YukiKamei/published_papers/54443076 Yuki Kamei Rina Sugitani Noa Onzawa Mana Akao Taiki Fushimi Mitsugu Akagawa Oleuropein stimulates peripheral serotonin secretion via voltage-dependent Ca2+ channels and acutely regulates central function bioRxiv null null 20260721 10.64898/2026.07.15.738825 YukiKamei/published_papers/53687595 Takeshi Katayoshi Takahisa Nakajo Natsuko Kitajima Wakana Naka Yuki Kamei Taiki Fushimi Masakatsu Kageyama Mitsugu Akagawa Kentaro Tsuji NMN protects vascular endothelial cells from M1 macrophage-derived IL-1β-induced hyperpermeability by inhibiting VE-cadherin degradation Background and aims Vascular endothelial (VE) dysfunction, particularly endothelial hyperpermeability, is a critical pathological process in various inflammatory vascular diseases, including atherosclerosis, vasculitis, and sepsis. Nicotinamide mononucleotide (NMN), an NAD ⁺ precursor, has shown anti-inflammatory and vascular protective effects in preclinical models. However, the mechanisms by which NMN preserves endothelial barrier integrity against macrophage-derived inflammatory stimuli remain unclear. This study examined the potential protective role of NMN in endothelial hyperpermeability induced by pro-inflammatory macrophages. Methods A three-dimensional co-culture model of human umbilical vein endothelial cells (HUVECs) and M1 macrophages was constructed to reproduce inflammatory vascular microenvironments. Endothelial permeability was evaluated by measuring fluorescently labelled dextran and LDL passages from the luminal (top) to the abluminal side (bottom) of the insert. Results M1 macrophage co-culture increased HUVEC permeability, and NMN pretreatment attenuated this hyperpermeability. Mechanistic analysis revealed that interleukin-1β (IL-1β) released by M1 macrophages was the primary contributor to endothelial hyperpermeability. NMN suppressed IL-1β-induced cell-cell gap formation and VE-cadherin degradation in HUVECs by inhibiting nuclear factor kappa B (NF- κ B) pathway activation. These findings indicate that NMN prevents IL-1β-induced NF- κ B activation and subsequent VE-cadherin degradation, thereby protecting against endothelial hyperpermeability caused by intercellular gap formation. Other NAD ⁺ precursors, including nicotinamide riboside, similarly protected against IL-1β-induced hyperpermeability and VE-cadherin degradation. Alternatively, the NAD ⁺ -dependent deacetylase sirtuin 1 (SIRT1) inhibitor EX527 or SIRT1 siRNA knockdown abrogated NMN-mediated suppression of hyperpermeability and VE-cadherin degradation. Therefore, the protective effect of NMN against IL-1β-mediated endothelial dysfunction is dependent on the NAD ⁺ - SIRT1 axis. Conclusions This in vitro mechanistic study suggests that the NAD⁺ - SIRT1 axis contributes to IL-1β-induced endothelial barrier disruption, supporting further investigation of NMN in inflammatory vascular diseases. Frontiers Media SA Frontiers in Cardiovascular Medicine 2297-055X 13 null null 20260518 10.3389/fcvm.2026.1748872 YukiKamei/published_papers/50118192 Ryo Hayakawa Takeshi Ishii Taiki Fushimi Yuki Kamei Ai Yamaguchi Kenji Sugimoto Hitoshi Ashida Mitsugu Akagawa Luteolin protects human ARPE-19 retinal pigment epithelium cells from blue light-induced phototoxicity through activation of Nrf2/Keap1 signaling. Age-related macular degeneration (AMD), a serious physical and mental health problem worldwide, is the leading cause of irreversible, severe