name":"堤 理恵"},{"name":"大谷 環樹"},{"name":"末政 直哉"},{"name":"升本 早枝子"},{"name":"黒田 雅士"},{"name":"阪上 浩"}]},"description":{"en":"F]-fluoro-2-deoxy-D-glucose (FDG). FDG-PET/CT imaging revealed that insulin administration and exercise load significantly increased FDG accumulation in the skeletal muscle of C57BL/6J mice. FDG accumulation was lower in the skeletal muscle of 14-week-old db/db diabetic model mice exhibiting remarkable insulin resistance compared to that of 7-week-old db/db mice. Based on the continuous observation of FDG accumulation over time in diet-induced obese (DIO) mice, FDG accumulation significantly decreased in 17-week-old mice after the acquisition of insulin resistance. Although insulin-induced glucose uptake in the skeletal muscle was markedly attenuated in 20-week-old DIO mice that had already developed insulin resistance, exercise load effectively increased FDG uptake in the skeletal muscle. Thus, we successfully confirmed that glucose uptake accompanied by insulin administration and exercise load increased in the skeletal muscle using PET-CT. FDG-PET/CT might be an effective tool that could noninvasively capture the chronological changes of metabolic abnormalities in the skeletal muscle of mice.","ja":"Measuring glucose uptake in the skeletal muscle in vivo is an effective method to determine glucose metabolism abnormalities as the skeletal muscle is the principal tissue responsible for glucose disposal and is a major site of peripheral insulin resistance. In this study, we investigated the pathological glucose metabolism dynamics of the skeletal muscle of C57BL/6J mice in a noninvasive and time-sequential manner using positron emission tomography/computed tomography (PET/CT), an imaging technique that uses radioactive substances to visualize and measure metabolic processes in the body, with ["},"publication_date":"2020-06-05","publication_name":{"en":"Biochemical and Biophysical Research Communications","ja":"Biochemical and Biophysical Research Communications"},"volume":"Vol.528","number":"No.3","starting_page":"499","ending_page":"505","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbrc.2020.05.165"],"issn":["1090-2104"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:9, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32451822","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367804","label":"url"}],"paper_title":{"en":"Differential regulation of Actn2 and Actn3 expression during unfolded protein response in C2C12 myotubes.","ja":"Differential regulation of Actn2 and Actn3 expression during unfolded protein response in C2C12 myotubes."},"authors":{"en":[{"name":"Harada Nagakatsu"},{"name":"Gotoda Yuka"},{"name":"Hatakeyama Adzumi"},{"name":"Nakagawa Tadahiko"},{"name":"Miyatake Yumiko"},{"name":"Kuroda Masashi"},{"name":"Masumoto Saeko"},{"name":"Tsutsumi Rie"},{"name":"Nakaya Yutaka"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"原田 永勝"},{"name":"後藤田 結香"},{"name":"畠山 あづみ"},{"name":"中川 忠彦"},{"name":"宮武 由実子"},{"name":"黒田 雅士"},{"name":"升本 早枝子"},{"name":"堤 理恵"},{"name":"中屋 豊"},{"name":"阪上 浩"}]},"description":{"en":"ACTN2 and ACTN3 encode sarcomeric α-actinin-2 and α-actinin-3 proteins, respectively, that constitute the Z-line in mammalian skeletal muscle fibers. In human ACTN3, a nonsense mutation at codon 577 that encodes arginine (R) produces the R577X polymorphism. Individuals having a homozygous 577XX genotype do not produce α-actinin-3 protein. The 577XX genotype reportedly occurs in sprint and power athletes in frequency lower than in the normal population, suggesting that α-actinin-3 deficiency diminishes fast-type muscle function. Among humans who carry 577R alleles, varying ACTN3 expression levels under certain conditions can have diverse effects on atheletic and muscle performance. However, the factors that regulate ACTN3 expression are unclear. Here we investigated whether the unfolded protein response (UPR) under endoplasmic reticulum (ER) stress regulates expression of Actn3 and its isoform Actn2 in mouse C2C12 myotubes. Among UPR-related transcription factors, XBP1 upregulated Actn2, whereas XBP1, ATF4 and ATF6 downregulated Actn3 promoter activity. Chemical induction of ER stress increased Actn2 mRNA levels, but decreased those for Actn3. ER stress also decreased α-actinin-3 protein levels, whereas levels of α-actinin-2 were unchanged. The intracellular composition of muscle contraction-related proteins was altered under ER stress, in that expression of parvalbumin (a fast-twitch muscle-specific protein) and troponin I type 1 (skeletal, slow) was suppressed. siRNA-induced suppression of Actn3 mimicked the inhibitory effect of ER stress on parvalbumin levels. Thus, endogenous expression levels of α-actinin-3 can be altered by ER stress, which may modulate muscle performance and athletic aptitudes, particularly in humans who carry ACTN3 577R alleles.","ja":"ACTN2 and ACTN3 encode sarcomeric α-actinin-2 and α-actinin-3 proteins, respectively, that constitute the Z-line in mammalian skeletal muscle fibers. In human ACTN3, a nonsense mutation at codon 577 that encodes arginine (R) produces the R577X polymorphism. Individuals having a homozygous 577XX genotype do not produce α-actinin-3 protein. The 577XX genotype reportedly occurs in sprint and power athletes in frequency lower than in the normal population, suggesting that α-actinin-3 deficiency diminishes fast-type muscle function. Among humans who carry 577R alleles, varying ACTN3 expression levels under certain conditions can have diverse effects on atheletic and muscle performance. However, the factors that regulate ACTN3 expression are unclear. Here we investigated whether the unfolded protein response (UPR) under endoplasmic reticulum (ER) stress regulates expression of Actn3 and its isoform Actn2 in mouse C2C12 myotubes. Among UPR-related transcription factors, XBP1 upregulated Actn2, whereas XBP1, ATF4 and ATF6 downregulated Actn3 promoter activity. Chemical induction of ER stress increased Actn2 mRNA levels, but decreased those for Actn3. ER stress also decreased α-actinin-3 protein levels, whereas levels of α-actinin-2 were unchanged. The intracellular composition of muscle contraction-related proteins was altered under ER stress, in that expression of parvalbumin (a fast-twitch muscle-specific protein) and troponin I type 1 (skeletal, slow) was suppressed. siRNA-induced suppression of Actn3 mimicked the inhibitory effect of ER stress on parvalbumin levels. Thus, endogenous expression levels of α-actinin-3 can be altered by ER stress, which may modulate muscle performance and athletic aptitudes, particularly in humans who carry ACTN3 577R alleles."