徳島大学 / 教育研究者総覧 --- 黒田雅士

個人のホームページ

https://researchmap.jp/kuroda-masashi (researchmap)

専門分野

○	ライフサイエンス (Life sciences) [栄養学、健康科学 (Nutrition and health science)]

研究テーマ

著書・論文

学術論文(審査論文):

1.	阪上浩, 黒田雅士, 堤理恵 : 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, 四国医学雑誌, Vol.78, No.1-2, 3-8, 2022年. (要約) 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. (キーワード) The elderly / 肥満症 (obesity) / 生活習慣病 (lifestyle-related disease) / 栄養 (nutrition) / High protein diet (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050010997647006592 (CiNii: 1050010997647006592)
2.	Kana Beppu, Rie Tsutsumi, Satoshi Ansai, Nana Ochiai, Mai Terakawa, Marie Mori, Masashi Kuroda, Kazuki Horikawa, Takumi Tomoi, Joe Sakamoto, Yasuhiro Kamei, Kiyoshi Naruse and Hiroshi Sakaue : Development of a screening system for agents that modulate taste receptor expression with the CRISPR-Cas9 system in medaka., Biochemical and Biophysical Research Communications, Vol.601, 65-72, 2022. (要約) 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. (キーワード) Animals / CRISPR-Cas Systems / Dysgeusia / 遺伝子発現 (gene expression) / Green Fluorescent Proteins / Oryzias / 生活の質 (quality of life) / Taste (徳島大学機関リポジトリ) ● Metadata: 116998 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2022.02.082 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35228123 ● Search Scopus @ Elsevier (PMID): 35228123 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2022.02.082 (徳島大学機関リポジトリ: 116998, DOI: 10.1016/j.bbrc.2022.02.082, PubMed: 35228123)
3.	堤理恵, 三島優奈, 川上歩花, 黒田雅士, 阪上浩 : 生活習慣病と栄養学 : 最近のトピックスを交えて, 四国医学雑誌, Vol.77, No.5-6, 187-192, 2021年. (要約) 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. (キーワード) 栄養 (nutrition) / metabolic syndrome / low carbohydrate / タンパク質 (protein) (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050292251404941184 (CiNii: 1050292251404941184)
4.	Atsushi Morio, Rie Tsutsumi, Shiho Satomi, Takashi Kondo, Hirotsugu Miyoshi, Takahiro Kato, Masashi Kuroda, Tadahiro Kitamura, Kenta Hara, Noboru Saeki, Hiroshi Sakaue and Yasuo M. Tsutsumi : Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model., Diabetology & Metabolic Syndrome, Vol.13, No.1, 2021. (要約) 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 (徳島大学機関リポジトリ) ● Metadata: 117442 (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s13098-021-00755-z (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34801078 ● Search Scopus @ Elsevier (PMID): 34801078 ● Search Scopus @ Elsevier (DOI): 10.1186/s13098-021-00755-z (徳島大学機関リポジトリ: 117442, DOI: 10.1186/s13098-021-00755-z, PubMed: 34801078)
5.	Rie Tsutsumi, Yuki Yamasaki, Jiro Takeo, Hiroko Miyahara, Mayu Sebe, Masahiro Bando, Yousuke Tanba, Yuna Mishima, Kana Takeji, Nanako Ueshima, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada, Daiju Fukuda, Ryoko Yoshimoto, Yasuo M. Tsutsumi, Ken-ichi Aihara, Masataka Sata and Hiroshi Sakaue : Long-chain monounsaturated fatty acids improve endothelial function with altering microbial flora, Translational Research : The Journal of Laboratory and Clinical Medicine, Vol.237, 16-30, 2021. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 116689 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.trsl.2021.03.016 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33775867 ● Summary page in Scopus @ Elsevier: 2-s2.0-85114290883 (徳島大学機関リポジトリ: 116689, DOI: 10.1016/j.trsl.2021.03.016, PubMed: 33775867, Elsevier: Scopus)
6.	Atsushi Morio, Rie Tsutsumi, Takashi Kondo, Hirotsugu Miyoshi, Takahiro Kato, Soshi Narasaki, Shiho Satomi, Erika Nakaya, Masashi Kuroda, Hiroshi Sakaue, Tadahiro Kitamura and Yasuo M. Tsutsumi : Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling., Nutrition, Metabolism, and Cardiovascular Diseases : NMCD, 2021. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.numecd.2021.06.025 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34362635 ● Search Scopus @ Elsevier (PMID): 34362635 ● Search Scopus @ Elsevier (DOI): 10.1016/j.numecd.2021.06.025 (DOI: 10.1016/j.numecd.2021.06.025, PubMed: 34362635)
7.	Yuko Okamatsu-Ogura, Masashi Kuroda, Rie Tsutsumi, Ayumi Tsubota, Masayuki Saito, Kazuhiro Kimura and Hiroshi Sakaue : UCP1-dependent and UCP1-independent metabolic changes induced by acute cold exposure in brown adipose tissue of mice., Metabolism: Clinical and Experimental, Vol.113, 154396, 2020. (要約) 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. (キーワード) 褐色脂肪組織 (brown adipose tissue) / Animals / Cold Temperature / 脂肪酸β酸化 (fatty acids β-oxidation) / Glutamine / メタボロミクス (metabolomics) / ノックアウトマウス (knockout mice) / Mice, Inbred C57BL / ノックアウトマウス (knockout mice) / Thermogenesis / Triglycerides / Uncoupling Protein 1 (徳島大学機関リポジトリ) ● Metadata: 116598 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.metabol.2020.154396 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33065161 ● Search Scopus @ Elsevier (PMID): 33065161 ● Search Scopus @ Elsevier (DOI): 10.1016/j.metabol.2020.154396 (徳島大学機関リポジトリ: 116598, DOI: 10.1016/j.metabol.2020.154396, PubMed: 33065161)