vision impairment and loss in older people. AMD is associated with multiple risk factors, many of which are closely linked to increased oxidative stress. Some studies have suggested that long-term and excessive exposure to blue light may be a potential risk factor for the development or progression of AMD. Recently, we demonstrated that blue light irradiation caused oxidative stress in all-trans-retinal (atRAL)-exposed human ARPE-19 retinal pigment epithelium cells by generating singlet oxygen (1O2), leading to apoptotic cell death. Luteolin, a flavonoid found in various edible plants, has been reported to possess divergent health-promoting properties including anti-oxidative and chemopreventive effects by up-regulating anti-oxidative and phase II detoxifying enzymes through activation of Keap1/Nrf2 signaling. Herein, we verified the cytoprotective action of luteolin against blue light irradiation using atRAL-exposed ARPE-19 cells. Our results established that luteolin effectively prevented blue light-induced apoptosis of ARPE-19 cells by mitigating oxidative stress. We also confirmed that luteolin suppressed intracellular accumulation of 1O2 and formation of atRAL-derived lipofuscin by increased expression of heme oxygenase-1 and aldehyde dehydrogenase 1A1 through activation of Keap1/Nrf2 signaling. Furthermore, our data implied that the luteolin-provoked activation of Keap1/Nrf2 signaling might be due to covalent binding of luteolin o-quinone to the critical cysteinyl thiol in Keap1. The present results suggest that luteolin could be helpful in the prevention and amelioration of blue light-induced retinal degeneration, including AMD. Free radical research 1 21 20250509 10.1080/10715762.2025.2503832 40340707 YukiKamei/published_papers/49991749 Yuki Nagara Kentaro Tsuji Yuki Kamei Mitsugu Akagawa Bergenin promotes mitochondrial biogenesis via the AMPK/SIRT1 axis in hepatocytes. Aging and obesity trigger liver mitochondrial decline, impairing liver function and energy metabolism. Effective hepatic mitochondrial biogenesis helps maintain and restore hepatocyte function. The effects of bergenin, a polyphenol with various pharmacological effects, on hepatic mitochondrial biogenesis remain unclear. Therefore, we aimed to determine its effects on mitochondrial biogenesis in hepatocytes. We measured mitochondrial content in human HepG2 hepatocytes using MitoTracker Green FM ; intracellular ATP content using an ATP assay kit ; and mitochondrial DNA (mtDNA) using the ratio of mtDNA to nuclear DNA by qPCR. Protein levels were analyzed using immunoblotting. Nuclear translocation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) was assessed by immunofluorescence staining and immunoblotting. In human HepG2 hepatocytes, bergenin increased mitochondrial content, elevated mitochondrial DNA and constituent proteins, and enhanced intracellular ATP levels and PGC-1α nuclear translocation, possibly promoting mitochondrial biosynthesis. SIRT1 expression was induced in bergenin-treated cells and may be responsible for bergenin-inducible mitochondrial biogenesis, which was abolished by the SIRT1 inhibitor EX-527. Furthermore, bergenin activated AMP-activated protein kinase (AMPK). Compound C, an AMPK inhibitor, abolished bergenin-induced SIRT1 expression and mitochondrial biogenesis. Overall, bergenin activates hepatic mitochondrial biogenesis through the AMPK / SIRT1 axis, which could help to prevent and ameliorate serious aging- and obesity-related liver diseases. J. Med. Invest. 