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KITANO Ryuji

    Department of Biological and Environmental Chemistry　Associate Professor
Last Updated :2024/05/15

Researcher Information

URL

ORCID ID

J-Global ID

Research Interests

  • 性ステロイド   ポリフェノール   腸内細菌   栄養代謝   GPCR   

Research Areas

  • Life sciences / Metabolism and endocrinology
  • Life sciences / Nutrition and health science
  • Life sciences / Applied biochemistry
  • Life sciences / Food sciences

Academic & Professional Experience

  • 2024/04 - Today  Kindai UniversityFaculty of Humanity-Oriented Science and Engineering Department of Biological and Environmental Chemistry准教授
  • 2021/01 - 2024/03  Kyoto University大学院薬学研究科 創発医薬科学専攻 代謝ゲノム薬学分野（兼務）助教
  • 2021/01 - 2024/03  京都大学大学院生命科学研究科 高次生命科学専攻 生体システム学分野助教
  • 2018/04 - 2020/12  東京農工大学大学院農学研究院 応用生命化学専攻 代謝機能制御学研究室特任講師
  • 2016/04 - 2018/03  国立病院機構 京都医療センター臨床研究センター内分泌代謝高血圧研究部博士研究員
  • 2013/12 - 2016/03  京都大学学際融合教育研究推進センター生理化学研究ユニット特定研究員

Education

  • 2009/04 - 2012/03  Kyoto University  Graduate School of Agriculture  Division of Food Science and Biotechnology
  • 2007/04 - 2009/03  Kyoto University  Graduate School of Agriculture  Division of Food Science and Biotechnology
  • 2003/04 - 2007/03  Kyoto University  Faculty of Agriculture  食品生物科学科

Association Memberships

  • 日本心血管内分泌代謝学会   日本内分泌学会   日本抗加齢医学会   日本食品免疫学会   日本肥満学会   日本栄養・食糧学会   日本農芸化学会   

Published Papers

  • Ryuji Ohue-Kitano; Yukika Banno; Yuki Masujima; Ikuo Kimura
    Scientific reports 14 (1) 1056 - 1056 2024/01 [Refereed]
     
    The gut microbiota has emerged as an important factor that potentially influences various physiological functions and pathophysiological processes such as obesity and type 2 diabetes mellitus. Accumulating evidence from human and animal studies suggests that gut microbial metabolites play a critical role as integral molecules in host-microbe interactions. Notably, several dietary environment-dependent fatty acid metabolites have been recognized as potent modulators of host metabolic homeostasis. More recently, nicotine, the primary active molecule in tobacco, has been shown to potentially affect host metabolism through alterations in the gut microbiota and its metabolites. However, the mechanisms underlying the interplay between host nutritional status, diet-derived microbial metabolites, and metabolic homeostasis during nicotine exposure remain unclear. Our findings revealed that nicotine administration had potential effects on weight regulation and metabolic phenotype, independent of reduced caloric intake. Moreover, nicotine-induced body weight suppression is associated with specific changes in gut microbial composition, including Lactobacillus spp., and KetoB, a nicotine-sensitive gut microbiota metabolite, which could be linked to changes in host body weight, suggesting its potential role in modulating host metabolism. Our findings highlight the remarkable impact of the interplay between nutritional control and the gut environment on host metabolism during smoking and smoking cessation.
  • Ryuji Ohue-Kitano; Yuki Masujima; Shota Nishikawa; Masayo Iwasa; Yosuke Nishitani; Hideaki Kawakami; Hiroshige Kuwahara; Ikuo Kimura
    Scientific reports 13 (1) 21246 - 21246 2023/12 [Refereed]
     
    3-(4-hydroxy-3-methoxyphenyl) propionic acid (HMPA) is a metabolite produced by the gut microbiota through the conversion of 4-hydroxy-3-methoxycinnamic acid (HMCA), which is a widely distributed hydroxycinnamic acid-derived metabolite found abundantly in plants. Several beneficial effects of HMPA have been suggested, such as antidiabetic properties, anticancer activities, and cognitive function improvement, in animal models and human studies. However, the intricate molecular mechanisms underlying the bioaccessibility and bioavailability profile following HMPA intake and the substantial modulation of metabolic homeostasis by HMPA require further elucidation. In this study, we effectively identified and characterized HMPA-specific GPR41 receptor, with greater affinity than HMCA. The activation of this receptor plays a crucial role in the anti-obesity effects and improvement of hepatic steatosis by stimulating the lipid catabolism pathway. For the improvement of metabolic disorders, our results provide insights into the development of functional foods, including HMPA, and preventive pharmaceuticals targeting GPR41.
  • Sato K; Ohno-Oishi M; Yoshida M; Sato T; Aizawa T; Sasaki Y; Maekawa S; Ishikawa M; Omodaka K; Kawano C; Ohue-Kitano R; Kimura I; Nakazawa T
    Glia 71 (11) 2609 - 2622 0894-1491 2023/07 [Refereed]
     