8.	Yumiko Miyatake, Yuna Mishima, Rie Tsutsumi, Tamaki Otani, Naoya Suemasa, Saeko Masumoto, Masashi Kuroda and Hiroshi Sakaue : Assessment of insulin resistance in the skeletal muscle of mice using positron emission tomography/computed tomography imaging., Biochemical and Biophysical Research Communications, Vol.528, No.3, 499-505, 2020. (要約) 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 [ (徳島大学機関リポジトリ) ● Metadata: 118304 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2020.05.165 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32513534 ● Search Scopus @ Elsevier (PMID): 32513534 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2020.05.165 (徳島大学機関リポジトリ: 118304, DOI: 10.1016/j.bbrc.2020.05.165, PubMed: 32513534)
9.	Nagakatsu Harada, Yuka Gotoda, Adzumi Hatakeyama, Tadahiko Nakagawa, Yumiko Miyatake, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue : Differential regulation of Actn2 and Actn3 expression during unfolded protein response in C2C12 myotubes., Journal of Muscle Research and Cell Motility, 2020. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s10974-020-09582-7 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32451822 ● Search Scopus @ Elsevier (PMID): 32451822 ● Search Scopus @ Elsevier (DOI): 10.1007/s10974-020-09582-7 (DOI: 10.1007/s10974-020-09582-7, PubMed: 32451822)
10.	Masashi Kuroda, Misa Nishiguchi, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Saya Okamoto, Waka Sasaki, Yumiko Miyatake, Mayu Sebe, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : Interferon regulatory factor 7 mediates obesity-associated MCP-1 transcription., PLoS ONE, Vol.15, No.5, e0233390, 2020. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 115245 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0233390 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32437400 ● Search Scopus @ Elsevier (PMID): 32437400 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0233390 (徳島大学機関リポジトリ: 115245, DOI: 10.1371/journal.pone.0233390, PubMed: 32437400)
11.	Tetsuya Hosooka, Yusei Hosokawa, Kaku Matsugi, Masakazu Shinohara, Yoko Senga, Yoshikazu Tamori, Chikako Aoki, Sho Matsui, Tsutomu Sasaki, Tadahiro Kitamura, Masashi Kuroda, Hiroshi Sakaue, Kazuhiro Nomura, Kei Yoshino, Yuko Nabatame, Yoshito Itoh, Kanji Yamaguchi, Yoshitake Hayashi, Jun Nakae, Domenico Accili, Takehiko Yokomizo, Susumu Seino, Masato Kasuga and Wataru Ogawa : The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B 4 axis, Proceedings of the National Academy of Sciences of the United States of America, Vol.117, No.21, 11674-11684, 2020. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1073/pnas.1921015117 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32393635 ● Search Scopus @ Elsevier (PMID): 32393635 ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.1921015117 (DOI: 10.1073/pnas.1921015117, PubMed: 32393635)
12.	Masashi Kuroda, Rumi Onoyama, Waka Sasaki, Mayu Sebe, Tadahiro Kitamura, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : DNA methylation status influences insulin-induced glucose transport in 3T3-L1 adipocytes by mediating p53 expression., Biochemical and Biophysical Research Communications, Vol.525, No.1, 39-45, 2020. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2020.02.038 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32070490 ● Search Scopus @ Elsevier (PMID): 32070490 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2020.02.038 (DOI: 10.1016/j.bbrc.2020.02.038, PubMed: 32070490)
13.	Mayu Sebe, Rie Tsutsumi, Takuro Oyama, T Yousuke Horikawa, Yuta Uemura, Nami Kakuta, Yoko Sakai, Atsushi Morio, Hirotsugu Miyoshi, Takashi Kondo, Tomoaki Urabe, Yuko Noda, Satoshi Kamiya, Noboru Saeki, Masashi Kuroda, Katsuya Tanaka, Yasuo Tsutsumi and Hiroshi Sakaue : Assessment of postoperative nutritional status and physical function between open surgical aortic valve replacement and transcatheter aortic valve implantation in elderly patients., The Journal of Medical Investigation : JMI, Vol.67, No.1.2, 139-144, 2020. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114644 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.67.139 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378597 ● Search Scopus @ Elsevier (PMID): 32378597 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.139 (徳島大学機関リポジトリ: 114644, DOI: 10.2152/jmi.67.139, PubMed: 32378597)
14.	Masahiro Bando, Saeko Masumoto, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : Effect of olive oil consumption on aging in a senescence-accelerated mice-prone 8 (SAMP8) model., The Journal of Medical Investigation : JMI, Vol.66, No.3.4, 241-247, 2019. (要約) 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. (キーワード) 加齢 (aging) / Animals / Avoidance Learning / Diet, Mediterranean / 記憶 (memory) / Mice / Models, Animal / Olive Oil / Organ Size / Triglycerides (徳島大学機関リポジトリ) ● Metadata: 113365 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.66.241 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31656282 ● Summary page in Scopus @ Elsevier: 2-s2.0-85074168190 (徳島大学機関リポジトリ: 113365, DOI: 10.2152/jmi.66.241, PubMed: 31656282, Elsevier: Scopus)