72 : 66-75, February, 2025. The journal of medical investigation : JMI 72 1.2 66 75 20250000 10.2152/jmi.72.66 40268458 YukiKamei/published_papers/47827450 Ryosuke Kamikubo Hiroki Yoshida Taiki Fushimi Yuki Kamei Mitsugu Akagawa β-Caryophyllene, a dietary phytocannabinoid, alleviates high-fat diet-induced hepatic steatosis in mice via AMPK activation Abstract β-Caryophyllene (BCP), a dietary phytocannabinoid, significantly suppresses palmitate-induced lipid accumulation in human HepG2 hepatocytes via activation of AMP-activated protein kinase (AMPK) signaling. The objective of the preset research was to assess whether oral administration of BCP alleviates obesity-induced hepatic steatosis in mice through AMPK activation. We examined the protective action of supplementation of 0.3% BCP (w/w) in a high-fat diet (HFD) on C57BL/6 J mice for 12 weeks. BCP supplementation evidently ameliorated histological hepatic steatosis features, and significantly reduced triglycerides and cholesterol levels in liver, and serum levels of aspartate aminotransferase and alanine aminotransferase as compared with non-supplemented HFD-fed mice. Immunoblotting revealed that BCP supplementation in HFD-fed mice also caused hepatic AMPK activation. Furthermore, treatment with BCP in HFD-fed mice significantly suppressed body weight gain and attenuated obesity-related phenotypes relative to the HFD mice. Our results suggest the usefulness of BCP in the prevention of obesity-related liver steatosis and liver injury. Oxford University Press (OUP) Bioscience, Biotechnology, and Biochemistry 1347-6947 null null 20240913 10.1093/bbb/zbae129 YukiKamei/published_papers/45527853 Yuki Mori Masashi Masuda Risa Yoshida-Shimizu Saki Aoyagi Yuichiro Adachi Nguyen The Anh Yusuke Maruyama Yosuke Okumura Yuki Kamei Maiko Sakai Kohta Ohnishi Hirokazu Ohminami Yutaka Taketani All-trans retinoic acid induces lipophagy through the activation of the AMPK-Beclin1 signaling pathway and reduces Rubicon expression in adipocytes. Lipophagy is defined as a lipolysis pathway that degrades lipid droplet (LD) via autophagy. All-trans retinoic acid (atRA), a metabolite of vitamin A, stimulates lipolysis through hormone-sensitive lipase and β-oxidation. However, the regulation of lipolysis by atRA-induced autophagy in adipocytes remains unclear. In this study, we investigated the effect of atRA on autophagy in epididymal fat of mice and the molecular mechanisms of autophagy in 3T3-L1 adipocytes. Western blotting showed that atRA decreased the expression of p62, a cargo receptor for autophagic degradation, and increased the expression of the lipidated LC3B (LC3B-II), an autophagy marker, in epididymal fat. Next, we confirmed that atRA increased autophagic flux in differentiated 3T3-L1 cells using the GFP-LC3-RFP-LC3ΔG probe. Immunofluorescent staining revealed that the colocalization of LC3B with perilipin increased in differentiated 3T3-L1 cells treated with atRA. The knockdown of Atg5, an essential gene in autophagy induction, partly suppressed the atRA-induced release of non-esterified fatty acid (NEFA) from LDs in differentiated 3T3-L1 cells. atRA time-dependently elicited the phosphorylation of AMPK and Beclin1, autophagy-inducing factors, in mature 3T3-L1 adipocytes. Inversely, atRA decreased the protein expression of Rubicon, an autophagy repressor, in differentiated 3T3-L1 