},"publication_date":"2020-05-25","publication_name":{"en":"Journal of Muscle Research and Cell Motility","ja":"Journal of Muscle Research and Cell Motility"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10974-020-09582-7"],"issn":["1573-2657"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:10, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115245","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32437400","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367803","label":"url"}],"paper_title":{"en":"Interferon regulatory factor 7 mediates obesity-associated MCP-1 transcription.","ja":"Interferon regulatory factor 7 mediates obesity-associated MCP-1 transcription."},"authors":{"en":[{"name":"Kuroda Masashi"},{"name":"Nishiguchi Misa"},{"name":"Ugawa Naho"},{"name":"Ishikawa Etsuko"},{"name":"Kawabata Yasuyo"},{"name":"Okamoto Saya"},{"name":"Sasaki Waka"},{"name":"Miyatake Yumiko"},{"name":"Sebe Mayu"},{"name":"Masumoto Saeko"},{"name":"Tsutsumi Rie"},{"name":"Harada Nagakatsu"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"黒田 雅士"},{"name":"西口 実佐"},{"name":"宇川 菜穂"},{"name":"石川 悦子"},{"name":"川端 康代"},{"name":"岡本 彩椰"},{"name":"佐々木 和佳"},{"name":"宮武 由実子"},{"name":"瀬部 真由"},{"name":"升本 早枝子"},{"name":"堤 理恵"},{"name":"原田 永勝"},{"name":"阪上 浩"}]},"description":{"en":"Hypertrophy, associated with adipocyte dysfunction, causes increased pro-inflammatory adipokine, and abnormal glucose and lipid metabolism, leading to insulin resistance and obesity-related-health problems. By combining DNA microarray and genomic data analyses to predict DNA binding motifs, we identified the transcription factor Interferon Regulatory Factor 7 (IRF7) as a possible regulator of genes related to adipocyte hypertrophy. To investigate the role of IRF7 in adipocytes, we examined gene expression patterns in 3T3-L1 cells infected with a retrovirus carrying the IRF7 gene and found that enforced IRF7 expression induced the expression of monocyte chemoattractant protein-1 (MCP-1), a key initial adipokine in the chronic inflammation of obesity. CRISPR/Cas9 mediated-suppression of IRF7 significantly reduced MCP-1 mRNA. Luciferase assays, chromatin immunoprecipitation PCR analysis and gel shift assay showed that IRF7 transactivates the MCP-1 gene by binding to its proximal Interferon Stimulation Response Element (ISRE), a putative IRF7 binding motif. IRF7 knockout mice exhibited lower expression of MCP-1 in epidydimal white adipose tissue under high-fat feeding conditions, suggesting the transcription factor is physiologically important for inducing MCP-1. Taken together, our results suggest that IRF7 transactivates MCP-1 mRNA in adipocytes, and it may be involved in the adipose tissue inflammation associated with obesity.","ja":"Hypertrophy, associated with adipocyte dysfunction, causes increased pro-inflammatory adipokine, and abnormal glucose and lipid metabolism, leading to insulin resistance and obesity-related-health problems. By combining DNA microarray and genomic data analyses to predict DNA binding motifs, we identified the transcription factor Interferon Regulatory Factor 7 (IRF7) as a possible regulator of genes related to adipocyte hypertrophy. To investigate the role of IRF7 in adipocytes, we examined gene expression patterns in 3T3-L1 cells infected with a retrovirus carrying the IRF7 gene and found that enforced IRF7 expression induced the expression of monocyte chemoattractant protein-1 (MCP-1), a key initial adipokine in the chronic inflammation of obesity. CRISPR/Cas9 mediated-suppression of IRF7 significantly reduced MCP-1 mRNA. Luciferase assays, chromatin immunoprecipitation PCR analysis and gel shift assay showed that IRF7 transactivates the MCP-1 gene by binding to its proximal Interferon Stimulation Response Element (ISRE), a putative IRF7 binding motif. IRF7 knockout mice exhibited lower expression of MCP-1 in epidydimal white adipose tissue under high-fat feeding conditions, suggesting the transcription factor is physiologically important for inducing MCP-1. Taken together, our results suggest that IRF7 transactivates MCP-1 mRNA in adipocytes, and it may be involved in the adipose tissue inflammation associated with obesity."},"publication_date":"2020-05-21","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.15","number":"No.5","starting_page":"e0233390","ending_page":"e0233390","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0233390"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:11, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32393635","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367802","label":"url"}],"paper_title":{"en":"The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B 4 axis","ja":"The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B 4 axis"},"authors":{"en":[{"name":"Hosooka Tetsuya"},{"name":"Hosokawa Yusei"},{"name":"Matsugi Kaku"},{"name":"Shinohara Masakazu"},{"name":"Senga Yoko"},{"name":"Tamori Yoshikazu"},{"name":"Aoki Chikako"},{"name":"Matsui Sho"},{"name":"Sasaki Tsutomu"},{"name":"Kitamura Tadahiro"},{"name":"Kuroda Masashi"},{"name":"Sakaue Hiroshi"},{"name":"Nomura Kazuhiro"},{"name":"Yoshino Kei"},{"name":"Nabatame Yuko"},{"name":"Itoh Yoshito"},{"name":"Yamaguchi Kanji"},{"name":"Hayashi Yoshitake"},{"name":"Nakae Jun"},{"name":"Accili Domenico"},{"name":"Yokomizo Takehiko"},{"name":"Seino Susumu"},{"name":"Kasuga Masato"},{"name":"Ogawa Wataru"}],"ja":[{"name":"Hosooka Tetsuya"},{"name":"Hosokawa Yusei"},{"name":"Matsugi Kaku"},{"name":"Shinohara Masakazu"},{"name":"Senga Yoko"},{"name":"Tamori Yoshikazu"},{"name":"Aoki Chikako"},{"name":"Matsui Sho"},{"name":"Sasaki Tsutomu"},{"name":"Kitamura Tadahiro"},{"name":"黒田 雅士"},{"name":"阪上 浩"},{"name":"Nomura Kazuhiro"},{"name":"Yoshino Kei"},{"name":"Nabatame Yuko"},{"name":"Itoh Yoshito"},{"name":"Yamaguchi Kanji"},{"name":"Hayashi Yoshitake"},{"name":"Nakae