15.	堤理恵, 瀬部真由, 別府香名, 渡辺涼乃, 尾平優, 黒田雅士, 阪上浩 : 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), 日本静脈経腸栄養学会雑誌, Vol.33, No.4, 1019-1024, 2018年. (要約) <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> (キーワード) 味覚障害 / 嗅覚障害 / 化学療法 (出版サイトへのリンク) ● Publication site (DOI): 10.11244/jspen.33.1019 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282763059771520 ● Search Scopus @ Elsevier (DOI): 10.11244/jspen.33.1019 (DOI: 10.11244/jspen.33.1019, CiNii: 1390282763059771520)
16.	Nagakatsu Harada, Adzumi Hatakeyama, Maiko Okuyama, Yumiko Miyatake, Tadahiko Nakagawa, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue : Readthrough of ACTN3 577X nonsense mutation produces full-length α-actinin-3 protein., Biochemical and Biophysical Research Communications, Vol.502, No.3, 422-428, 2018. (要約) , 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 (キーワード) Actinin / Caffeine / Codon, Nonsense / Gentamicins / HEK293 Cells / Humans / Muscle, Skeletal / Mutant Proteins / Peptide Chain Termination, Translational / RNA Stability / RNA, Messenger / Transfection (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2018.05.193 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29857001 ● Search Scopus @ Elsevier (PMID): 29857001 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.05.193 (DOI: 10.1016/j.bbrc.2018.05.193, PubMed: 29857001)
17.	Chikugo Momoko, Sebe Mayu, Rie Tsutsumi, Iuchi Marina, Jun Kishi, Masashi Kuroda, Nagakatsu Harada, Yasuhiko Nishioka and Hiroshi Sakaue : Effect of Janus kinase inhibition by tofacitinib on body composition and glucose metabolism., The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 166-170, 2018. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 112232 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.65.166 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282855 ● Search Scopus @ Elsevier (PMID): 30282855 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.166 (徳島大学機関リポジトリ: 112232, DOI: 10.2152/jmi.65.166, PubMed: 30282855)
18.	Nagakatsu Harada, Maiko Okuyama, Aya Yoshikatsu, Hironori Yamamoto, Saori Ishiwata, Chikako Hamada, Tomoyo Hirose, Masayuki Shono, Masashi Kuroda, Rie Tsutsumi, Jiro Takeo, Yutaka Taketani, Yutaka Nakaya and Hiroshi Sakaue : Endoplasmic Reticulum Stress in Mice Increases Hepatic Expression of Genes Carrying a Premature Termination Codon via a Nutritional Status-Independent GRP78-Dependent Mechanism., Journal of Cellular Biochemistry, Vol.118, No.11, 3810-3824, 2017. (出版サイトへのリンク) ● Publication site (DOI): 10.1002/jcb.26031 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28383761 ● Search Scopus @ Elsevier (PMID): 28383761 ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.26031 (DOI: 10.1002/jcb.26031, PubMed: 28383761)
19.	Masato Miyake, Masashi Kuroda, Hiroshi Kiyonari, Kenji Takehana, Satoshi Hisanaga, Masatoshi Morimoto, Jun Zhang, Miho Oyadomari, Hiroshi Sakaue and Seiichi Oyadomari : Ligand-induced rapid skeletal muscle atrophy in HSA-Fv2E-PERK transgenic mice., PLoS ONE, Vol.12, No.6, e0179955, 2017. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114340 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0179955 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28644884 ● Search Scopus @ Elsevier (PMID): 28644884 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0179955 (徳島大学機関リポジトリ: 114340, DOI: 10.1371/journal.pone.0179955, PubMed: 28644884)
20.	Yumiko Miyatake, Tetsuya Shiuchi, Kazuaki Mawatari, Satomi Toda, Yasuko Taniguchi, Akari Futami, Fukiko Sato, Masashi Kuroda, Mayu Sebe, Rie Tsutsumi, Nagakatsu Harada, Yasuhiko Minokoshi, Tadahiro Kitamura, Koro Gotoh, Masaki Ueno, Yutaka Nakaya and Hiroshi Sakaue : Intracerebroventricular injection of ghrelin decreases wheel running activity in rats., Peptides, Vol.87, 12-19, 2017. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 113364 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.peptides.2016.11.005 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27825986 ● Summary page in Scopus @ Elsevier: 2-s2.0-84995961350 (徳島大学機関リポジトリ: 113364, DOI: 10.1016/j.peptides.2016.11.005, PubMed: 27825986, Elsevier: Scopus)
21.	Masashi Kuroda, Ayako Tominaga, Kasumi Nakagawa, Misa Nishiguchi, Mayu Sebe, Yumiko Miyatake, Tadahiro Kitamura, Rie Tsutsumi, Nagakatsu Harada, Yutaka Nakaya and Hiroshi Sakaue : DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes., PLoS ONE, Vol.11, No.8, e0160532, 2016. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 110107 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0160532 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27494408 ● Search Scopus @ Elsevier (PMID): 27494408 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0160532 (徳島大学機関リポジトリ: 110107, DOI: 10.1371/journal.pone.0160532, PubMed: 27494408)