cells and epididymal fat. Interestingly, the expression of ALDH1A1, atRA-synthesizing enzymes, increased in epididymal fat with decreased protein expression of Rubicon in aged mice. These results suggest that atRA may partially induce lipolysis through lipophagy by activating the AMPK-Beclin1 signaling pathway in the adipocytes and increased atRA levels may contribute to decreased Rubicon expression in the epididymal fat of aged mice. (248/250 words). The Journal of nutritional biochemistry 109589 109589 20240129 10.1016/j.jnutbio.2024.109589 38295886 YukiKamei/published_papers/44482302 Yosuke Okumura Kotaro Abe Shoko Sakai Yuki Kamei Yuki Mori Yuichiro Adachi Masaki Takikawa Ayano Kitamura Hirokazu Ohminami Kohta Ohnishi Masashi Masuda Taiho Kambe Hironori Yamamoto Yutaka Taketani Elevated luminal inorganic phosphate suppresses intestinal Zn absorption in 5/6 nephrectomized rats. Zinc (Zn) is an essential trace element in various biological processes. Chronic kidney disease (CKD) often leads to hypozincemia, resulting in further progression of CKD. In CKD, intestinal Zn absorption, the main regulator of systemic Zn metabolism, is often impaired; however, the mechanism underlying Zn malabsorption remains unclear. Here, we evaluated intestinal Zn absorption capacity in a rat model of CKD induced by 5/6 nephrectomy (5/6 Nx). Rats were given Zn and the incremental area under the plasma Zn concentration-time curve (iAUC) was measured, as well as expression of ZIP4, an intestinal Zn transporter. We found that 5/6 Nx rats showed lower iAUC than sham-operated rats, but expression of ZIP4 protein was upregulated. We therefore focused on other Zn absorption regulators to explore the mechanism by which Zn absorption was substantially decreased. Because some phosphate compounds inhibit Zn absorption by co-precipitation and hyperphosphatemia is a common symptom in advanced CKD, we measured inorganic phosphate (Pi) levels. Pi was elevated not only in serum but also in the intestinal lumen of 5/6 Nx rats. Furthermore, intestinal intraluminal Pi administration decreased the iAUC in a dose-dependent manner in normal rats. In vitro, increased Pi concentration decreased Zn solubility under physiological conditions. Furthermore, dietary Pi restriction ameliorated hypozincemia in 5/6 Nx rats. We conclude that hyperphosphatemia or excess Pi intake is a factor in Zn malabsorption and hypozincemia in CKD. Appropriate management of hyperphosphatemia will be useful for prevention and treatment of hypozincemia in CKD patients. American journal of physiology. Renal physiology null null 20240118 10.1152/ajprenal.00310.2023 38234299 YukiKamei/published_papers/43922126 Yuki Kamei Yosuke Okumura Yuichiro Adachi Yuki Mori Maiko Sakai Kohta Ohnishi Hirokazu Ohminami Masashi Masuda Hisami Yamanaka-Okumura Yutaka Taketani Humoral and cellular factors inhibit phosphate-induced vascular calcification during the growth period. Hyperphosphatemia is an independent and non-classical risk factor of cardiovascular disease and mortality in patients with chronic kidney disease (CKD). Increased levels of extracellular inorganic phosphate (Pi) are known to directly induce vascular calcification, but the detailed underlying mechanism has not been clarified. Although serum Pi levels during the growth period are as high as those observed in hyperphosphatemia in adult CKD, vascular calcification does not usually occur during growth. Here, we have