    Resident microglia are important to maintain homeostasis in the central nervous system, which includes the retina. The retinal microglia become activated in numerous pathological conditions, but the molecular signatures of these changes are poorly understood. Here, using an approach based on FACS and RNA-seq, we show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury. Most importantly, we found that the microglial cells strongly expressed Tnf and Il1α, both of which are known to induce neurotoxic reactive astrocytes, and were characterized by Gpr84high-expressing cells in a particular subpopulation. Moreover, ripasudil, a Rho kinase inhibitor, significantly blunted Gpr84 expression and cytokine induction in vitro and in vivo. Finally, GPR84-deficient mice prevented RGC loss in optic nerve-injured retina. These results reveal that Rho kinase-mediated GPR84 alteration strongly contribute to microglial activation and promote neurotoxicity, suggesting that Rho-ROCK and GPR84 signaling may be potential therapeutic targets to prevent the neurotoxic microglial phenotype induced by optic nerve damage, such as occurs in traumatic optic neuropathy and glaucoma.
  • Ryuji Ohue-Kitano; Hazuki Nonaka; Akari Nishida; Yuki Masujima; Daisuke Takahashi; Takako Ikeda; Akiharu Uwamizu; Miyako Tanaka; Motoyuki Kohjima; Miki Igarashi; Hironori Katoh; Tomohiro Tanaka; Asuka Inoue; Takayoshi Suganami; Koji Hase; Yoshihiro Ogawa; Junken Aoki; Ikuo Kimura
    JCI insight 8 (2) e165469  2023/01 [Refereed]
     
    Medium-chain triglycerides (MCTs), which consist of medium-chain fatty acids (MCFAs), are unique forms of dietary fat with various health benefits. GPR84 acts as a receptor for MCFAs (especially C10:0 and C12:0); however, GPR84 is still considered an orphan receptor, and the nutritional signaling of endogenous and dietary MCFAs via GPR84 remains unclear. Here, we showed that endogenous MCFA-mediated GPR84-signaling protected hepatic functions from diet-induced lipotoxicity. Under high-fat diet (HFD) conditions, GPR84-deficient mice exhibited non-alcoholic steatohepatitis (NASH) and the progression of hepatic fibrosis but not steatosis. With markedly increased hepatic MCFA levels under HFD, GPR84 suppressed lipotoxicity-induced macrophage over-activation. Thus, GPR84 is an immunomodulating receptor that suppresses excessive dietary fat intake-induced toxicity by sensing increases in MCFAs. Additionally, administering MCTs, MCFAs (C10:0 or C12:0, but not C8:0), or GPR84 agonists effectively impreoved NASH in mouse models. Exogenous GPR84 stimulation is therefore a potential strategy for treating NASH.
  • Yuka Yamanouchi; Seita Chudan; Riko Ishibashi; Ryuji Ohue‐Kitano; Miyu Nishikawa; Yoshiaki Tabuchi; Ikuo Kimura; Yoshinori Nagai; Shinichi Ikushiro; Yukihiro Furusawa
    Molecular Nutrition & Food Research Wiley 66 (22) e2200063  1613-4125 2022/11 [Refereed]
  • Hazuki Nonaka; Ryuji Ohue-Kitano; Yuki Masujima; Miki Igarashi; Ikuo Kimura
    Frontiers in Nutrition Frontiers Media SA 9 848450  2022/03 [Refereed]
     
    Background Dietary triglycerides are an important energy source; however, their excess intake causes metabolic diseases such as obesity and type 2 diabetes. Medium-chain triglycerides (MCTs) as triglyceride forms of medium-chain fatty acids (MCFAs) are applied to meet the energy demands of athletes, the elderly, and people with stunted growth, because MCFAs are efficiently converted into energy for immediate utilization by the organs and do not accumulate as fat. Although the intake of each MCT type (octanoate; C8:0, decanoate; C10:0, and dodecanoate; C12:0) exhibits beneficial metabolic effects, individual functional differences remain unclear. Methods MCTs or MCFAs were administrated to male GPR84-deficient mice with a C57BL/6J background and mouse enteroendocrine cell line STC-1, and the effects on glucose homeostasis and gut hormone GLP-1 secretion were evaluated. Results C10:0 intake improves glucose metabolism through the MCFA receptor GPR84-mediated GLP-1 secretion. Each MCT intake showed resistance to obesity and improved metabolic parameters compared with lard intake. Moreover, oral administration of MCTs enhanced glucose tolerance, especially C10:0 administration, which sufficiently increased plasma GLP-1 levels. Additionally, C10:0 stimulation promoted GLP-1 secretion via GPR84 in STC-1, enhanced glucose tolerance through GPR84-mediated GLP-1 secretion, and showed resistance to high-fat diet (HFD)-induced obesity in mice. Conclusions Dietary MCT (C10:0) intake efficiently may protect against obesity and improve insulin resistance via GLP-1 secretion.
  • Keita Watanabe; Mayu Yamano; Yuki Masujima; Ryuji Ohue-Kitano; Ikuo Kimura
    Biochemistry and Biophysics Reports Elsevier BV 27 101095  2405-5808 2021/08 [Refereed]
  • Toru Kusakabe; Shigefumi Yokota; Mika Shimizu; Takayuki Inoue; Masashi Tanaka; Ryuji Ohue-Kitano; Kazuya Muranaka; Hajime Yamakage; Hiromichi Wada; Koji Hasegawa; Noriko Satoh-Asahara
    BMJ Open Diabetes Research & Care BMJ 8 (1) e001303  2020/09 [Refereed]
     