学術論文(紀要・その他):

1.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 黒井俊哉, 植木歩夢, 堤理恵, 阪上浩, 小瀧歩, 工藤千秋 : 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, 日本早期認知症学会誌, Vol.13, No.1, 42-48, 2020年. (要約) 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) (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / *認知症(診断) 早期診断チェックリスト Mini-Mental State 老研式活動能力指標ヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1523669556040598272 (CiNii: 1523669556040598272)

総説・解説:

1.	黒田雅士, 堤理恵, 阪上浩 : 【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, 月刊糖尿病, Vol.14, No.1, 28-34, 2022年1月.
2.	黒田雅士, 堤理恵, 阪上浩 : 脂肪細胞分化に対するエピジェネティック制御機構, 実験医学増刊, Vol.39, No.5, 32-38, 2021年3月.
3.	黒田雅士, 堤理恵, 阪上浩 : 【個人差の理解へ向かう肥満症研究 GWAS，エピゲノム，腸内細菌，栄養学的知見から多様な病態を解明し，Precision Medicineをめざす】(第1章)代謝(エネルギー消費)の分子・細胞・個体メカニズム脂肪細胞分化に対するエピジェネティック制御機構, 実験医学, Vol.39, No.5, 654-660, 2021年3月. (要約) 生体はヒストン修飾やDNAメチル化などのエピジェネティクスによる制御機構により染色体の局所構造を変化させて，ゲノムDNA中の膨大な情報の中から必要な遺伝子を選択して活性化・不活性化している．このエピジェネティクスによる遺伝子発現制御は幹・前駆細胞がある特定の機能をもった細胞へ分化する際にも重要な意義をもち，分化誘導中の時系列遺伝子発現プロファイルの形成に貢献している．脂肪細胞では分化のマスターレギュレーターPPARγを中心に，その誘導や標的遺伝子の活性化にかかわるエピゲノムの変化が解明されている．(著者抄録) (キーワード) Histones Histone-Lysine N-Methyltransferase 遺伝子発現調節クロマチン DNAメチル化 CCAAT-Enhancer-Binding Protein-Beta 非翻訳RNA エピジェネティックプロセス褐色脂肪細胞 Jumonji Domain-Containing Histone Demethylases 脂肪細胞分化ベージュ脂肪細胞細胞発生 Jmjd3 Protein KDM3A Protein EHMT1 Protein ヒト
4.	原加奈子, 堤理恵, 中西信人, 三島優奈, 待田京香, 黒田雅士, 大藤純, 阪上浩 : 重症患者における筋萎縮と尿中タイチン濃度測定の意義, 四国医学雑誌, Vol.76, No.5-6, 267-272, 2020年12月. (要約) タイチンは，骨格筋において最初に分解される蛋白質として注目されている．尿中のタイチンN末端断片濃度を測定できるELISAが開発され，筋ジストロフィー患者では健常人の数百倍のタイチンN末端断片が検出されることが報告されている．これまでに行った，重症病態における筋萎縮，筋機能低下のバイオマーカーとしての尿中タイチン濃度測定の有用性についての研究を中心に概説した． (キーワード) バイオマーカー(尿) ICU 筋萎縮症(診断,X線診断) 筋節 X線CT 病勢悪化 Connectin(尿) ヒト (徳島大学機関リポジトリ) ● Metadata: 115785 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050287363395004928 (徳島大学機関リポジトリ: 115785, CiNii: 1050287363395004928)
5.	黒田雅士, 阪上浩 : 脂肪細胞熱産生機構における転写因子による制御, 糖尿病·内分泌代謝科, Vol.51, No.1, 23-27, 2020年7月. (キーワード) thermogenesis / brown adipocytes / transcriptional control (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1521699229687059584 (CiNii: 1521699229687059584)
6.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 黒田雅士, 阪上浩 : 【糖・エネルギー代謝ネットワークupdate】脂肪細胞熱産生機構における転写因子による制御, 糖尿病·内分泌代謝科, Vol.51, No.1, 23-27, 2020年7月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / DNA-Binding Proteins 転写因子肥満トランスアクチベーター熱産生 Interferon Regulatory Factors RNA-Binding Protein EWS エピジェネティックプロセス *褐色脂肪細胞脂肪細胞分化 Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-Alpha PRDM16 Protein Interferon Regulatory Factor-4 EBF1 Protein ヒト (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1521699229687059584 (CiNii: 1521699229687059584)
7.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 三島優奈, 堤理恵, 阪上浩 : 代謝動態の連関による生体機能制御骨格筋と代謝調節に注目して, 糖尿病·内分泌代謝科, Vol.51, No.1, 71-77, 2020年7月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / エネルギー代謝肝臓飢餓筋萎縮症脂肪組織身体運動絶食ホメオスタシス *骨格筋廃用症候群ヒト (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520010380610834688 (CiNii: 1520010380610834688)
8.	黒田雅士, 阪上浩 : ADCY3遺伝子異常と肥満, 内分泌·糖尿病·代謝内科, Vol.48, No.3, 214-218, 2019年3月. (キーワード) ADCY3 / Leptin / Melanocortin 4 receptor (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1521417755406689664 (CiNii: 1521417755406689664)
9.	Masashi Kuroda and Hiroshi Sakaue : Adipocyte Death and Chronic Inflammation in Obesity, The Journal of Medical Investigation : JMI, Vol.64, No.3,4, 193-196, Aug. 2017. (要約) Cell death is closely linked to many diseases including cancer, neurodegenerative diseases, autoimmune diseases, and metabolic disorders. Increased adipocyte death has been reported during the development of obesity. Adipocyte death may be caused by excessive stress during obesity-related adipose tissue remodeling. Adipose tissue macrophages are key players in obesity-related inflammation and systemic insulin resistance. Accumulating evidence suggests that adipocyte death is involved in immune cell function and initiates inflammation through an interaction with macrophages; however, the precise mechanisms remain largely unknown. This review focuses on the contribution of dead cells (particularly dead adipocytes in adipose tissue) to the pathophysiological conditions associated with obesity. J. Med. Invest. 64: 193-196, August, 2017. (キーワード) Adipocytes / Cell Death / Chronic Disease / Humans / Inflammation / Macrophages / Obesity (徳島大学機関リポジトリ) ● Metadata: 111114 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.64.193 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954980 ● Search Scopus @ Elsevier (PMID): 28954980 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.193 (徳島大学機関リポジトリ: 111114, DOI: 10.2152/jmi.64.193, PubMed: 28954980)
10.	黒田雅士, 阪上浩 : 肥満・2型糖尿病におけるビタミンD・カルシウムの役割, Clinical Calcium, Vol.26, No.3, 349-354, 2016年3月. (要約) Obesity, induced by unhealthy lifestyle choices, could be involved in the development of chronic diseases like type 2 diabete. Obesity is largely due to the imbalance of energy intake and expenditure, therefore we have put more emphasis on the amount of macronutrients including carbohydrates, fats and proteins as dietary therapy for obesity and related-conditions. On the other hand, several studies revealed obese or diabetic patients were more likely to have micronutrient deficiencies such as vitamins and minerals. Besides the effects on bone metabolism, vitamin D and calcium might contribute to metabolic disorder accompanied by obesity. However, it has not been concluded supplementation of these two nutrients has a benefit in obese or diabetic individuals. Further studies are needed. (キーワード) Animals / カルシウム (calcium) / Diabetes Mellitus, Type 2 / Dietary Proteins / Energy Intake / Humans / 肥満症 (obesity) / ビタミンD (vitamin D) (出版サイトへのリンク) ● Publication site (DOI): 10.20837/4201603009 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26923970 ● Search Scopus @ Elsevier (PMID): 26923970 ● Search Scopus @ Elsevier (DOI): 10.20837/4201603009 (DOI: 10.20837/4201603009, PubMed: 26923970)

