Updated on 2024/04/18

写真a

 
YAMAMOTO Shusei
 
Organization
Faculty of Health Sciences Assistant Professor
Position
Assistant Professor
Homepage
https://cell-physiology-immunology-lab.jimdofree.com/
External link

Degree

  • Doctor ( 2023.9   Okayama University )

  • Master ( 2021.3   Okayama University )

  • Bachelor ( 2019.3   Okayama University )

Research Interests

  • Bile acid

  • Nonalcoholic Steatohepatitis

  • Cardiovascular Disease

  • Sarcopenia

Research Areas

  • Others / Others  / 病態検査学

  • Life Science / Nutrition science and health science

Education

  • Okayama University   大学院保健学研究科   検査技術科学分野 博士後期課程

    2021.4 - 2023.9

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    Country： Japan

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  • Okayama University   大学院保健学研究科   検査技術科学分野 博士前期課程

    2019.4 - 2021.3

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    Country： Japan

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  • Okayama University   医学部   保健学科 検査技術科学専攻

    2015.4 - 2019.3

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    Country： Japan

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Research History

  • Okayama University   Academic Field of Health Sciences   Assistant Professor

    2021.10

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    Country：Japan

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  • Japan Society for Promotion of Science

    2021.4 - 2021.9

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  • Okayama University   Graduate School of Medicine , Dentistry and Pharmaceutical Sciences

    2019.4 - 2021.3

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Professional Memberships

  • SHR等疾患モデル共同研究会

    2023.1

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  • 日本臨床検査学教育協議会

    2022.4

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  • 日本サルコペニア・フレイル学会

    2021.10

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  • 日本臨床衛生検査技師会

    2020.10

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  • 日本動脈硬化学会

    2019.12

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  • 高血圧関連疾患モデル学会

    2019.7 - 2024.3

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  • The Butterfly Science Society of Japan

    2015.4

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Papers

  • Uric Acid Elevation by Fructose Overload Exacerbates Nash and Atherosclerosis via Oxidative Stress Reviewed

    Moe Fujii, Mai Kakimoto, Ikumi Sato, Koki Honma, Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Satoshi Hirohata, Kazuya Kitamori, Shang Ran, Shusei Yamamoto, Shogo Watanabe

    Current Nutrition and Food Science   20 ( 2 )   250 - 261   2024

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    Publishing type：Research paper (scientific journal)  

    Background: Nonalcoholic steatohepatitis (NASH) is well associated with an increased risk of cardiovascular disease (CVD), regardless of risk factors for metabolic syndrome. However, intermediary factors between NASH and CVD remain unknown. In recent years, hyperuricemia has been associated not only with gout but also with several other organ diseases, such as hypertension, chronic renal failure, and metabolic syndrome. In addition, hyperuricemia was shown to frequently occur in patients with NASH and could be a risk factor for CVD. Furthermore, serum uric acid (UA) levels have been linked with fructose intake. Objectives: We hypothesized that fructose loading elevates UA levels and exacerbates NASH and atherosclerosis via oxidative stress. Methods: Stroke-prone spontaneously hypertensive rats (SHRSP5/Dmcr), between 14 to 24 weeks of age, were divided into two groups and fed a high-fat and high-cholesterol (HFC) diet. In addition to the HFC diet, the fructose group was subjected to 10% fructose loading. The oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed at 25-week-old, followed by blood sampling, animal sacrifice, endothelial function test, blood biochemistry, histopathological staining, xanthine oxidase activity test, and genetic analysis performed at 26-week-old. Results: Fructose loading increased UA and oxidative stress levels. In addition, fructose loading induced insulin resistance. The fructose group exhibited aggravated hepatic fibrosis and lipid depo-sition, as well as enhanced lipid accumulation in the mesenteric arteries. Conclusion: In the SHRSP5/Dmcr rat model, elevated UA levels were a risk factor for the exacer-bation of NASH and atherosclerosis via oxidative stress.