    IntroductionTreatment using sodium-glucose cotransporter (SGLT) 2 inhibitor and low-carbohydrate diet (LCD) for obesity and type 2 diabetes are similar in terms of carbohydrate limitation. However, their mechanisms of action differ, and the effects on the body remain unclear. We investigated the effects of SGLT2 inhibitor and LCD on body composition and metabolic profile using the db/db mouse model for obesity and type 2 diabetes. Research design and methodsEight-week-old male db/db mice were divided into four groups: mice receiving normal diet and vehicle or canagliflozin (Cana) administration and mice receiving LCD and vehicle or Cana administration for 8 weeks. Consumed calories were adjusted to be equal among the groups. ResultsBoth Cana administration and LCD feeding resulted in significant weight gain. Cana administration significantly decreased plasma glucose levels and increased plasma insulin levels with preservation of pancreatic β cells. However, LCD feeding did not improve plasma glucose levels but deteriorated insulin sensitivity. LCD feeding significantly reduced liver weight and hepatic triglyceride content; these effects were not observed with Cana administration. Combined treatment with LCD did not lead to an additive increase in blood β-ketone levels. ConclusionsSGLT2 inhibitors and LCD exert differential effects on the body. Their combined use may achieve better metabolic improvements in obesity and type 2 diabetes.
  • Ikuo Kimura; Junki Miyamoto; Ryuji Ohue-Kitano; Keita Watanabe; Takahiro Yamada; Masayoshi Onuki; Ryo Aoki; Yosuke Isobe; Daiji Kashihara; Daisuke Inoue; Akihiko Inaba; Yuta Takamura; Satsuki Taira; Shunsuke Kumaki; Masaki Watanabe; Masato Ito; Fumiyuki Nakagawa; Junichiro Irie; Hiroki Kakuta; Masakazu Shinohara; Ken Iwatsuki; Gozoh Tsujimoto; Hiroaki Ohno; Makoto Arita; Hiroshi Itoh; Koji Hase
    Science American Association for the Advancement of Science (AAAS) 367 (6481) eaaw8429 - eaaw8429 0036-8075 2020/02 [Refereed]
     
    Antibiotics and dietary habits can affect the gut microbial community, thus influencing disease susceptibility. Although the effect of microbiota on the postnatal environment has been well documented, much less is known regarding the impact of gut microbiota at the embryonic stage. Here we show that maternal microbiota shapes the metabolic system of offspring in mice. During pregnancy, short-chain fatty acids produced by the maternal microbiota dictate the differentiation of neural, intestinal, and pancreatic cells through embryonic GPR41 and GPR43. This developmental process helps maintain postnatal energy homeostasis, as evidenced by the fact that offspring from germ-free mothers are highly susceptible to metabolic syndrome, even when reared under conventional conditions. Thus, our findings elaborate on a link between the maternal gut environment and the developmental origin of metabolic syndrome.
  • Ikuo Kimura; Atsuhiko Ichimura; Ryuji Ohue-Kitano; Miki Igarashi
    Physiological reviews 100 (1) 171 - 210 2020/01 [Refereed]
     
    Fatty acids are metabolized and synthesized as energy substrates during biological responses. Long- and medium-chain fatty acids derived mainly from dietary triglycerides, and short-chain fatty acids (SCFAs) produced by gut microbial fermentation of the otherwise indigestible dietary fiber, constitute the major sources of free fatty acids (FFAs) in the metabolic network. Recently, increasing evidence indicates that FFAs serve not only as energy sources but also as natural ligands for a group of orphan G protein-coupled receptors (GPCRs) termed free fatty acid receptors (FFARs), essentially intertwining metabolism and immunity in multiple ways, such as via inflammation regulation and secretion of peptide hormones. To date, several FFARs that are activated by the FFAs of various chain lengths have been identified and characterized. In particular, FFAR1 (GPR40) and FFAR4 (GPR120) are activated by long-chain saturated and unsaturated fatty acids, while FFAR3 (GPR41) and FFAR2 (GPR43) are activated by SCFAs, mainly acetate, butyrate, and propionate. In this review, we discuss the recent reports on the key physiological functions of the FFAR-mediated signaling transduction pathways in the regulation of metabolism and immune responses. We also attempt to reveal future research opportunities for developing therapeutics for metabolic and immune disorders.
  • Hidenori Shimizu; Yuki Masujima; Chihiro Ushiroda; Rina Mizushima; Satsuki Taira; Ryuji Ohue-Kitano; Ikuo Kimura
    Scientific Reports Springer Science and Business Media LLC 9 (1) 16574  2019/11 [Refereed]
     