国際会議:

1.	Masashi Kuroda, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Saya Okamoto, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : Transcription factor IRF7 and energy metabolism, The 11th Scientific Meeting of the Asian Association for the Study of Diabetes., May 2019.
2.	Masashi Kuroda : Adipose tissue-derived protein, MFG-E8, regulates chronic inflammation and obesity-related liver disease, Asia-Pacific Diabetes and Obesity Study Group symposium 2018, 兵庫県神戸市, Oct. 2018.

国内講演発表:

1.	和田安純, 黒田雅士, 田村優実, 茶本凜, 富永玲奈, 小林久呂枝, 松村英里佳, 瀧下美由紀, 藤田めい, 堤理恵, 阪上浩 : 脂肪組織由来MFG-E8はNASHでの肝慢性炎症・線維化を促進する, 第42回日本肥満学会, 2022年3月.
2.	黒田雅士, 富永玲奈, 田村優実, 茶本凜, 松村英里佳, 小林久呂枝, 和田安純, 瀧下美由紀, 藤田めい, 志内哲也, 堤理恵, 阪上浩 : エネルギー代謝調節機構における転写因子IRF7生理的意義の検討, 第25回アディポサイエンス・シンポジウム, 2022年2月.
3.	黒田雅士, 茶本凜, 田村優実, 富永玲奈, 小林久呂枝, 松村英里佳, 和田安純, 瀧下美由紀, 藤田めい, 堤理恵, 阪上浩 : DNAメチル化による熱産生関連遺伝子制御機構の検討, 第 54 回日本栄養•食糧学会中国•四国支部大会, 2021年10月.
4.	和田安純, 茶本凜, 田村優実, 富永玲奈, 小林久呂枝, 松村英里佳, 瀧下美由紀, 藤田めい, 黒田雅士, 堤理恵, 阪上浩 : NASH病態形成における脂肪組織由来分泌タンパク質MFG-E8の関与, 第263回徳島医学会, 2021年8月.
5.	黒田雅士, 茶本凜, 富永玲奈, 田村優実, 松村英里佳, 小川美季, 堤理恵, 阪上浩 : DNAメチル化による脂肪細胞機能制御についての検討, 第64回日本糖尿病学会年次学術集会, 2021年5月.
6.	出葉祥恵, 山下果穂, 竹治香菜, 山崎幸, 黒田雅士, 堤理恵, 阪上浩 : ストレプトゾトシン抵抗性ラットに認められた消化管・膵臓連関, 糖尿病, Vol.64, No.Suppl.1, III-94-6, 2021年5月.
7.	三島優奈, 堤理恵, 大谷環樹, 原加奈子, 藤本紗織, 黒田雅士, 阪上浩 : PET/CTを用いたマウス骨格筋インスリン抵抗性の評価, 第41回日本肥満学会, 2021年3月.
8.	岡松優子, 黒田雅士, 堤理恵, 坪田あゆみ, 斉藤昌之, 木村和弘, 阪上浩 : マウス褐色脂肪組織において寒冷刺激により誘導されるUCP1依存的および非依存的代謝変化, 第41回日本肥満学会, 2021年3月.
9.	松村英里佳, 黒田雅士, 富永玲奈, 田村優実, 茶本凜, 小林久呂枝, 和田安純, 瀧下美由紀, 藤田めい, 志内哲也, 堤理恵, 阪上浩 : 転写因子IRF7によるエネルギー代謝調節機構の解明, 第42回日本肥満学会, 2021年3月.
10.	三島優奈, 堤理恵, 黒田雅士, 阪上浩, 大谷環樹 : PET/CTを用いたマウス骨格筋インスリン抵抗性の評価, 四国医学雑誌, Vol.76, No.5-6, 342, 2020年12月. (キーワード) インスリン抵抗性(実験的) 骨格筋(X線診断,放射性核種診断) *PET-CT検査マウス動物
11.	瀬部真由, 堤理恵, 瀬野浦聖佳, 岸潤, 黒田雅士, 木下成三, 中屋豊, 堤保夫, 西岡安彦, 阪上浩 : 脂質の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, 学会誌JSPEN, Vol.2, No.Suppl.1, 824, 2020年11月. (キーワード) 関節リウマチ(病因,合併症,実験的) 食品中の脂肪(毒性・副作用) 病勢悪化筋肉減少症(病因,合併症,実験的) *高脂肪食(有害作用) ヒトマウス動物中年(45~64) 女
12.	徳里望, 堤理恵, 黒田雅士, 升本早枝子, 庄野仁志, 阿部亮, 大西皓貴, 佐藤豪, 北村嘉章, 阿部晃治, 阪上浩, 武田憲昭 : 食事へのグルタミン酸Na添加が頭頸部癌患者の化学療法による舌粘膜の味覚受容体遺伝子発現に与える影響, 日本耳鼻咽喉科学会会報, Vol.123, No.4, 1065, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Sodium Glutamate(治療的利用,薬理学) 遺伝子発現口腔粘膜抗腫瘍剤(治療的利用,毒性・副作用) 頭頸部腫瘍(薬物療法) 味覚障害(化学的誘発,薬物療法) 味蕾舌粘膜ヒト
13.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 河相舞香, 竹治香菜, 山崎幸, 松本裕華, 堤理恵, 黒田雅士, 阪上浩 : ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, 糖尿病, Vol.63, No.9, 642, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Insulin Streptozocin(毒性・副作用) 薬物抵抗性細胞保護 *インスリン分泌細胞 Ghrelin(血液) Glucagon-Like Peptide 1(血液) ラット動物
14.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 原加奈子, 堤理恵, 三島優奈, 松本裕華, 黒田雅士, 大谷環樹, 阪上浩 : PET/CTを用いた代謝性疾患モデルマウス骨格筋糖取り込みの評価, 糖尿病, Vol.63, No.9, 649, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 高インスリン症(実験的) 疾患モデル(動物) 骨格筋(X線診断,放射性核種診断) Fluorodeoxyglucose F18(診断的利用) PET-CT検査マウス動物オス