    DOI： 10.2174/1573401319666230508150159

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  • Therapeutic effect of ouabagenin, a novel liver X receptor agonist, on atherosclerosis in nonalcoholic steatohepatitis in SHRSP5/Dmcr rat model. Reviewed International journal

    Shusei Yamamoto, Ikumi Sato, Moe Fujii, Mai Kakimoto, Koki Honma, Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Satoru Tamura, Minoru Ueda, Satoshi Hirohata, Shogo Watanabe

    Canadian journal of physiology and pharmacology   101 ( 9 )   455 - 465   2023.9

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    The liver X receptor (LXR) can enhance cholesterol transporters, which could remove excess cholesterol from foam cells in atheromas. LXR has two subtypes: LXRα, which aggravates hepatic lipid accumulation, and LXRβ, which does not. In 2018, ouabagenin (OBG) was reported as a potential LXRβ-specific agonist. We aimed to examine whether OBG specifically affects LXRβ in nonalcoholic steatohepatitis (NASH); it did not aggravate hepatic steatosis and can suppress the development of atherosclerosis. SHRSP5/Dmcr rats fed a high-fat and high-cholesterol diet were divided into four groups as follows: (I) L-NAME group, (II) L-NAME/OBG group, (III) OBG (-) group, and (IV) OBG (+) group. All groups' rats were intraperitoneally administered L-NAME. The L-NAME/OBG group's rats were intraperitoneally administered OBG and L-NAME simultaneously. After L-NAME administration, the OBG (+) group's rats were administered OBG, while the OBG (-) group's rats were not. Although all rats developed NASH, OBG did not exacerbate steatosis (L-NAME/OBG and OBG (+) groups). In addition, endothelial cells were protected in the L-NAME/OBG group and foam cells in the atheroma were reduced in the OBG (+) group. OBG is an LXRβ-specific agonist and has a potential therapeutic effect on atherosclerosis without developing lipid accumulation in the liver.

    DOI： 10.1139/cjpp-2022-0532

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  • Selective autophagy associated with iron overload aggravates non-alcoholic steatohepatitis via ferroptosis. Reviewed International journal

    Koki Honma, Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Toshiaki Ohara, Kazuya Kitamori, Ikumi Sato, Satoshi Hirohata, Moe Fujii, Shusei Yamamoto, Shang Ran, Shogo Watanabe

    Experimental biology and medicine (Maywood, N.J.)   15353702231191197 - 15353702231191197   2023.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    Non-alcoholic steatohepatitis (NASH) is a progressive form of non-alcoholic fatty liver disease (NAFLD) that causes cirrhosis and hepatocellular carcinoma. Iron is an essential trace element in the body; however, excess iron can cause tissue damage and dysfunction. Iron overload is often observed in patients with NASH, and the amount of iron accumulated in the liver positively correlates with the histological severity of NASH. Ferroptosis, a novel form of iron-dependent cell death, is caused by the accumulation of lipid peroxidation and oxidative stress and is related to NASH. In addition, ferroptosis is closely related to autophagy, an intracellular self-degradation process. Although autophagy has many beneficial effects, it may also be harmful to the organism, for example, inducing ferroptosis. It is unclear whether iron overload aggravates NASH via autophagy. The aim of this research is to determine the mechanism by which iron overload induces ferroptosis via autophagy and aggravates NASH. Stroke-prone spontaneously hypertensive rats (SHRSP5/Dmcr) were divided into two groups and fed a high-fat and high-cholesterol (HFC) diet for eight weeks. Iron dextran was administered to the Fe group in addition to the HFC diet. Blood analysis, histological staining, calcineurin activity assay, quantitative reverse transcription polymerase chain reaction (RT-PCR), immunofluorescence staining, and electron microscopy were performed. The results showed that iron overload promoted autophagy via nuclear translocation of transcription factor EB (TFEB) and induced ferritinophagy, which is the autophagic degradation of ferritin. In addition, the HFC diet induced lipophagy, the autophagic degradation of lipid droplets. The Fe group also exhibited promoted ferroptosis and aggravated hepatic inflammation and fibrosis. In conclusion, iron overload accelerates ferritinophagy and lipophagy, aggravating NASH pathology via ferroptosis. These findings indicate the therapeutic potential of inhibiting autophagy and ferroptosis for treating NASH.