examined whether the defence system against Pi-induced vascular calcification can exist during the growth period using mice model. We found that calcification propensity of young serum (aged 3 weeks) was significantly lower than that of adult serum (10 months), possibly due to high fetuin-A levels. In addition, when the aorta was cultured in high Pi medium in vitro, obvious calcification was observed in the adult aorta but not in the young aorta. Furthermore, culture in high Pi medium increased the mRNA level of tissue-nonspecific alkaline phosphatase (TNAP), which degrades pyrophosphate, only in the adult aorta. Collectively, our findings indicate that the aorta in growing mouse may be resistant to Pi-induced vascular calcification via a mechanism in which high serum fetuin-A levels and suppressed TNAP expression. The Society for Free Radical Research Japan Journal of clinical biochemistry and nutrition 1880-5086 73 3 198 204 20231100 10.3164/jcbn.23-11 37970550 YukiKamei/published_papers/43914568 Mana Kitao Ai Yamaguchi Takuma Tomioka Kenji Kai Yuki Kamei Kenji Sugimoto Mitsugu Akagawa Astaxanthin protects human ARPE-19 retinal pigment epithelium cells from blue light-induced phototoxicity by scavenging singlet oxygen. Age-related macular degeneration (AMD) is one of an increasing number of diseases that causes irreversible impairment and loss of vision in the elderly. AMD occurs by oxidative stress-mediated apoptosis of retinal pigment epithelium cells. The onset of AMD may be positively correlated with the exposure to blue light. We screened food-derived carotenoids for cytoprotective action against blue light irradiation using human ARPE-19 retinal pigment epithelium cells. This study revealed that blue light irradiation triggered apoptosis and oxidative stress in all-trans-retinal (atRAL)-exposed ARPE-19 cells by generating singlet oxygen (1O2), leading to significant cell death. We found that astaxanthin, a potent anti-oxidative xanthophyll abundant in several marine organisms including microalgae, salmon, and shrimp, significantly suppresses blue light-induced apoptotic cell death of atRAL-exposed ARPE-19 cells by scavenging 1O2. Mechanistic studies using the blue-light irradiated cells also demonstrated that the cytoprotective effects of astaxanthin can be attributed to scavenging of 1O2 directly. Our results suggest the potential value of astaxanthin as a dietary strategy to prevent blue light-induced retinal degeneration including AMD. Free radical research 1 35 20231028 10.1080/10715762.2023.2277144 37897411 YukiKamei/published_papers/42060104 Yilimulati Yimamu Ayako Ohtani Yuichiro Takei Airi Furuichi Yuki Kamei Hisami Yamanaka-Okumura Hirokazu Ohminami Masashi Masuda Makoto Miyazaki Hironori Yamamoto Yutaka Taketani 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1) induces ectopic calcification. Vascular calcification is an important pathogenesis related to cardiovascular disease and high mortality rate in chronic kidney disease (CKD) patients. It has been well-known that hyper-phosphatemia induces osteochondrogenic transition of vascular smooth muscle cells (VSMCs) resulting ectopic calcification in aortic media, cardiac valve, and kidney. However, the detailed mechanism of the ectopic calcification has been not clarified yet. Here, we found that the co-localization of CYP27B1 with the calcified lesions of aorta and arteries in kidney of klotho mutant (kl/kl) mice, and then