15.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 森万理恵, 別府香名, 堤理恵, 森博康, 松久宗英, 阪上浩, 神田彩恵, 堤理恵, 三島優奈, 上嶋奈々子, 松本裕華, 原加奈子, 黒田雅士, 阪上浩 : ロイシンの抗動脈硬化作用の検討, 糖尿病, Vol.63, No.9, 657, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 血液透析糸球体濾過量腎不全-慢性(治療,合併症) 糖尿病(合併症) 味覚障害(病因) 味蕾 Leptin(血液) G-Protein-Coupled Receptors T1R Receptor ヒト / Cholesterol(血液) Leucine(治療的利用) LDL Cholesterol(血液) 動脈硬化症(薬物療法,実験的) マウス動物メス
16.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 岡本彩椰, 黒田雅士, 川端康代, 田村優実, 富永玲奈, 堤理恵, 阪上浩 : NASH病態形成における脂肪組織由来分泌タンパク質MFG-E8の関与, 糖尿病, Vol.63, No.9, 668, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Aspartate Aminotransferases(血液) 表面抗原脂肪組織糖尿病(合併症) 乳タンパク質肝線維症肝疾患-非アルコール性脂肪性(実験的,合併症) MFGE8 Protein マウス動物
17.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 瀬部真由, 堤理恵, 黒田雅士, 阪上浩 : 高脂肪食摂取が関節リウマチ病態に与える影響, 糖尿病, Vol.63, No.9, 668, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 関節リウマチ(実験的) 肥満 CD4陽性T細胞リスク評価 Interleukin-17 高脂肪食マウス動物
18.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子 : リンゴ由来プロシアニジンの摂取が老化モデルマウスの肥満・認知機能に及ぼす影響, 糖尿病, Vol.63, No.9, 668, 2020年9月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物
19.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 原加奈子, 堤理恵, 中西信人, 阪上浩 : 【重症患者の長期予後を見据えた栄養療法と運動療法】重症病態における代謝変化とアミノ酸代謝の見解, 外科と代謝·栄養, Vol.54, No.3, 143-146, 2020年8月. (要約) 熱傷や多発外傷，敗血症といった重症病態では，健常時と比較して代謝動態は著しく変化する．侵襲時での炎症性サイトカインや免疫細胞の活性化によって解糖経路の亢進やミトコンドリアの機能不全による酸化的リン酸化の抑制が生じる．このような代謝の変化によってエネルギー代謝の倹約と乳酸の過剰産生が示唆される．また，代謝動態への影響は糖代謝のみではなくアミノ酸代謝にも及ぶ．特に分岐鎖アミノ酸(BCAA)の代謝動態は重要なシグナル因子となっている可能性が考えられる．敗血症においては，骨格筋でのロイシン抵抗性が懸念されるが，一方でロイシンの投与によって骨格筋減少抑制効果があることも報告されている．重症病態において代謝機構の変化に合わせたエネルギー投与量の調整ともに，アミノ酸代謝の意義を究明する必要がある．(著者抄録) (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Amino Acids(血液) Branched-Chain Amino Acids 運動療法活性酸素筋萎縮症(予防) 代謝栄養管理ヒト
20.	瀬部真由, 堤理恵, 瀬野浦聖佳, 岸潤, 黒田雅士, 木下成三, 中屋豊, 堤保夫, 西岡安彦, 阪上浩 : 飽和脂肪酸の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, 糖尿病, Vol.63, No.Suppl.1, S-329, 2020年8月. (キーワード) 関節リウマチ(食事療法) 脂肪酸(毒性・副作用) 骨格筋病勢悪化 *筋肉減少症(化学的誘発) 筋量ヒト女
21.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 堤理恵, 瀬部真由, 岸潤, 木下成三, 西岡安彦, 阪上浩 : 飽和脂肪酸の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, 日本臨床分子医学会学術総会プログラム・抄録集, No.9, 75, 2020年4月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 関節リウマチ(病因) 脂肪酸骨格筋病勢悪化 *筋肉減少症(病因) 高脂肪食ヒトマウス動物女
22.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 瀬部真由, 堤理恵, 瀬野浦聖佳, 黒田雅士, 中屋豊, 阪上浩, 岸潤, 木下成三, 堤保夫, 西岡安彦 : 飽和脂肪酸の過剰摂取は関節リウマチを増悪させ骨格筋量の減少を引き起こす, 四国医学雑誌, Vol.76, No.1-2, 120-121, 2020年4月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 栄養評価関節リウマチ(実験的,合併症,診断) 脂肪酸(薬理学) *骨格筋身体組成筋肉減少症(実験的,合併症,診断) ヒトマウス動物中年(45~64) 女
23.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 武田英二, 佐藤美智子, 隅田奈美, 久米寛子, 大前博司, 森下照大, 川浦昭彦, 片山貴文, 堤理恵, 阪上浩, 竹谷豊 : 骨格筋肉量，機能，栄養素吸収におよぼす1日1000IUのビタミンD摂取効果, ビタミン, Vol.94, No.4, 277, 2020年4月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Hydroxycholecalciferols(血液) Vitamin D(薬理学) 筋骨格系生理学的現象乳骨格筋身体組成生理的吸収筋量ヒト成人(19~44) 中年(45~64) 高齢者(65~79) 男女