    Abstract Fermented foods represent a significant portion of human diets with several beneficial effects. Foods produced by bacterial fermentation are enriched in short-chain fatty acids (SCFAs), which are functional products of dietary fibers via gut microbial fermentation. In addition to energy sources, SCFAs also act as signaling molecules via G-protein coupled receptors such as FFAR2 and FFAR3. Hence, dietary SCFAs in fermented foods may have a direct influence on metabolic functions. However, the detailed mechanism by dietary SCFAs remains unclear. Here, we show that dietary SCFAs protected against high-fat diet-induced obesity in mice in parallel with increased plasma SCFAs without changing cecal SCFA or gut microbial composition. Dietary SCFAs suppressed hepatic weight and lipid synthesis. These effects were abolished in FFAR3-deficient mice but not FFAR2-deficient. Thus, SCFAs supplementation improved hepatic metabolic functions via FFAR3 without influencing intestinal environment. These findings could help to promote the development of functional foods using SCFAs.
  • Junki Miyamoto; Ryuji Ohue-Kitano; Hiromi Mukouyama; Akari Nishida; Keita Watanabe; Miki Igarashi; Junichiro Irie; Gozoh Tsujimoto; Noriko Satoh-Asahara; Hiroshi Itoh; Ikuo Kimura
    Proceedings of the National Academy of Sciences Proceedings of the National Academy of Sciences 116 (47) 23813 - 23821 0027-8424 2019/11 [Refereed]
     
    Ketone bodies, including β-hydroxybutyrate and acetoacetate, are important alternative energy sources during energy shortage. β-Hydroxybutyrate also acts as a signaling molecule via specific G protein-coupled receptors (GPCRs); however, the specific associated GPCRs and physiological functions of acetoacetate remain unknown. Here we identified acetoacetate as an endogenous agonist for short-chain fatty acid (SCFA) receptor GPR43 by ligand screening in a heterologous expression system. Under ketogenic conditions, such as starvation and low-carbohydrate diets, plasma acetoacetate levels increased markedly, whereas plasma and cecal SCFA levels decreased dramatically, along with an altered gut microbiota composition. In addition, Gpr43-deficient mice showed reduced weight loss and suppressed plasma lipoprotein lipase activity during fasting and eucaloric ketogenic diet feeding. Moreover, Gpr43-deficient mice exhibited minimal weight decrease after intermittent fasting. These observations provide insight into the role of ketone bodies in energy metabolism under shifts in nutrition and may contribute to the development of preventive medicine via diet and foods.
  • Regulation of host energy metabolism by gut microbiota-derived short-chain fatty acids
    Hidenori Shimizu; Ryuji Ohue-Kitano; Ikuo Kimura
    Glycative Stress Research 6 (3) 181 - 191 2019/09 [Refereed]
  • Ryuji Ohue-Kitano; Satsuki Taira; Keita Watanabe; Yuki Masujima; Toru Kuboshima; Junki Miyamoto; Yosuke Nishitani; Hideaki Kawakami; Hiroshige Kuwahara; Ikuo Kimura
    Nutrients MDPI AG 11 (5) 1036  2019/05 [Refereed]
     
    4-Hydroxy-3-methoxycinnamic acid (HMCA), a hydroxycinnamic acid derivative, is abundant in fruits and vegetables, including oranges, carrots, rice bran, and coffee beans. Several beneficial effects of HMCA have been reported, including improvement of metabolic abnormalities in animal models and human studies. However, its mitigating effects on high-fat diet (HFD)-induced obesity, and the mechanism underlying these effects, remain to be elucidated. In this study, we demonstrated that dietary HMCA was efficacious against HFD-induced weight gain and hepatic steatosis, and that it improved insulin sensitivity. These metabolic benefits of HMCA were ascribable to 3-(4-hydroxy-3-methoxyphenyl)propionic acid (HMPA) produced by gut microbiota. Moreover, conversion of HMCA into HMPA was attributable to a wide variety of microbes belonging to the phylum Bacteroidetes. We further showed that HMPA modulated gut microbes associated with host metabolic homeostasis by increasing the abundance of organisms belonging to the phylum Bacteroidetes and reducing the abundance of the phylum Firmicutes. Collectively, these results suggest that HMPA derived from HMCA is metabolically beneficial, and regulates hepatic lipid metabolism, insulin sensitivity, and the gut microbial community. Our results provide insights for the development of functional foods and preventive medicines, based on the microbiota of the intestinal environment, for the prevention of metabolic disorders.
  • M. Tanaka; H. Yamakage; S. Masuda; T. Inoue; R. Ohue-Kitano; R. Araki; Y. Matoba; M. Saito; T. Nagaoka; K. Yonezawa; T. Tanaka; M. Suzuki; M. Sawamura; M. Nishimura; S. Odori; H. Wada; K. Kotani; T. Kusakabe; A. Shimatsu; K. Hasegawa; N. Satoh-Asahara
    Diabetes & Metabolism Elsevier BV 45 (1) 86 - 89 1262-3636 2019/01 [Refereed]
  • Masashi Tanaka; Shinya Masuda; Hajime Yamakage; Takayuki Inoue; Ryuji Ohue-Kitano; Shigefumi Yokota; Toru Kusakabe; Hiromichi Wada; Kiyoshi Sanada; Kojiro Ishii; Koji Hasegawa; Akira Shimatsu; Noriko Satoh-Asahara
    Diabetes Research and Clinical Practice Elsevier BV 142 195 - 202 0168-8227 2018/08 [Refereed]
  • S. Masuda; M. Tanaka; T. Inoue; R. Ohue-Kitano; H. Yamakage; K. Muranaka; T. Kusakabe; A. Shimatsu; K. Hasegawa; N. Satoh-Asahara
    Acta Physiologica Wiley 222 (3) e12975  1748-1708 2018/03 [Refereed]
  • Ryuji Ohue‐Kitano; Yumiko Yasuoka; Tsuyoshi Goto; Nahoko Kitamura; Si‐Bum Park; Shigenobu Kishino; Ikuo Kimura; Mayu Kasubuchi; Haruya Takahashi; Yongjia Li; Yu‐Sheng Yeh; Huei‐Fen Jheng; Mari Iwase; Masashi Tanaka; Shinya Masuda; Takayuki Inoue; Hajime Yamakage; Toru Kusakabe; Fumito Tani; Akira Shimatsu; Nobuyuki Takahashi; Jun Ogawa; Noriko Satoh‐Asahara; Teruo Kawada
    The FASEB Journal Wiley 32 (1) 304 - 318 0892-6638 2018/01 [Refereed]
     