    DOI： 10.1177/15353702231191197

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  • Antioxidant action of xanthine oxidase inhibitor febuxostat protects the liver and blood vasculature in SHRSP5/Dmcr rats. Reviewed International journal

    Mai Kakimoto, Moe Fujii, Ikumi Sato, Koki Honma, Hinako Nakayama, Sora Kirihara, Taketo Fukuoka, Shang Ran, Satoshi Hirohata, Kazuya Kitamori, Shusei Yamamoto, Shogo Watanabe

    Journal of applied biomedicine   21 ( 2 )   80 - 90   2023.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Xanthine oxidase (XO) generates reactive oxygen species during uric acid production. Therefore, XO inhibitors, which suppress oxidative stress, may effectively treat non-alcoholic steatohepatitis (NASH) and atherosclerosis via uric acid reduction. In this study, we examined the antioxidant effect of the XO inhibitor febuxostat on NASH and atherosclerosis in stroke-prone spontaneously hypertensive 5 (SHRSP5/Dmcr) rats. METHODS: SHRSP5/Dmcr rats were divided into three groups: SHRSP5/Dmcr + high-fat and high-cholesterol (HFC) diet [control group, n = 5], SHRSP5/Dmcr + HFC diet + 10% fructose (40 ml/day) [fructose group, n = 5], and SHRSP5/Dmcr + HFC diet + 10% fructose (40 ml/day) + febuxostat (1.0 mg/kg/day) [febuxostat group, n = 5]. Glucose and insulin resistance, blood biochemistry, histopathological staining, endothelial function, and oxidative stress markers were evaluated. RESULTS: Febuxostat reduced the plasma uric acid levels. Oxidative stress-related genes were downregulated, whereas antioxidant factor-related genes were upregulated in the febuxostat group compared with those in the fructose group. Febuxostat also ameliorated inflammation, fibrosis, and lipid accumulation in the liver. Mesenteric lipid deposition decreased in the arteries, and aortic endothelial function improved in the febuxostat group. CONCLUSIONS: Overall, the XO inhibitor febuxostat exerted protective effects against NASH and atherosclerosis in SHRSP5/Dmcr rats.

    DOI： 10.32725/jab.2023.009

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  • SHRSP5/Dmcr rats fed a high-fat and high-cholesterol diet develop disease-induced sarcopenia as nonalcoholic steatohepatitis progresses. Reviewed International journal

    Shusei Yamamoto, Koki Honma, Moe Fujii, Mai Kakimoto, Sora Kirihara, Hinako Nakayama, Kazuya Kitamori, Ikumi Sato, Satoshi Hirohata, Shogo Watanabe

    Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft   249   152104   2023.5

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Secondary sarcopenia develops as a result of a bedridden state and illnesses, such as cachexia, liver disease, and diabetes. However, there is a lack of animal models to investigate the underlying mechanisms and potential treatments for secondary sarcopenia. Recently, secondary sarcopenia has been associated with the prognosis of nonalcoholic steatohepatitis. This study aimed to investigate whether stroke-prone spontaneously hypertensive rat 5 (SHRSP5/Dmcr) which developed severe nonalcoholic steatohepatitis by a high-fat and high-cholesterol (HFC; containing 2% cholic acid) diet is a useful model of secondary sarcopenia. METHODS: SHRSP5/Dmcr rats were divided into 6 groups fed with a Stroke-Prone (SP: normal chow) or HFC diets for different periods (4, 12, and 20 weeks), and WKY/Izm rats were divided into 2 groups fed an SP or HFC diet. Body weight, food intake, and muscle force were measured weekly for all rats. After the end of the diet period, skeletal muscle strength evoked by electrical stimulation was recorded, blood was collected, and organ weight was measured. The sera were used for biochemical analysis and the organs were used for histopathological analysis. RESULTS: SHRSP5/Dmcr rats fed an HFC diet developed nonalcoholic steatohepatitis, and their skeletal muscles, especially fast muscles, showed atrophy, indicating that muscle atrophy is aggravated by the progression of nonalcoholic steatohepatitis. In contrast, WKY/Izm rats fed an HFC diet did not exhibit sarcopenia. CONCLUSIONS: This study suggests that SHRSP5/Dmcr rats could be a useful novel model for investigate the mechanism of secondary sarcopenia disorder associated with nonalcoholic steatohepatitis.