Jun"},{"name":"Accili Domenico"},{"name":"Yokomizo Takehiko"},{"name":"Seino Susumu"},{"name":"Kasuga Masato"},{"name":"Ogawa Wataru"}]},"description":{"en":"Although adipocytes are major targets of insulin, the influence of impaired insulin action in adipocytes on metabolic homeostasis remains unclear. We here show that adipocyte-specific PDK1 (3'-phosphoinositide-dependent kinase 1)-deficient (A-PDK1KO) mice manifest impaired metabolic actions of insulin in adipose tissue and reduction of adipose tissue mass. A-PDK1KO mice developed insulin resistance, glucose intolerance, and hepatic steatosis, and this phenotype was suppressed by additional ablation of FoxO1 specifically in adipocytes (A-PDK1/FoxO1KO mice) without an effect on adipose tissue mass. Neither circulating levels of adiponectin and leptin nor inflammatory markers in adipose tissue differed between A-PDK1KO and A-PDK1/FoxO1KO mice. Lipidomics and microarray analyses revealed that leukotriene B4 (LTB4) levels in plasma and in adipose tissue as well as the expression of 5-lipoxygenase (5-LO) in adipose tissue were increased and restored in A-PDK1KO mice and A-PDK1/FoxO1KO mice, respectively. Genetic deletion of the LTB4 receptor BLT1 as well as pharmacological intervention to 5-LO or BLT1 ameliorated insulin resistance in A-PDK1KO mice. Furthermore, insulin was found to inhibit LTB4 production through down-regulation of 5-LO expression via the PDK1-FoxO1 pathway in isolated adipocytes. Our results indicate that insulin signaling in adipocytes negatively regulates the production of LTB4 via the PDK1-FoxO1 pathway and thereby maintains systemic insulin sensitivity.","ja":"Although adipocytes are major targets of insulin, the influence of impaired insulin action in adipocytes on metabolic homeostasis remains unclear. We here show that adipocyte-specific PDK1 (3'-phosphoinositide-dependent kinase 1)-deficient (A-PDK1KO) mice manifest impaired metabolic actions of insulin in adipose tissue and reduction of adipose tissue mass. A-PDK1KO mice developed insulin resistance, glucose intolerance, and hepatic steatosis, and this phenotype was suppressed by additional ablation of FoxO1 specifically in adipocytes (A-PDK1/FoxO1KO mice) without an effect on adipose tissue mass. Neither circulating levels of adiponectin and leptin nor inflammatory markers in adipose tissue differed between A-PDK1KO and A-PDK1/FoxO1KO mice. Lipidomics and microarray analyses revealed that leukotriene B4 (LTB4) levels in plasma and in adipose tissue as well as the expression of 5-lipoxygenase (5-LO) in adipose tissue were increased and restored in A-PDK1KO mice and A-PDK1/FoxO1KO mice, respectively. Genetic deletion of the LTB4 receptor BLT1 as well as pharmacological intervention to 5-LO or BLT1 ameliorated insulin resistance in A-PDK1KO mice. Furthermore, insulin was found to inhibit LTB4 production through down-regulation of 5-LO expression via the PDK1-FoxO1 pathway in isolated adipocytes. Our results indicate that insulin signaling in adipocytes negatively regulates the production of LTB4 via the PDK1-FoxO1 pathway and thereby maintains systemic insulin sensitivity."},"publication_date":"2020-05-11","publication_name":{"en":"Proceedings of the National Academy of Sciences of the United States of America","ja":"Proceedings of the National Academy of Sciences of the United States of America"},"volume":"Vol.117","number":"No.21","starting_page":"11674","ending_page":"11684","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1073/pnas.1921015117"],"issn":["1091-6490"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:12, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32070490","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367800","label":"url"}],"paper_title":{"en":"DNA methylation status influences insulin-induced glucose transport in 3T3-L1 adipocytes by mediating p53 expression.","ja":"DNA methylation status influences insulin-induced glucose transport in 3T3-L1 adipocytes by mediating p53 expression."},"authors":{"en":[{"name":"Kuroda Masashi"},{"name":"Onoyama Rumi"},{"name":"Sasaki Waka"},{"name":"Sebe Mayu"},{"name":"Kitamura Tadahiro"},{"name":"Masumoto Saeko"},{"name":"Tsutsumi Rie"},{"name":"Harada Nagakatsu"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"黒田 雅士"},{"name":"小野山 瑠美"},{"name":"佐々木 和佳"},{"name":"瀬部 真由"},{"name":"Kitamura Tadahiro"},{"name":"升本 早枝子"},{"name":"堤 理恵"},{"name":"原田 永勝"},{"name":"阪上 浩"}]},"description":{"en":"Researchers frequently use 3T3-L1 adipocytes as a fat cell line, but the capacity of this line for insulin-mediated glucose transport is lower than that of primary isolated fat cells. In this study, we found that 5-azacytidine (5-aza-C), DNA methyltransferase 1 inhibitor, enhanced insulin-stimulated 2-deoxyglucose (2-DG) transport in 3T3-L1 cells after adipogenic differentiation. We next examined the expression of the genes related to glucose transport and insulin signal transduction. The insulin independent glucose transporter, glucose transporter 1 (GLUT1), showed lower expression in 5-aza-C pre-treated 3T3-L1 adipocytes, than in un-treated control adipocytes, while the expression of insulin dependent transporter GLUT4 remained unchanged. In addition, insulin receptor substrate-1 (IRS-1) was highly expressed in 5-aza-C pre-treated adipocytes. Based on DNA microarray and functional annotation analysis, we noticed that 5-aza-C pretreatment activated the tumor suppressor p53 pathway. We confirmed that in 5-aza-C adipocytes, p53 expression was markedly higher, and the methylation level of CpGs in its promoter region was lower than in un-treated control adipocytes. Moreover, pharmacological inhibition of p53 restored GLUT1 and IRS-1 expression to the same level as in un-treated 3T3-L1 adipocytes, and significantly decreased insulin-mediated 2-DG uptake. These results suggest that glucose transport capacity in adipocytes is influenced by DNA methylation status, and demethylation induced by 5-aza-C increased it possibly through the p53 signaling pathway.","ja":"Researchers frequently use 3T3-L1 adipocytes as a fat cell line, but the capacity of this line for insulin-mediated glucose transport is lower than that of primary isolated fat cells. In this study, we found that 5-azacytidine (5-aza-C), DNA