24.	瀬部真由, 堤理恵, 瀨野浦聖佳, 岸潤, 黒田雅士, 木下成三, 中屋豊, 堤保夫, 西岡安彦, 阪上浩 : 飽和脂肪酸の過剰摂取は関節リウマチ病態の憎悪・骨格筋量の減少を引き起こす, 第23回日本病態栄養学会年次学術集会, 2020年1月.
25.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 瀬部真由, 堤理恵, 瀬野浦聖佳, 岸潤, 黒田雅士, 木下成三, 中屋豊, 堤保夫, 西岡安彦, 阪上浩 : 飽和脂肪酸の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, 日本病態栄養学会誌, Vol.23, No.Suppl., S-1, 2020年1月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 関節リウマチ(化学的誘発,実験的) 危険因子脂肪酸(毒性・副作用) 骨格筋病勢悪化過栄養(化学的誘発,実験的) 筋肉減少症(化学的誘発,実験的) 筋量マウス動物
26.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 阿久根愛実, 堤理恵, 植木歩夢, 瀬部真由, 黒井俊哉, 藤田智子, 小瀧歩, 工藤千秋, 阪上浩 : 認知機能低下と食事摂取・口腔細菌叢の関連性の検討, 日本病態栄養学会誌, Vol.23, No.Suppl., S-46, 2020年1月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 細菌食行動食肉食品中のタンパク質無機栄養素野菜認知機能低下(予防,診断) 消化管微生物叢 *口腔内細菌ヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
27.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 三島優奈, 堤理恵, 松本裕華, 原加奈子, 大谷環樹, 上嶋菜々子, 神田彩恵, 黒田雅士, 阪上浩 : 廃用性筋萎縮モデルにおける骨格筋・肝代謝動態の連関による生体機能制御, 日本病態栄養学会誌, Vol.23, No.Suppl., S-54, 2020年1月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 遺伝子発現エネルギー代謝筋萎縮症(実験的) 骨格筋糖代謝廃用症候群(実験的) Large Neutral Amino Acid-Transporter 1 マウス動物
28.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 橘高久未子, 山本智子, 堤理恵, 中西信人, 阪上浩 : 重症病態における血中遊離アミノ酸の意義, 日本病態栄養学会誌, Vol.23, No.Suppl., S-57, 2020年1月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Amino Acids ICU エネルギー代謝前向き研究 *メタボロミクスヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
29.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 竹治香菜, 山崎幸, 河相舞香, 松本裕華, 黒田雅士, 堤理恵, 阪上浩 : ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, 日本病態栄養学会誌, Vol.23, No.Suppl., S-57, 2020年1月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Streptozocin(毒性・副作用) 糖尿病(実験的) 薬物抵抗性インスリン分泌細胞 Glucagon-Like Peptide 1(血液) ラット動物
30.	竹治香菜, 山崎幸, 河相舞香, 松本裕華, 黒田雅士, 堤理恵, 阪上浩 : ストレプドゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, 第23回日本病態栄養学会年次学術集会, 2020年1月.
31.	三島優奈, 堤理恵, 松本裕華, 原加奈子, 大谷環樹, 上嶋菜々子, 神田彩恵, 黒田雅士, 阪上浩 : 廃用性筋萎縮モデルにおける骨格筋・艦隊者動態の連関による生体機能制御, 第23回日本病態栄養学会年次学術集会, 2020年1月.
32.	堤理恵, 瀬部真由, 岸潤, 瀨野浦聖佳, 黒田雅士, 西岡安彦, 阪上浩 : 飽和脂肪酸はインスリン抵抗性誘導を介して慢性関節リウマチを増悪させる, 第40回日本肥満学会, 2019年11月.
33.	川端康代, 黒田雅士, 岡本彩椰, 田村優実, 富永玲奈, 堤理恵, 阪上浩 : エネルギー代謝調節機構における転写因子IRF7の役割, 第40回日本肥満学会, 2019年11月.
34.	竹治香菜, 山崎幸, 河相舞香, 松本裕華, 黒田雅士, 堤理恵, 阪上浩 : ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, 第40回日本肥満学会, 2019年11月.
35.	川端康代, 黒田雅士, 岡本彩椰, 田村優実, 富永玲奈, 堤理恵, 阪上浩 : エネルギー代謝調節機構における転写因子IRF7の役割, 第24回アディポサイエンス・シンポジウム, 2019年8月.
36.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 阪上浩, 堤理恵 : 肥満をもう一度考える:新たな肥満症から治療まで肥満から読み解く高齢者栄養の問題点と管理の実際, 日本抗加齢医学会総会プログラム・抄録集, No.9, 137, 2019年6月. (キーワード) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 危険因子肥満(合併症,治療) 栄養管理筋肉減少症(合併症,治療) 認知機能低下(病因,治療) フレイル(病因,治療) ヒト高齢者(65~79) 高齢者(80~)