    Among dietary fatty acids with immunologic effects, ω-3 polyunsaturated fatty acids, such as α-linolenic acid (ALA), have been considered as factors that contribute to the differentiation of M2-type macrophages (M2 macrophages). In this study, we examined the effect of ALA and its gut lactic acid bacteria metabolites 13-hydroxy-9(Z),15(Z)-octadecadienoic acid (13-OH) and 13-oxo-9(Z),15(Z)-octadecadienoic acid (13-oxo) on the differentiation of M2 macrophages from bone marrow-derived cells (BMDCs) and investigated the underlying mechanisms. BMDCs were stimulated with ALA, 13-OH, or 13-oxo in the presence of IL-4 or IL-13 for 24 h, and significant increases in M2 macrophage markers CD206 and Arginase-1 (Arg1) were observed. In addition, M2 macrophage phenotypes were less prevalent following cotreatment with GPCR40 antagonists or inhibitors of PLC-β and MEK under these conditions, suggesting that GPCR40 signaling is involved in the regulation of M2 macrophage differentiation. In further experiments, remarkable M2 macrophage accumulation was observed in the lamina propria of the small intestine of C57BL/6 mice after intragastric treatments with ALA, 13-OH, or 13-oxo at 1 g/kg of body weight per day for 3 d. These findings suggest a novel mechanism of M2 macrophage differentiation involving fatty acids from gut lactic acid bacteria and GPCR40 signaling.-Ohue-Kitano, R., Yasuoka, Y., Goto, T., Kitamura, N., Park, S.-B., Kishino, S., Kimura, I., Kasubuchi, M., Takahashi, H., Li, Y., Yeh, Y.-S., Jheng, H.-F., Iwase, M., Tanaka, M., Masuda, S., Inoue, T., Yamakage, H., Kusakabe, T., Tani, F., Shimatsu, A., Takahashi, N., Ogawa, J., Satoh-Asahara, N., Kawada, T. α-Linolenic acid-derived metabolites from gut lactic acid bacteria induce differentiation of anti-inflammatory M2 macrophages through G protein-coupled receptor 40.
  • Minji Kim; Tomoya Furuzono; Kanae Yamakuni; Yongjia Li; Young‐Il Kim; Haruya Takahashi; Ryuji Ohue‐Kitano; Huei‐Fen Jheng; Nobuyuki Takahashi; Yuriko Kano; Rina Yu; Shigenobu Kishino; Jun Ogawa; Kunitoshi Uchida; Jun Yamazaki; Makoto Tominaga; Teruo Kawada; Tsuyoshi Goto
    The FASEB Journal Wiley 31 (11) 5036 - 5048 0892-6638 2017/11 [Refereed]
     