methyltransferase 1 inhibitor, enhanced insulin-stimulated 2-deoxyglucose (2-DG) transport in 3T3-L1 cells after adipogenic differentiation. We next examined the expression of the genes related to glucose transport and insulin signal transduction. The insulin independent glucose transporter, glucose transporter 1 (GLUT1), showed lower expression in 5-aza-C pre-treated 3T3-L1 adipocytes, than in un-treated control adipocytes, while the expression of insulin dependent transporter GLUT4 remained unchanged. In addition, insulin receptor substrate-1 (IRS-1) was highly expressed in 5-aza-C pre-treated adipocytes. Based on DNA microarray and functional annotation analysis, we noticed that 5-aza-C pretreatment activated the tumor suppressor p53 pathway. We confirmed that in 5-aza-C adipocytes, p53 expression was markedly higher, and the methylation level of CpGs in its promoter region was lower than in un-treated control adipocytes. Moreover, pharmacological inhibition of p53 restored GLUT1 and IRS-1 expression to the same level as in un-treated 3T3-L1 adipocytes, and significantly decreased insulin-mediated 2-DG uptake. These results suggest that glucose transport capacity in adipocytes is influenced by DNA methylation status, and demethylation induced by 5-aza-C increased it possibly through the p53 signaling pathway."},"publication_date":"2020-02-16","publication_name":{"en":"Biochemical and Biophysical Research Communications","ja":"Biochemical and Biophysical Research Communications"},"volume":"Vol.525","number":"No.1","starting_page":"39","ending_page":"45","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbrc.2020.02.038"],"issn":["1090-2104"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:13, {"insert":{"user_id":"B000344297","type":"published_papers","id":"33414385"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114644","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32378597","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367801","label":"url"}],"paper_title":{"en":"Assessment of postoperative nutritional status and physical function between open surgical aortic valve replacement and transcatheter aortic valve implantation in elderly patients.","ja":"Assessment of postoperative nutritional status and physical function between open surgical aortic valve replacement and transcatheter aortic valve implantation in elderly patients."},"authors":{"en":[{"name":"Sebe Mayu"},{"name":"Tsutsumi Rie"},{"name":"Oyama Takuro"},{"name":"Horikawa Yousuke T"},{"name":"Uemura Yuta"},{"name":"Kakuta Nami"},{"name":"Sakai Yoko"},{"name":"Morio Atsushi"},{"name":"Miyoshi Hirotsugu"},{"name":"Kondo Takashi"},{"name":"Urabe Tomoaki"},{"name":"Noda Yuko"},{"name":"Kamiya Satoshi"},{"name":"Saeki Noboru"},{"name":"Kuroda Masashi"},{"name":"Tanaka Katsuya"},{"name":"Tsutsumi Yasuo"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"瀬部 真由"},{"name":"堤 理恵"},{"name":"大山 拓朗"},{"name":"Horikawa Yousuke T"},{"name":"植村 勇太"},{"name":"角田 奈美"},{"name":"酒井 陽子"},{"name":"Morio Atsushi"},{"name":"Miyoshi Hirotsugu"},{"name":"Kondo Takashi"},{"name":"Urabe Tomoaki"},{"name":"Noda Yuko"},{"name":"Kamiya Satoshi"},{"name":"Saeki Noboru"},{"name":"黒田 雅士"},{"name":"田中 克哉"},{"name":"堤 保夫"},{"name":"阪上 浩"}]},"description":{"en":"Background and aims : Severe aortic stenosis (AS) has been normally treated with surgical aortic valve replacement (AVR) whereas recently, transcatheter aortic valve implantation (TAVI) has been introduced as a minimally invasive operation for patients with high surgical risk and frailty. In this study, we have evaluated postoperative physical function and nutrition intake in the patients following AVR and TAVI. Methods : This prospective observational study involved 9 patients with surgical aortic valve replacement (AVR) and 7 patients with transcatheter aortic valve implantation (TAVI). Body composition was measured one day prior surgery, postoperative day (POD) 1, POD 3, POD 5 and POD 7. Hand grip strength, calf circumference and gait speed were measured one day before surgery and on the day of discharge. Results : Skeletal muscle was significantly decreased in AVR patients at postoperative day 3 and 7, while there was no change in TAVI patients. Patients with TAVI showed higher dietary intake after surgery compared to patients with AVR, and they maintained hand grip strength and calf circumference at discharge. Conclusions : In elderly patients with AS, TAVI can improve post-operative recovery maintaining nutritional status and physical function even. J. Med. Invest. 67 : 139-144, February, 2020.","ja":"Background and aims : Severe aortic stenosis (AS) has been normally treated with surgical aortic valve replacement (AVR) whereas recently, transcatheter aortic valve implantation (TAVI) has been introduced as a minimally invasive operation for patients with high surgical risk and frailty. In this study, we have evaluated postoperative physical function and nutrition intake in the patients following AVR and TAVI. Methods : This prospective observational study involved 9 patients with surgical aortic valve replacement (AVR) and 7 patients with transcatheter aortic valve implantation (TAVI). Body composition was measured one day prior surgery, postoperative day (POD) 1, POD 3, POD 5 and POD 7. Hand grip strength, calf circumference and gait speed were measured one day before surgery and on the day of discharge. Results : Skeletal muscle was significantly decreased in AVR patients at postoperative day 3 and 7, while there was no change in TAVI patients. Patients with TAVI showed higher dietary intake after surgery compared to patients with AVR, and they maintained hand grip strength and calf circumference at discharge. Conclusions : In elderly patients with AS, TAVI can improve post-operative recovery maintaining nutritional status and physical function even. J. Med. Invest. 67 : 139-144, February, 2020."