investigated the role of CYP27B1 in the mineralization of the VSMCs. Under high phosphate condition, overexpression of CYP27B1 induced calcification and osteocalcin mRNA expression in the VSMCs. Inversely, siRNA-CYP27B1 inhibited high phosphate-induced calcification of the VSMCs. We also found that the accumulated CYP27B1 protein was glycosylated in the kidney of kl/kl mice. Therefore, overexpression of CYP27B1-N310A and CYP27B1-T439A, which are a mutation for N-linked glycosylation site (N310A) and a mutation for O-linked glycosylation site (T439A) in CYP27B1, decreased calcium deposition and expression of RUNX2 induced by high phosphate medium in VSMCs compared with wild-type CYP27B1. These results suggest that extra-renal expression of glycosylated CYP27B1 would be required for ectopic calcification of VSMCs under hyperphosphatemia. Journal of clinical biochemistry and nutrition 71 2 103 111 20220900 10.3164/jcbn.22-16 36213783 YukiKamei/published_papers/42060123 Yuichiro Adachi Masashi Masuda Iori Sakakibara Takayuki Uchida Yuki Niida Yuki Mori Yuki Kamei Yosuke Okumura Hirokazu Ohminami Kohta Ohnishi Hisami Yamanaka-Okumura Takeshi Nikawa Yutaka Taketani All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal. All-trans retinoic acid (ATRA) increases the sensitivity to unfolded protein response in differentiating leukemic blasts. The downstream transcriptional factor of PERK, a major arm of unfolded protein response, regulates muscle differentiation. However, the role of growth arrest and DNA damage-inducible protein 34 (GADD34), one of the downstream factors of PERK, and the effects of ATRA on GADD34 expression in muscle remain unclear. In this study, we identified ATRA increased the GADD34 expression independent of the PERK signal in the gastrocnemius muscle of mice. ATRA up-regulated GADD34 expression through the transcriptional activation of GADD34 gene via inhibiting the interaction of homeobox Six1 and transcription co-repressor TLE3 with the MEF3-binding site on the GADD34 gene promoter in skeletal muscle. ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on GADD34 mRNA via p-38 MAPK, resulting in the instability of GADD34 mRNA. Overexpressed GADD34 in C2C12 cells changes the type of myosin heavy chain in myotubes. These results suggest ATRA increases GADD34 expression via transcriptional and post-transcriptional regulation, which changes muscle fiber type. Life science alliance 5 7 null null 20220300 10.26508/lsa.202101345 35318262 YukiKamei/misc/54247907 亀井優輝 西久保菜花 榊彩伽 麻田穂香 松本陽菜 伏見太希 赤川貢 乳児期マウスにおける内因的なビタミンK₂産生機構の解析 ビタミン 0006-386X 100 3 null null 20260000 YukiKamei/misc/54247915 島田渚 亀井優輝 伏見太希 辻健太郎 赤川貢 血管石灰化を抑制する香辛料の探索 日本栄養・食糧学会大会講演要旨集 79th null null 20250000 YukiKamei/misc/54247914 上野秀花 亀井優輝 伏見太希 片吉健史 辻健太郎 赤川貢 α-Humuleneの細胞内NAD⁺濃度上昇作用を介した細胞老化抑制効果の解明 日本栄養・食糧学会大会講演要旨集 79th null null 20250000 YukiKamei/misc/54247913 上野秀花 亀井優輝 伏見太希 赤川貢 片吉健史 辻健太郎 α-Humuleneの細胞内NAD+濃度上昇作用を介した細胞老化抑制効果の解明 四国医学雑誌(Web) 2758-3279 81 1-2 null null 20250000 YukiKamei/misc/54247912 赤川貢 西川綾花 辻健太郎 飯泉陽介 伏見太希 亀井優輝 阪本龍司 Cytoprotective Effects of Spermine on Dicarbonyl Stress ジカルボニルストレスに対するスペルミンの細胞保護効果の解明 日本農芸化学会大会講演要旨集(Web) 2186-7976 2025 null null 20250000 YukiKamei/misc/54247911 上野秀花 亀井優輝 伏見太希 片吉健史 辻健太郎 赤川貢 α-Humulene increases intracellular NAD⁺ concentration via upregulation of NAMPT Expression α-HumuleneによるNAMPT発現増加を介した細胞内NAD⁺濃度上昇作用の解明 日本農芸化学会大会講演要旨集(Web) 2186-7976 2025 null null 20250000 YukiKamei/misc/54247910 