    Gut microbiota can regulate the host energy metabolism; however, the underlying mechanisms that could involve gut microbiota-derived compounds remain to be understood. Therefore, in this study, we investigated the effects of KetoA [10-oxo-12(Z)-octadecenoic acid]-a linoleic acid metabolite produced by gut lactic acid bacteria-on whole-body energy metabolism and found that dietary intake of KetoA could enhance energy expenditure in mice, thereby protecting mice from diet-induced obesity. By using Ca2+ imaging and whole-cell patch-clamp methods, KetoA was noted to potently activate transient receptor potential vanilloid 1 (TRPV1) and enhance noradrenalin turnover in adipose tissues. In addition, KetoA up-regulated genes that are related to brown adipocyte functions, including uncoupling protein 1 (UCP1) in white adipose tissue (WAT), which was later diminished in the presence of a β-adrenoreceptor blocker. By using obese and diabetic model KK-Ay mice, we further show that KetoA intake ameliorated obesity-associated metabolic disorders. In the absence of any observed KetoA-induced antiobesity effect or UCP1 up-regulation in TRPV1-deficient mice, we prove that the antiobesity effect of KetoA was caused by TRPV1 activation-mediated browning in WAT. KetoA produced in the gut could therefore be involved in the regulation of host energy metabolism.-Kim, M., Furuzono, T., Yamakuni, K., Li, Y., Kim, Y.-I., Takahashi, H., Ohue-Kitano, R., Jheng, H.-F., Takahashi, N., Kano, Y., Yu, R., Kishino, S., Ogawa, J., Uchida, K., Yamazaki, J., Tominaga, M., Kawada, T., Goto, T. 10-oxo-12(Z)-octadecenoic acid, a linoleic acid metabolite produced by gut lactic acid bacteria, enhances energy metabolism by activation of TRPV1.
  • Ryo Inoue; Ryuji Ohue-Kitano; Takamitsu Tsukahara; Masashi Tanaka; Shinya Masuda; Takayuki Inoue; Hajime Yamakage; Toru Kusakabe; Koji Hasegawa; Akira Shimatsu; Noriko Satoh-Asahara
    Journal of Clinical Biochemistry and Nutrition The Society for Free Radical Research Japan 61 (3) 217 - 221 0912-0009 2017/11 [Refereed]
  • Ha-Eun Yang; Yongjia Li; Akira Nishimura; Huei-Fen Jheng; Ana Yuliana; Ryuji Kitano-Ohue; Wataru Nomura; Nobuyuki Takahashi; Chu-Sook Kim; Rina Yu; Nahoko Kitamura; Si-Bum Park; Shigenobu Kishino; Jun Ogawa; Teruo Kawada; Tsuyoshi Goto
    Molecular Nutrition & Food Research Wiley 61 (10) 1700064  1613-4125 2017/10 [Refereed]
  • Takayuki Inoue; Masashi Tanaka; Shinya Masuda; Ryuji Ohue-Kitano; Hajime Yamakage; Kazuya Muranaka; Hiromichi Wada; Toru Kusakabe; Akira Shimatsu; Koji Hasegawa; Noriko Satoh-Asahara
    Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids Elsevier BV 1862 (5) 552 - 560 1388-1981 2017/05 [Refereed]
  • Masashi Tanaka; Hajime Yamakage; Takayuki Inoue; Shinya Masuda; Ryuji Ohue-Kitano; Toru Kusakabe; Noriko Satoh-Asahara
    Journal of Alzheimer’s Disease & Parkinsonism OMICS Publishing Group 7 (5) 380  2017 [Refereed]
  • Tsuyoshi Goto; Young-Il Kim; Tomoya Furuzono; Nobuyuki Takahashi; Kanae Yamakuni; Ha-Eun Yang; Yongjia Li; Ryuji Ohue; Wataru Nomura; Tatsuya Sugawara; Rina Yu; Nahoko Kitamura; Si-Bum Park; Shigenobu Kishino; Jun Ogawa; Teruo Kawada
    Biochemical and Biophysical Research Communications Elsevier BV 459 (4) 597 - 603 0006-291X 2015/04 [Refereed]
  • Ryuji Ohue; Masahiro Nakamoto; Naofumi Kitabatake; Fumito Tani
    Cytotechnology Springer Science and Business Media LLC 64 (3) 221 - 230 0920-9069 2012/05 [Refereed]
  • Ryuji Ohue; Kei Hashimoto; Masahiro Nakamoto; Yuichi Furukawa; Tetsuya Masuda; Naofumi Kitabatake; Fumito Tani
    Journal of Innate Immunity S. Karger AG 3 (6) 605 - 613 1662-811X 2011 [Refereed]
  • R. Ohue; F. Tani; N. Kitabatake
    Nucleic Acids Symposium Series Oxford University Press (OUP) 52 (1) 647 - 648 0261-3166 2008/09 [Refereed]

Books etc

  • 腸内細菌代謝物とアンチエイジング
    大植 隆司; 木村 郁夫 (Joint workL章.マイクロバイオームとアンチエイジング（抗加齢）医学)アンチエイジング医学の基礎と臨床 2023
  • 腸内微生物叢と代謝制御システム
    大植 隆司; 清水 秀憲; 木村 郁夫 (Joint work)腸内微生物叢最前線 2021
  • 短鎖脂肪酸の産生と生理機能調節
    大植 隆司; 平 さつき; 木村 郁夫 (Joint work)食品機能性脂質の基礎と応用 2018

Conference Activities & Talks

  • 中鎖脂肪酸受容体GPR84を介した代謝調節機構の解明
    大植隆司; 木村郁夫
    第65回日本脂質生化学会  2023/06
  • The role of the medium-chain fatty acid receptor GPR84 on metabolic homeostasis.
    大植隆司
    GUTS FORUM 2021  2021/07
  • 中鎖脂肪酸受容体を介した新規代謝調節機構
    大植隆司
    生理学研究所2020年度研究会  2020/12
  • 細胞膜上性ステロイドホルモン受容体を介した代謝機能制御
    大植隆司
    生理学研究所2018年度研究会  2018/09
  • 食由来成分を基質とした腸内細菌代謝物による宿主のエネルギー代謝制御
    大植隆司
    日本内分泌学会第36回内分泌代謝学サマーセミナーYECシンポジウムB  2018/08
  • 腸内細菌叢を標的とした新規心血管病予防法とオーダーメイド栄養プログラムの開発
    大植隆司
    アンチエイジングフェア2017  2017/09