37.	川端康代, 黒田雅士, 宇川菜穂, 石川悦子, 岡本彩椰, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 : 肥大化脂肪細胞における転写因子IRF7の同定と生理的役割の検討, 第62回日本糖尿病学会, 2019年5月.
38.	三島優奈, 堤理恵, 宮武由実子, 末政直哉, 大谷環樹, 兒玉直子, 丹波洋介, 黒田雅士, 升本早枝子, 阪上浩 : PET/CTを用いた代謝異常時の骨格筋における糖取り込みの測定, 第62回日本糖尿病学会, 2019年5月.
39.	黒田雅士, 石川悦子, 宇川菜穂, 岡本彩椰, 川端康代, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 : 脂肪組織慢性炎症及びNASH病態形成における分泌タンパク質MFG-E8の関与, 第62回日本糖尿病学会, 2019年5月.
40.	佐々木和佳, 黒田雅士, 石川悦子, 宇川菜穂, 川端康代, 升本早枝子, 堤理恵, 阪上浩 : 脱メチル化3T3-L1脂肪細胞のインスリン感受性調節因子の探索, 第39回日本肥満学会, 2018年10月.
41.	川端康代, 黒田雅士, 石川悦子, 宇川菜穂, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 : 肥大化脂肪細胞における転写因子IRF7の同定と生理的役割の検討, 第39回日本肥満学会, 2018年10月.
42.	黒田雅士, 阪上浩 : 肥満病態形成におけるIRF7の二つの役割, 第39回日本肥満学会, 2018年10月.
43.	黒田雅士, 宇川菜穂, 石川悦子, 川端康代, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 : エネルギー代謝における転写因子IRF7の役割, 第23回アディポサイエンス・シンポジウム, 2018年8月.
44.	宇川菜穂, 黒田雅士, 石川悦子, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 : 肥大化脂肪細胞における転写因子 IRF7 の同定と機能解析, 第61回日本糖尿病学会, 2018年5月.
45.	黒田雅士, 石川悦子, 宇川菜穂, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 : 脂肪組織慢性炎症及びNASH病態形成に対するMFG-E8の関与, 第61回日本糖尿病学会, 2018年5月.
46.	Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : Adipose tissue-derived protein, MFG-E8, regulates chronic inflammation and obesity-related liver disease, 第91回日本内分泌学会, Apr. 2018.
47.	堤理恵, 竹尾仁良, 板東正浩, 瀬部真由, 山﨑幸, 丹波洋介, 宮原裕子, 黒田雅士, 升本早枝子, 原田永勝, 阪上浩 : 魚油由来長鎖モノエン脂肪酸の上腕動脈内皮機能に与える効果の検討, 第38回日本肥満学会, 2017年10月.
48.	小野山瑠美, 黒田雅士, 西口実佐, 宇川菜穂, 石川悦子, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 : 転写制御領域解析システムを用いた3T3-L1脂肪細胞のインスリン感受性調節因子の探索, 第38回日本肥満学会, 2017年10月.
49.	石川悦子, 黒田雅士, 西口実佐, 小野山瑠美, 宇川菜穂, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 : 脂肪組織慢性炎症及びNASH病態形成に対するMFG-E8の関与, 第38回日本肥満学会, 2017年10月.
50.	黒田雅士, 西口実佐, 小野山瑠美, 宇川菜穂, 石川悦子, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 : 脂肪細胞における転写因子IRF7の同定及び機能解析, 第22回アディポサイエンス・シンポジウム, 2017年8月.
51.	西口実佐, 黒田雅士, 小野山瑠美, 宇川菜穂, 堤理恵, 原田永勝, 阪上浩 : 肥大化脂肪細胞における転写因子IRF7の同定と機能解析, 第60回日本糖尿病学会年次学術集会, 2017年5月.
52.	小野山瑠美, 黒田雅士, 西口実佐, 宇川菜穂, 堤理恵, 原田永勝, 阪上浩 : 3T3-L1脂肪細胞のインスリン感受性に対するDNAメチル化の制御機構, 第60回日本糖尿病学会年次学術集会, 2017年5月.
53.	黒田雅士, 西口実佐, 小野山瑠美, 宇川菜穂, 堤理恵, 原田永勝, 阪上浩 : 新規肥満関連転写因子IRF7によるMCP-1発現制御機構の解析, 第90回日本内分泌学会学術集会, 2017年4月.
54.	丹波洋介, 竹尾仁良, 板東正浩, 瀬部真由, 山崎幸, 福田大受, 宮原裕子, 宮武由実子, 末政直哉, 黒田雅士, 升本早枝子, 原田永勝, 堤理恵, 佐田政隆, 阪上浩 : 魚油由来長鎖モノエン脂肪酸は抗動脈硬化作用を有する, 第21回病態栄養学会年次学術集会, 2017年1月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

サルコペニアの診断と発症予防法の開発を目指した基盤・応用研究 (研究課題/領域番号: 22H03535 )
肥満形成過程における褐色脂肪機能不全メカニズムの解明 (研究課題/領域番号: 20K19709 )
抗動脈硬化作用を有する極長鎖一価不飽和脂肪酸の基盤・応用研究 (研究課題/領域番号: 19H04055 )
脂肪組織由来分泌タンパク質による肝マクロファージ機能制御とNASH病態への関与 (研究課題/領域番号: 18K16205 )
研究者番号（00803579）による検索

黒田 雅士

研究活動

個人のホームページ

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

学術論文(紀要・その他):

総説・解説:

国際会議:

国内講演発表:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

黒田雅士