},"publication_date":"2020","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.67","number":"No.1.2","starting_page":"139","ending_page":"144","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.67.139"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:14, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113365","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31656282","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85074168190&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=367799","label":"url"}],"paper_title":{"en":"Effect of olive oil consumption on aging in a senescence-accelerated mice-prone 8 (SAMP8) model.","ja":"Effect of olive oil consumption on aging in a senescence-accelerated mice-prone 8 (SAMP8) model."},"authors":{"en":[{"name":"Bando Masahiro"},{"name":"Masumoto Saeko"},{"name":"Kuroda Masashi"},{"name":"Tsutsumi Rie"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"板東 正浩"},{"name":"升本 早枝子"},{"name":"黒田 雅士"},{"name":"堤 理恵"},{"name":"阪上 浩"}]},"description":{"en":"Background : Mediterranean diets have been linked to a reduced risk of cancer, vascular illnesses, Parkinson's and Alzheimer's disease. Olive oil is the primary fat source in the Mediterranean diet ; however, only a few studies have investigated the effect of olive oil on aging. In the present study, we aimed to determine whether consumption of olive oil significantly influences aging and memory in senescence-accelerated mouse-prone 8 (SAMP8). Methods : SAMP8 and senescence-accelerated mouse resistant 1 (SAMR1) mice were fed either 7% soy oil or 1% olive oil and 6% soy oil during a six-month study period. Reduction in memory in passive avoidance learning was examined after two months from the initiation of the experiment. Results : The weight of organs including the liver, kidney, spleen, and fat tissue changed significantly and memory performance was reduced in SAMP8 than in SAMR1 mice. There were no significant differences in SAMP8 and SAMR1 mice; however, blood triglyceride level decreased significantly in SAMP8 mice fed on olive oil. Conclusions : These results suggest that consuming olive oil may not have a protective role in aging and memory recall, but beneficial effects may be related to improvement in lipid metabolism. J. Med. Invest. 66 : 241-247, August, 2019.","ja":"Background : Mediterranean diets have been linked to a reduced risk of cancer, vascular illnesses, Parkinson's and Alzheimer's disease. Olive oil is the primary fat source in the Mediterranean diet ; however, only a few studies have investigated the effect of olive oil on aging. In the present study, we aimed to determine whether consumption of olive oil significantly influences aging and memory in senescence-accelerated mouse-prone 8 (SAMP8). Methods : SAMP8 and senescence-accelerated mouse resistant 1 (SAMR1) mice were fed either 7% soy oil or 1% olive oil and 6% soy oil during a six-month study period. Reduction in memory in passive avoidance learning was examined after two months from the initiation of the experiment. Results : The weight of organs including the liver, kidney, spleen, and fat tissue changed significantly and memory performance was reduced in SAMP8 than in SAMR1 mice. There were no significant differences in SAMP8 and SAMR1 mice; however, blood triglyceride level decreased significantly in SAMP8 mice fed on olive oil. Conclusions : These results suggest that consuming olive oil may not have a protective role in aging and memory recall, but beneficial effects may be related to improvement in lipid metabolism. J. Med. Invest. 66 : 241-247, August, 2019."},"publication_date":"2019","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.66","number":"No.3.4","starting_page":"241","ending_page":"247","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.66.241"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:15, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://repo.lib.tokushima-u.ac.jp/113717","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282763059771520/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=359327","label":"url"}],"paper_title":{"en":"Management of dysgeusia and dysosmia caused by chemotherapy","ja":"化学療法に伴う味覚・嗅覚障害への対応 (特集 化学療法時の栄養管理)"},"authors":{"en":[{"name":"Tsutsumi Rie"},{"name":"瀬部 真由"},{"name":"別府 香名"},{"name":"渡辺 涼乃"},{"name":"尾平 優"},{"name":"Kuroda Masashi"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"堤 理恵"},{"name":"瀬部 真由"},{"name":"別府 香名"},{"name":"渡辺 涼乃"},{"name":"尾平 優"},{"name":"黒田 雅士"},{"name":"阪上 浩"}]},"description":{"en":"<p>がんの化学療法中に味覚・嗅覚障害は頻繁に生じ，患者のquality of life(以下，QOLと略)だけでなく，体重低下や栄養状態の悪化を引き起こす深刻な副作用である．しかしながらこれまで確立された治療法や予防策はなく，食事内容や形態の工夫が主な対処法であった．味覚障害は薬剤による亜鉛のキレート化が原因であるとされているが，これに加えて味覚受容体遺伝子の発現変化や口腔粘膜障害の影響も報告されている．本稿では，化学療法中に生じる味覚・嗅覚障害の実態とともに，これに対する栄養的なアプローチを紹介する．</p>","ja":"<p>がんの化学療法中に味覚・嗅覚障害は頻繁に生じ，患者のquality of life(以下，QOLと略)だけでなく，体重低下や栄養状態の悪化を引き起こす深刻な副作用である．しかしながらこれまで確立された治療法や予防策はなく，食事内容や形態の工夫が主な対処法であった．味覚障害は薬剤による亜鉛のキレート化が原因であるとされているが，これに加えて味覚受容体遺伝子の発現変化や口腔粘膜障害の影響も報告されている．本稿では，化学療法中に生じる味覚・嗅覚障害の実態とともに，これに対する栄養的なアプローチを紹介する．</p>"},"publication_date":"2018-09","publication_name":{"en":"The Journal of Japanese Society for Parenteral and Enteral Nutrition","ja":"日本静脈経腸栄養学会雑誌"},"volume":"Vol.33","number":"No.4","starting_page":"1019","ending_page":"1024","languages":["jpn"],"referee":true,"identifiers":{"doi":["10.11244/jspen.33.1019"],"issn":["2189-0161"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:16, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29857001","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=354246","label":"url"}],"paper_title":{"en":"Readthrough of ACTN3 577X nonsense mutation produces full-length α-actinin-3 protein.","ja":"Readthrough of ACTN3 577X nonsense mutation produces full-length α-actinin-3 protein."