MISC

  • ケトン体の新たな受容体の発見の意義
    塩野 勝之; 北野(大植)隆司; 木村 郁夫  循環器内科  92-  (1)  77  -83  2022/07
  • 腸内フローラ・口腔フローラ改善によるウェルネスアップ
    大植 隆司; 木村 郁夫  食と健康  2022
  • 妊娠期の腸内環境と子供の代謝
    野仲 葉月; 大植 隆司; 木村 郁夫  糖尿病・内分泌代謝科  54-  (1)  52  -60  2022/01
  • ケトン体受容体による生体機能制御
    大植隆司; 西田朱里; 木村郁夫  医学のあゆみ  276-  (12)  1098  -1103  2021
  • 腸内細菌と肥満症
    大植 隆司; 加藤 裕教; 木村 郁夫  実験医学（増刊号）  39-  (5)  188  -194  2021
  • 低炭水化物食における分子栄養メカニズム
    西田 朱里; 宮本 潤基; 大植 隆司; 木村 郁夫  Pharma Medica  38-  (9)  79  -83  2020
  • 腸内細菌代謝物と生体機能—循環器・代謝疾患の治療への応用—
    清水 秀憲; 大植 隆司; 木村 郁夫  CARDIAC PRACTICE  29-  (4)  23  -27  2019
  • 内分泌・代謝疾患を診る 日本人2型糖尿病におけるPICRUSt予測メタゲノム解析を用いた腸内細菌叢プロファイルと宿主の糖代謝との関連解析
    浅原 哲子; 北野 隆司; 井上 亮; 塚原 隆充; 田中 将志; 井上 隆之; 村中 和哉; 山陰 一; 日下部 徹; 島津 章  国立病院総合医学会講演抄録集  72回-  100  -100  2018/11
  • 肥満患者における骨格筋由来液性因子・マイオスタチンを介した耐糖能悪化と骨格筋萎縮
    田中 将志; 増田 慎也; 山陰 一; 井上 隆之; 北野 隆司; 横田 繁史; 村中 和哉; 日下部 徹; 和田 啓道; 真田 樹義; 石井 好二郎; 長谷川 浩二; 島津 章; 浅原 哲子  糖尿病  61-  (Suppl.1)  S  -321  2018/04
  • 日本人2型糖尿病におけるPICRUSt予測メタゲノム解析を用いた腸内細菌叢プロファイルと宿主の糖代謝との機能的連関
    浅原 哲子; 北野 隆司; 井上 亮; 塚原 隆充; 田中 将志; 井上 隆之; 横田 繁史; 村中 和哉; 山陰 一; 日下部 徹; 長谷川 浩二; 島津 章  糖尿病  61-  (Suppl.1)  S  -389  2018/04
  • 肥満症・2型糖尿病とプロバイオティクス
    大植隆司; 平さつき; 木村郁夫  臨床と研究  95-  (9)  51  -56  2018
  • 食物繊維由来腸内細菌代謝物、短鎖脂肪酸と宿主代謝制御
    平さつき; 渡辺啓太; 大植隆司; 木村郁夫  ルミナコイド研究  22-  (2)  53  -62  2018
  • 糖尿病・肥満における新規認知症予知バイオマーカーの検討 TREM2の病態意義の解明
    田中 将志; 山陰 一; 増田 慎也; 井上 隆之; 北野 隆司; 村中 和哉; 小鳥 真司; 村瀬 永子; 大谷 良; 中村 道三; 和田 啓道; 小谷 和彦; 日下部 徹; 島津 章; 長谷川 浩二; 浅原 哲子  肥満研究  23-  (Suppl.)  176  -176  2017/09
  • ω3不飽和脂肪酸によるSIRT1経路を介したミクログリア活性抑制
    井上 隆之; 田中 将志; 増田 慎也; 山陰 一; 北野 隆司; 村中 和哉; 日下部 徹; 和田 啓道; 島津 章; 長谷川 浩二; 浅原 哲子  肥満研究  23-  (Suppl.)  218  -218  2017/09
  • 日本人2型糖尿病におけるPICRUSt予測メタゲノム解析を用いた腸内細菌叢の病態生理学的意義の解明
    北野 隆司; 井上 亮; 塚原 隆充; 田中 将志; 増田 慎也; 井上 隆之; 山陰 一; 日下部 徹; 長谷川 浩二; 島津 章; 浅原 哲子  肥満研究  23-  (Suppl.)  227  -227  2017/09
  • 肥満・糖尿病における新規認知症予知バイオマーカーの探索 TREM2の病態生理学的意義の解明
    田中 将志; 山陰 一; 増田 慎也; 井上 隆之; 北野 隆司; 村中 和哉; 小鳥 真司; 和田 啓道; 小谷 和彦; 日下部 徹; 島津 章; 長谷川 浩二; 浅原 哲子  日本動脈硬化学会総会プログラム・抄録集  49回-  197  -197  2017/06
  • 糖尿病・肥満における新規認知症予知バイオマーカー 血清TREM2の病態意義の解明
    田中 将志; 山陰 一; 増田 慎也; 井上 隆之; 北野 隆司; 村中 和哉; 小鳥 真司; 和田 啓道; 小谷 和彦; 日下部 徹; 島津 章; 長谷川 浩二; 浅原 哲子  日本内分泌学会雑誌  93-  (1)  259  -259  2017/04
  • 糖尿病における認知機能低下・認知症の発症予知バイオマーカーの探索 TREM2の病態生理学的意義の解明
    田中 将志; 山陰 一; 増田 慎也; 井上 隆之; 北野 隆司; 村中 和哉; 小鳥 真司; 和田 啓道; 小谷 和彦; 日下部 徹; 島津 章; 長谷川 浩二; 浅原 哲子  糖尿病  60-  (Suppl.1)  S  -441  2017/04
  • マウス活性化ミクログリアにおけるω3不飽和脂肪酸によるSIRT1を介した炎症抑制作用機序の解明
    井上 隆之; 田中 将志; 増田 慎也; 山陰 一; 北野 隆司; 村中 和哉; 日下部 徹; 和田 啓道; 島津 章; 長谷川 浩二; 浅原 哲子  日本内分泌学会雑誌  93-  (1)  367  -367  2017/04
  • ω3不飽和脂肪酸によるSIRT1を介した抗炎症作用とミクログリア活性化抑制機序の解明
    井上 隆之; 田中 将志; 増田 慎也; 山陰 一; 北野 隆司; 村中 和哉; 日下部 徹; 和田 啓道; 島津 章; 長谷川 浩二; 浅原 哲子  糖尿病  60-  (Suppl.1)  S  -241  2017/04
  • 腸内細菌と食事療法
    浅原哲子; 北野隆司  月刊糖尿病  9-  (5)  43  -56  2017
  • 肥満症における腸内細菌とエクオールの関与
    浅原哲子; 北野隆司  内分泌・糖尿病・代謝内科  45-  (1)  14  -21  2017
  • 肥満・糖尿病における認知症予知バイオマーカーの探索 血清TREM2の病態意義
    田中 将志; 山陰 一; 増田 慎也; 井上 隆之; 北野 隆司; 村中 和哉; 和田 啓道; 長谷川 浩二; 荒木 里香; 的場 ゆか; 齋藤 美穂; 長岡 匡; 米澤 一也; 田中 剛史; 大谷 すみれ; 澤村 守夫; 西村 元伸; 島津 章; 浅原 哲子  肥満研究  22-  (Suppl.)  239  -239  2016/09
  • 活性化ミクログリアにおけるSIRT1を介したω3不飽和脂肪酸による炎症抑制作用機序の解明
    井上 隆之; 田中 将志; 増田 慎也; 山陰 一; 北野 隆司; 村中 和哉; 和田 啓道; 長谷川 浩二; 島津 章; 浅原 哲子  肥満研究  22-  (Suppl.)  245  -245  2016/09