伏見太希 廣木健登 藤井靖之 亀井優輝 赤川貢 須原義智 越阪部奈緒美 Biological activities of the flavonoids with different C-ring depend on their redox properties C環構造の異なるフラボノイド類のRedox特性依存的な生理活性発現の解明 日本農芸化学会大会講演要旨集(Web) 2186-7976 2025 null null 20250000 YukiKamei/misc/54247909 恩澤乃愛 亀井優輝 杉谷里菜 伏見太希 赤川貢 オリーブ由来ポリフェノールOleuropeinによる腸セロトニン分泌機構とその中枢作用の解明 日本ポリフェノール学会学術集会プログラム・講演抄録集 18th null null 20250000 YukiKamei/misc/54247908 伏見太希 平畠千会 亀井優輝 赤川貢 須原義智 越阪部奈緒美 C環構造の違いによる交感神経刺激作用の差異の検証 日本ポリフェノール学会学術集会プログラム・講演抄録集 18th null null 20250000 YukiKamei/misc/54247906 伏見太希 平畠千絵 廣木健登 亀井優輝 赤川貢 越阪部奈緒美 Cyanidin-3-O-glucosideの循環動態への影響とその作用メカニズムの検証 日本農芸化学会中四国支部講演会講演要旨集(Web) 71st null null 20250000 YukiKamei/misc/54247917 田副渚 辻シャフィカ 池本一人 亀井優輝 伏見太希 内田貴之 二川健 赤川貢 Pyrroloquinoline quinone(PQQ)の抗肥満作用の解明 日本フードファクター学会学術集会講演要旨集(CD-ROM) 29th null null 20240000 YukiKamei/misc/54247916 杉谷里菜 亀井優輝 伏見太希 内藤健太郎 赤川貢 オリーブ由来ポリフェノールOleuropeinはセロトニン分泌を促進する 日本フードファクター学会学術集会講演要旨集(CD-ROM) 29th null null 20240000 YukiKamei/misc/47841180 永良祐樹 亀井優輝 内藤健太郎 赤川貢 アカメガシワ由来ポリフェノール,ベルゲニンによるミトコンドリア新生促進作用の解明 日本栄養・食糧学会中国・四国支部大会講演要旨集(CD-ROM) 56th null null 20230000 YukiKamei/misc/47841160 亀井優輝 赤川貢 物理化学的に血管石灰化を抑制する食品因子の探索 日本フードファクター学会学術集会講演要旨集 28th (CD-ROM) null null 20230000 YukiKamei/misc/42437091 永良祐樹 亀井優輝 内藤健太郎 赤川貢 アカメガシワ由来ポリフェノール,ベルゲニンのPGC-1α/SIRT1経路を介したミトコンドリア新生促進作用の解明 日本栄養・食糧学会大会講演要旨集 77th null null 20230500 YukiKamei/misc/42437146 Yuki Kamei Yosuke Okumura Yuichiro Adachi Yuki Mori Hirokazu Ohminami Masashi Masuda Yutaka Taketani Inhibitory Mechanism of Ectopic Calcification during Growth Period. ASBMR 2022 Annual meeting Abstracts null null 20220900 YukiKamei/misc/42437139 亀井優輝 大南博和 増田真志 竹谷豊 成長期には血中リン濃度が高くても血管石灰化が生じないのはなぜか? 栄養学雑誌 0021-5147 80 5 Supplement 191 null 20220900 YukiKamei/misc/42473978 竹谷豊 亀井優輝 織田奈央子 織田奈央子 大南博和 奥村仙示 増田真志 山本浩範 ミネラル代謝の変動と生物への影響 リン 日本骨粗鬆症学会雑誌 2189-8383 7 Suppl.1 (CD-ROM) null null 20210900 YukiKamei/misc/42473950 竹谷豊 亀井優輝 内科医が知っておきたい栄養食事療法 ビタミン・微量元素不足が生じやすい状況と補充で期待される効果 Medical Practice 0910-1551 38 9 1343 1348 20210900 YukiKamei/misc/42437171 亀井優輝 大南博和 大西康太 増田真志 奥村仙示 竹谷豊 成長期における血管石灰化抑制機構の解明 日本栄養・食糧学会大会講演要旨集 75th 136 null 20210700 YukiKamei/misc/42437177 佐守美穂 亀井優輝 大西康太 足立雄一郎 増田真志 大南博和 奥村仙示 竹谷豊 羽田尚彦 井上淳詞 NSAIDs起因性小腸障害に対するほうれん草由来グリセロ糖脂質の影響 第53回日本栄養・食糧学会中国・四国支部大会 要旨集 null null 20201000 YukiKamei/misc/42437182 亀井優輝 大南博和 大西康太 増田真志 奥村仙示 竹谷豊 小児期における血中リン濃度とFetuin-A濃度との関係 第61回日本生化学会 中国・四国支部大会 要旨集 null null 20200500 YukiKamei/misc/42437188 亀井優輝 大南博和 大西康太 増田真志 奥村仙示 竹谷豊 小児期において血中Fetuin-A濃度とリン濃度は相関する 日本栄養・食糧学会中国・四国支部大会講演要旨集(CD-ROM) 52nd null null 20191000 YukiKamei/misc/42437196 織田奈央子 杉原康平 池田美萌 亀井優輝 吉本亜由美 上番増喬 奥村仙示 竹谷豊 食事性リンが腸内環境及び腸管上皮細胞に及ぼす影響 2018年度生理研研究会・体内環境の維持機構における上皮膜輸送の多角的・統合的理解 要旨集 null null 20180900 YukiKamei/misc/42437191 Naoko Oda Kohei Sugihara Ayumi Yoshimoto Yuki Kamei Takashi Uebanso Masashi Masuda Hisami Yamanaka-Okumura Yutaka Taketani Gut Microbiota Disturbance Caused by Dietary Phosphate in Mice. ISN Frontiers meetings 2018 Abstracts null null 20180200 YukiKamei/misc/42437202 織田奈央子 杉原康平 吉本亜由美 亀井優輝 上番増喬 増田真志 奥村仙示 竹谷豊 高リン食は腸内細菌叢の多様性を低下させる 日本病態栄養学会誌(Web) 1345-8167 21 Supplement null null 20180100 YukiKamei/presentations/54397404 食品因子による腸セロトニン制御とその意義 日本農芸化学会 中四国支部創立25周年記念 第44回若手研究者シンポジウム 20260710 YukiKamei/presentations/50713762 亀井 優輝 血管石灰化を予防する食事の最新情報 第271回徳島医学会学術集会 市民公開シンポジウム 20250727 徳島大学 Best Teacher of the Year 2024 20250300 日本農芸化学会 2024年 B.B.B.論文賞 20250300 公益財団法人 康楽会 康楽賞 20230200 徳島大学 徳島大学医学部優秀学生賞 20200300 日本栄養・食糧学会 第52回日本栄養・食糧学会中四国支部大会 学生奨励賞 20191000