},"authors":{"en":[{"name":"Harada Nagakatsu"},{"name":"Hatakeyama Adzumi"},{"name":"Okuyama Maiko"},{"name":"Miyatake Yumiko"},{"name":"Nakagawa Tadahiko"},{"name":"Kuroda Masashi"},{"name":"Masumoto Saeko"},{"name":"Tsutsumi Rie"},{"name":"Nakaya Yutaka"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"原田 永勝"},{"name":"畠山 あづみ"},{"name":"奥山 舞子"},{"name":"宮武 由実子"},{"name":"中川 忠彦"},{"name":"黒田 雅士"},{"name":"升本 早枝子"},{"name":"堤 理恵"},{"name":"中屋 豊"},{"name":"阪上 浩"}]},"description":{"en":"expression and thereby induced production of full-length α-actinin-3 protein in the presence of aminoglycoside. Together these results indicate that the ACTN3 R577X polymorphism could be a novel target for readthrough therapy, which may affect athletic and muscle performance in humans.","ja":", respectively) and transfected the constructs into HEK293 cells. Similar constructs for the ACTN3 577R gene were used as controls. HEK293 cells carrying the X gene, but not the X"},"publication_date":"2018-05-30","publication_name":{"en":"Biochemical and Biophysical Research Communications","ja":"Biochemical and Biophysical Research Communications"},"volume":"Vol.502","number":"No.3","starting_page":"422","ending_page":"428","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbrc.2018.05.193"],"issn":["1090-2104"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:17, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112232","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30282855","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=355562","label":"url"}],"paper_title":{"en":"Effect of Janus kinase inhibition by tofacitinib on body composition and glucose metabolism.","ja":"Effect of Janus kinase inhibition by tofacitinib on body composition and glucose metabolism."},"authors":{"en":[{"name":"Momoko Chikugo"},{"name":"Mayu Sebe"},{"name":"Tsutsumi Rie"},{"name":"Marina Iuchi"},{"name":"Kishi Jun"},{"name":"Kuroda Masashi"},{"name":"Harada Nagakatsu"},{"name":"Nishioka Yasuhiko"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"筑後 桃子"},{"name":"瀬部 真由"},{"name":"堤 理恵"},{"name":"井内 茉莉奈"},{"name":"岸 潤"},{"name":"黒田 雅士"},{"name":"原田 永勝"},{"name":"西岡 安彦"},{"name":"阪上 浩"}]},"description":{"en":"Tofacitinib is the first Janus Kinase (JAK) inhibitor to treat moderately to severely active RA. In this study, we investigated whether the effect of tofacitinib have any effects on body composition in mice and female patients with RA. Female C57BL/6 mice fed with a high-fat diet were treated with 30 mg/kg/day tofacitinib or vehicle for 70 days. Following treatment, trunk muscle, subcutaneous fat, and visceral fats were measured using X-ray computed tomography CT scan. Glucose tolerance and insulin sensitivity were assessed. In female RA patients treated with biological disease modified anti-rheumatic-drugs (biological DMARDs) or tofacitinib (n=4 per group), we also evaluated the body composition after 3 months from the start of treatment initiation using bioelectrical impedance analysis. Treatment with tofacitinib did not affect the body weight, and body composition in C57BL/6 mice. It also did not affect glucose, and insulin tolerance in mice. In patients with RA, treatment with biological DMARDs did not affect the body composition whereas the muscle mass was unchanged after receiving tofacitinib and the fat mass was significantly increased. J. Med. Invest. 65:166-170, August, 2018.","ja":"Tofacitinib is the first Janus Kinase (JAK) inhibitor to treat moderately to severely active RA. In this study, we investigated whether the effect of tofacitinib have any effects on body composition in mice and female patients with RA. Female C57BL/6 mice fed with a high-fat diet were treated with 30 mg/kg/day tofacitinib or vehicle for 70 days. Following treatment, trunk muscle, subcutaneous fat, and visceral fats were measured using X-ray computed tomography CT scan. Glucose tolerance and insulin sensitivity were assessed. In female RA patients treated with biological disease modified anti-rheumatic-drugs (biological DMARDs) or tofacitinib (n=4 per group), we also evaluated the body composition after 3 months from the start of treatment initiation using bioelectrical impedance analysis. Treatment with tofacitinib did not affect the body weight, and body composition in C57BL/6 mice. It also did not affect glucose, and insulin tolerance in mice. In patients with RA, treatment with biological DMARDs did not affect the body composition whereas the muscle mass was unchanged after receiving tofacitinib and the fat mass was significantly increased. J. Med. Invest. 65:166-170, August, 2018."},"publication_date":"2018","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.65","number":"No.3.4","starting_page":"166","ending_page":"170","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.65.166"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:18, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28383761","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=332553","label":"url"}],"paper_title":{"en":"Endoplasmic Reticulum Stress in Mice Increases Hepatic Expression of Genes Carrying a Premature Termination Codon via a Nutritional Status-Independent GRP78-Dependent Mechanism.","ja":"Endoplasmic Reticulum Stress in Mice Increases Hepatic Expression of Genes Carrying a Premature Termination Codon via a Nutritional Status-Independent GRP78-Dependent Mechanism."},"authors":{"en":[{"name":"Harada Nagakatsu"},{"name":"Okuyama Maiko"},{"name":"Yoshikatsu Aya"},{"name":"Yamamoto Hironori"},{"name":"Ishiwata Saori"},{"name":"Hamada Chikako"},{"name":"Hirose Tomoyo"},{"name":"Shono Masayuki"},{"name":"Kuroda Masashi"},{"name":"Tsutsumi Rie"},{"name":"Takeo Jiro"},{"name":"Taketani Yutaka"},{"name":"Nakaya Yutaka"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"原田 永勝"},{"name":"Okuyama Maiko"},{"name":"Yoshikatsu Aya"},{"name":"Yamamoto Hironori"},{"name":"Ishiwata Saori"},{"name":"Hamada Chikako"},{"name":"Hirose Tomoyo"},{"name":"Shono Masayuki"},{"name":"黒田 雅士"},{"name":"堤 理恵"},{"name":"Takeo Jiro"},{"name":"竹谷 豊"},{"name":"中屋 豊"},{"name":"阪上 浩"}]},"publication_date":"2017-11","publication_name":{"en":"Journal of Cellular Biochemistry","ja":"Journal of Cellular Biochemistry"},"volume":"Vol.118","number":"No.11","starting_page":"3810","ending_page":"3824","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/jcb.26031"],"issn":["1097-4644"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:19, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114340","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28644884","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=329734","label":"url"}],"paper_title":{"en":"Ligand-induced rapid skeletal muscle atrophy in HSA-Fv2E-PERK transgenic mice.","ja":"Ligand-induced rapid skeletal muscle atrophy in HSA-Fv2E-PERK transgenic mice."