Awards & Honors

  • 2021/11 GPCR研究会 第16回GPCR研究会 松尾研究奨励賞
  • 2019/07 日本内分泌学会 第37回内分泌代謝学サマーセミナー ポスター賞
  • 2017/10 日本肥満学会 第38回日本肥満学会 肥満症学「適塾」Award

Research Grants & Projects

  • 中鎖脂肪酸受容体GPR84を介した消化管ホルモン分泌機構の解明
    群馬大学生体調節研究所：令和５年度 「内分泌・代謝学共同研究拠点」共同研究費
    Date (from‐to) : 2023/04
  • ケトジェニック環境下におけるGPCRを介した新規代謝制御メカニズムの 解明
    ロッテ財団：第8回（2021年度）奨励研究助成A
    Date (from‐to) : 2021/04
  • ケトン体受容体を介したメタボリックシグナルに基づく新規エネルギー代謝調節機構
    日本学術振興会：令和2年度科学研究費補助金 基盤研究（C）
    Date (from‐to) : 2020/04
  • 機能性食品成分-GPR30システムによる腸管免疫を介した血管機能改善機構の解明
    日本学術振興会：平成30年度科学研究費補助金（若手）
    Date (from‐to) : 2018/04
  • 腸内細菌叢を標的とした新規心血管病予防法とオーダーメイド栄養プログラムの開発
    特定非営利活動法人（NPO）ヒューマンセンター21：平成29年度「若手研究者育成の為の研究助成」
    Date (from‐to) : 2017/08
  • 心血管病予防の為の新規栄養指導プログラムの開発 －時間栄養学に基づく効果的な魚類摂取法の検討－
    やずや食と健康研究所：2016年度研究助成
    Date (from‐to) : 2016/11

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