},"authors":{"en":[{"name":"Miyake Masato"},{"name":"Kuroda Masashi"},{"name":"Kiyonari Hiroshi"},{"name":"Takehana Kenji"},{"name":"Hisanaga Satoshi"},{"name":"Morimoto Masatoshi"},{"name":"Zhang Jun"},{"name":"Oyadomari Miho"},{"name":"Sakaue Hiroshi"},{"name":"Oyadomari Seiichi"}],"ja":[{"name":"三宅 雅人"},{"name":"黒田 雅士"},{"name":"Kiyonari Hiroshi"},{"name":"Takehana Kenji"},{"name":"久永 哲"},{"name":"森本 雅俊"},{"name":"Zhang Jun"},{"name":"親泊 美帆"},{"name":"阪上 浩"},{"name":"親泊 政一"}]},"description":{"en":"As a novel model of muscle wasting, HSA-Fv2E-PERK Tg mice provide a convenient tool for studying the pathogenesis of muscle loss and for assessing putative therapeutics.","ja":"As a novel model of muscle wasting, HSA-Fv2E-PERK Tg mice provide a convenient tool for studying the pathogenesis of muscle loss and for assessing putative therapeutics."},"publication_date":"2017-06-23","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.12","number":"No.6","starting_page":"e0179955","ending_page":"e0179955","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0179955"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:20, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113364","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27825986","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84995961350&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=356781","label":"url"}],"paper_title":{"en":"Intracerebroventricular injection of ghrelin decreases wheel running activity in rats.","ja":"Intracerebroventricular injection of ghrelin decreases wheel running activity in rats."},"authors":{"en":[{"name":"Miyatake Yumiko"},{"name":"Shiuchi Tetsuya"},{"name":"Mawatari Kazuaki"},{"name":"Toda Satomi"},{"name":"Taniguchi Yasuko"},{"name":"Futami Akari"},{"name":"Sato Fukiko"},{"name":"Kuroda Masashi"},{"name":"Sebe Mayu"},{"name":"Tsutsumi Rie"},{"name":"Harada Nagakatsu"},{"name":"Minokoshi Yasuhiko"},{"name":"Kitamura Tadahiro"},{"name":"Gotoh Koro"},{"name":"Ueno Masaki"},{"name":"Nakaya Yutaka"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"Miyatake Yumiko"},{"name":"志内 哲也"},{"name":"馬渡 一諭"},{"name":"Toda Satomi"},{"name":"Taniguchi Yasuko"},{"name":"Futami Akari"},{"name":"Sato Fukiko"},{"name":"黒田 雅士"},{"name":"Sebe Mayu"},{"name":"堤 理恵"},{"name":"原田 永勝"},{"name":"Minokoshi Yasuhiko"},{"name":"Kitamura Tadahiro"},{"name":"Gotoh Koro"},{"name":"Ueno Masaki"},{"name":"中屋 豊"},{"name":"阪上 浩"}]},"description":{"en":"There is an increasing interest in elucidating the molecular mechanisms by which voluntary exercise is regulated. In this study, we examined how the central nervous system regulates exercise. We used SPORTS rats, which were established in our laboratory as a highly voluntary murine exercise model. SPORTS rats showed lower levels of serum ghrelin compared with those of the parental line of Wistar rats. Intracerebroventricular and intraperitoneal injection of ghrelin decreased wheel-running activity in SPORTS rats. In addition, daily injection of the ghrelin inhibitor JMV3002 into the lateral ventricles of Wistar rats increased wheel-running activity. Co-administration of obestatin inhibited ghrelin-induced increases in food intake but did not inhibit ghrelin-induced suppression of voluntary exercise in rats. Growth hormone secretagogue receptor (GHSR) in the hypothalamus and hippocampus of SPORTS rats was not difference that in control rats. We created an arcuate nucleus destruction model by administering monosodium glutamate (MSG) to neonatal SPORTS rats. Injection of ghrelin into MSG-treated rats decreased voluntary exercise but did not increase food intake, suggesting that wheel-running activity is not controlled by the arcuate nucleus neurons that regulate feeding. These results provide new insights into the mechanism by which ghrelin regulates voluntary activity independent of arcuate nucleus neurons.","ja":"There is an increasing interest in elucidating the molecular mechanisms by which voluntary exercise is regulated. In this study, we examined how the central nervous system regulates exercise. We used SPORTS rats, which were established in our laboratory as a highly voluntary murine exercise model. SPORTS rats showed lower levels of serum ghrelin compared with those of the parental line of Wistar rats. Intracerebroventricular and intraperitoneal injection of ghrelin decreased wheel-running activity in SPORTS rats. In addition, daily injection of the ghrelin inhibitor JMV3002 into the lateral ventricles of Wistar rats increased wheel-running activity. Co-administration of obestatin inhibited ghrelin-induced increases in food intake but did not inhibit ghrelin-induced suppression of voluntary exercise in rats. Growth hormone secretagogue receptor (GHSR) in the hypothalamus and hippocampus of SPORTS rats was not difference that in control rats. We created an arcuate nucleus destruction model by administering monosodium glutamate (MSG) to neonatal SPORTS rats. Injection of ghrelin into MSG-treated rats decreased voluntary exercise but did not increase food intake, suggesting that wheel-running activity is not controlled by the arcuate nucleus neurons that regulate feeding. These results provide new insights into the mechanism by which ghrelin regulates voluntary activity independent of arcuate nucleus neurons."},"publication_date":"2017-01-05","publication_name":{"en":"Peptides","ja":"Peptides"},"volume":"Vol.87","starting_page":"12","ending_page":"19","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.peptides.2016.11.005"],"issn":["1873-5169"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:21, {"insert":{"user_id":"B000344297","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/110107","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27494408","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=356784","label":"url"}],"paper_title":{"en":"DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes.","ja":"DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes."},"authors":{"en":[{"name":"Kuroda Masashi"},{"name":"Tominaga Ayako"},{"name":"Nakagawa Kasumi"},{"name":"Nishiguchi Misa"},{"name":"Sebe Mayu"},{"name":"Miyatake Yumiko"},{"name":"Kitamura Tadahiro"},{"name":"Tsutsumi Rie"},{"name":"Harada Nagakatsu"},{"name":"Nakaya Yutaka"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"黒田 雅士"},{"name":"Tominaga Ayako"},{"name":"Nakagawa Kasumi"},{"name":"Nishiguchi Misa"},{"name":"Sebe Mayu"},{"name":"Miyatake Yumiko"},{"name":"Kitamura Tadahiro"},{"name":"Tsutsumi Rie"},{"name":"Harada Nagakatsu"},{"name":"Nakaya Yutaka"},{"name":"阪上 浩"}]},"description":{"en":"Leptin is a key regulator of energy intake and expenditure. This peptide hormone is expressed in mouse white adipose tissue, but hardly expressed in 3T3-L1 adipocytes. Using bisulfite sequencing, we found that CpG islands in the leptin promoter are highly methylated in 3T3-L1cells. 5-azacytidine, an inhibitor of DNA methyltransferase, markedly increased leptin expression as pre-adipocytes matured into adipocytes. Remarkably, leptin expression was stimulated by insulin in adipocytes derived from precursor cells exposed to 5-azacytidine, but suppressed by thiazolidinedione and dexamethasone. In contrast, adipocytes derived from untreated precursor cells were unresponsive to both 5-azacytidine and hormonal stimuli, although lipid accumulation was sufficient to boost leptin expression in the absence of demethylation. Taken together, the results suggest that leptin expression in 3T3-L1 cells requires DNA demethylation prior to adipogenesis, transcriptional activation during adipogenesis, and lipid accumulation after adipogenesis.","ja":"Leptin is a key regulator of energy intake and expenditure. This peptide hormone is expressed in mouse white adipose tissue, but hardly expressed in 3T3-L1 adipocytes. Using bisulfite sequencing, we found that CpG islands in the leptin promoter are highly methylated in 3T3-L1cells. 5-azacytidine, an inhibitor of DNA methyltransferase, markedly increased leptin expression as pre-adipocytes matured into adipocytes. Remarkably, leptin expression was stimulated by insulin in adipocytes derived from precursor cells exposed to 5-azacytidine, but suppressed by thiazolidinedione and dexamethasone. In contrast, adipocytes derived from untreated precursor cells were unresponsive to both 5-azacytidine and hormonal stimuli, although lipid accumulation was sufficient to boost leptin expression in the absence of demethylation. Taken together, the results suggest that leptin expression in 3T3-L1 cells requires DNA demethylation prior to adipogenesis, transcriptional activation during adipogenesis, and lipid accumulation after adipogenesis."},"publication_date":"2016-08-05","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.11","number":"No.8","starting_page":"e0160532","ending_page":"e0160532","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0160532"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:22, {"insert":{"user_id":"B000344297","type":"published_papers","id":"33489727"},"force":{"see_also":[{"@id":"http://search.jamas.or.jp/link/ui/2020348007","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1523669556040598272/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=381373","label":"url"}],"paper_title":{"en":"認知症超早期発見チェックシート(Q-ESD)と老研式活動能力指標(TMIG-IC)との相関性の検討","ja":"認知症超早期発見チェックシート(Q-ESD)と老研式活動能力指標(TMIG-IC)との相関性の検討"},"authors":{"en":[{"name":"徳里 望"},{"name":"Sakaue Hiroshi"},{"name":"Tsutsumi Rie"},{"name":"Kuroda Masashi"},{"name":"Masumoto Saeko"},{"name":"黒井 俊哉"},{"name":"植木 歩夢"},{"name":"Tsutsumi Rie"},{"name":"Sakaue Hiroshi"},{"name":"小瀧 歩"},{"name":"工藤 千秋"}],"ja":[{"name":"徳里 望"},{"name":"阪上 浩"},{"name":"堤 理恵"},{"name":"黒田 雅士"},{"name":"升本 早枝子"},{"name":"黒井 俊哉"},{"name":"植木 歩夢"},{"name":"堤 理恵"},{"name":"阪上 浩"},{"name":"小瀧 歩"},{"name":"工藤 千秋"}]},"description":{"en":"目的:急速な高齢化において認知症の早期発見・早期予防が重要であるが，プレクリニカル期における簡易的に検出可能なスクリーニング方法は開発されていない．今回，我々は，認知機能低下と関係の深い日常生活の変化を捉えるべく，認知症の超早期段階における発見チェックシート;The Questionnaires for Earlier Stage of Dementia(Q-ESD)を開発した．認知症と診断されていない高齢者を対象としてQ-ESDを実施し，その有用性に関して老研式活動能力指標との関連性を比較・検討した．対象と方法:全国13施設において，認知症簡易スクリーニング法TOP-Qスコアが1点以下の認知機能低下を認めない高齢者に対し，導入時と4ヵ月後にQ-ESDと老研式活動能力指標の調査をした．結果:対象者134名(男/女=25/109)の平均年齢は75.2±12.0歳，平均Q-ESDスコアは25.0±7.0点であった．Q-ESDと老研式活動能力指標の合計スコアに負の相関(P<0.05)がみられた．Q-ESDの改善・維持群，悪化群では初回調査時の手段的，知的，社会的ADLが有意に低値であった(p<0.05)．結論:Q-ESDは生活機能の低下を早期に検出し，Q-ESDのスコアの高値は将来の認知症発症の予備軍となり得る可能性が示唆された．(著者抄録)","ja":"目的:急速な高齢化において認知症の早期発見・早期予防が重要であるが，プレクリニカル期における簡易的に検出可能なスクリーニング方法は開発されていない．今回，我々は，認知機能低下と関係の深い日常生活の変化を捉えるべく，認知症の超早期段階における発見チェックシート;The Questionnaires for Earlier Stage of Dementia(Q-ESD)を開発した．認知症と診断されていない高齢者を対象としてQ-ESDを実施し，その有用性に関して老研式活動能力指標との関連性を比較・検討した．対象と方法:全国13施設において，認知症簡易スクリーニング法TOP-Qスコアが1点以下の認知機能低下を認めない高齢者に対し，導入時と4ヵ月後にQ-ESDと老研式活動能力指標の調査をした．結果:対象者134名(男/女=25/109)の平均年齢は75.2±12.0歳，平均Q-ESDスコアは25.0±7.0点であった．Q-ESDと老研式活動能力指標の合計スコアに負の相関(P<0.05)がみられた．Q-ESDの改善・維持群，悪化群では初回調査時の手段的，知的，社会的ADLが有意に低値であった(p<0.05)．結論:Q-ESDは生活機能の低下を早期に検出し，Q-ESDのスコアの高値は将来の認知症発症の予備軍となり得る可能性が示唆された．(著者抄録)"},"publication_date":"2020-06","publication_name":{"en":"The Journal of Japan Society for Early Stage of Dementia","ja":"日本早期認知症学会誌"},"volume":"Vol.13","number":"No.1","starting_page":"42","ending_page":"48","languages":["jpn"],"identifiers":{"issn":["2187-3402"]},"published_paper_type":"research_institution"},"priority":"input_data"}
==== end registerFile(/WWW/pub2/data/ERD/person/323761/researchmap/published_papers.jsonl, V5DuEY8BzHGxATo5YCY5) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/323761/researchmap/misc.jsonl) ====
line:1, {"insert":{"user_id":"B000344297","type":"misc","id":"39637303"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=389316","label":"url"}],"paper_title":{"en":"【脂肪細胞・アディポサイトカインと糖尿病】脂肪細胞と糖尿病 褐色脂肪細胞と糖尿病","ja":"【脂肪細胞・アディポサイトカインと糖尿病】脂肪細胞と糖尿病 褐色脂肪細胞と糖尿病"},"authors":{"en":[{"name":"Kuroda Masashi"},{"name":"Tsutsumi Rie"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"黒田 雅士"},{"name":"堤 理恵"},{"name":"阪上 浩"}]},"publication_date":"2022-01","publication_name":{"en":"月刊糖尿病","ja":"月刊糖尿病"},"volume":"Vol.14","number":"No.1","starting_page":"28","ending_page":"34","languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"B000344297","type":"misc","id":"33414386"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=380326","label":"url"}],"paper_title":{"en":"脂肪細胞分化に対するエピジェネティック制御機構","ja":"脂肪細胞分化に対するエピジェネティック制御機構"},"authors":{"en":[{"name":"Kuroda Masashi"},{"name":"Tsutsumi Rie"},{"name":"Sakaue Hiroshi"}],"ja":[{"name":"黒田 雅士"},{"name":"堤 理恵"},{"name":"阪上 浩"}]},"publication_date":"2021-03-20","publication_name":{"en":"実験医学増刊","ja":"実験医学増刊"},"volume":"Vol.39","number":"No.5","starting_page":"32","ending_page":"38","languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
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