    DOI： 10.1016/j.aanat.2023.152104

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  • Increased Glycine-conjugated and Unconjugated Bile Acid Levels Associated with Aggravation of Nonalcoholic Steatohepatitis and Cardiovascular Disease in SHRSP5/Dmcr Rat. Reviewed

    Shusei Yamamoto, Ikumi Sato, Moe Fujii, Mai Kakimoto, Koki Honma, Natsumi Akiyama, Miku Sakai, Natsuki Fukuhama, Shota Kumazaki, Satoshi Hirohata, Kazuya Kitamori, Yukio Yamori, Shogo Watanabe

    Acta medica Okayama   77 ( 1 )   29 - 36   2023.2

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    The SHRSP5/Dmcr is a useful animal model for the development of nonalcoholic steatohepatitis (NASH) pathology when fed a high-fat, high-cholesterol diet, and further drug interventions can lead to concomitant cardiovascular disease. While SHRSP5/Dmcr rats have been used for basic research related to NASH, details of their bile acid metabolism in this condition are unknown. In this study, we aimed to clarify the changes in the serum bile acid (BA) fractions associated with NASH and found that glycine-conjugated and unconjugated bile acid increased with worsening NASH and cardiovascular disease while taurine-conjugated BA relatively decreased.

    DOI： 10.18926/AMO/64358

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  • Suppression of nitric oxide synthase aggravates non-alcoholic steatohepatitis and atherosclerosis in SHRSP5/Dmcr rat via acceleration of abnormal lipid metabolism. Reviewed International journal

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Shota Kumazaki, Mami Matsui, Hinako Nakayama, Sora Kirihara, Shang Ran, Shinichi Usui, Ryoko Shinohata, Kazuya Kitamori, Satoshi Hirohata, Shogo Watanabe

    Pharmacological reports : PR   74 ( 4 )   669 - 683   2022.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Non-alcoholic steatohepatitis (NASH) is a progressive subtype of non-alcoholic fatty liver disease (NAFLD) that is closely related to cardiovascular disease (CVD). Nitric oxide (NO) plays a critical role in the control of various biological processes. Dysfunction of the NO signaling pathway is associated with various diseases such as atherosclerosis, vascular inflammatory disease, and diabetes. Recently, it has been reported that NO is related to lipid and cholesterol metabolism. Chronic NO synthase (NOS) inhibition accelerates NAFLD by increasing hepatic lipid deposition. However, the detailed relationship between NO and abnormal lipid and cholesterol metabolism in NAFLD/NASH has not been completely explained. We aimed to determine the effects of NOS inhibition by N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME), a NOS inhibitor, on NASH and CVD via lipid and cholesterol metabolism. METHODS: Stroke-prone spontaneously hypertensive rats were fed a high-fat and high-cholesterol diet for 8 weeks and administered L-NAME for the last 2 weeks. Following blood and tissue sampling, biochemical analysis, histopathological staining, quantitative RT-PCR analysis, and western blotting were performed. RESULTS: L-NAME markedly increased hepatic triglyceride (TG) and cholesterol levels by promoting TG synthesis and cholesterol absorption from the diet. L-NAME increased the mRNA levels of inflammatory markers and fibrotic areas in the liver. Cholesterol secretion from the liver was promoted in rats administered L-NAME, which increased serum cholesterol. L-NAME significantly increased the level of oxidative stress marker and lipid deposition in the arteries. CONCLUSIONS: NOS inhibition simultaneously aggravates NASH and atherosclerosis via hepatic lipid and cholesterol metabolism.

    DOI： 10.1007/s43440-022-00380-1

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  • Potential of a Novel Chemical Compound Targeting Matrix Metalloprotease-13 for Early Osteoarthritis: An In Vitro Study. Reviewed International journal

    Junko Inagaki, Airi Nakano, Omer Faruk Hatipoglu, Yuka Ooka, Yurina Tani, Akane Miki, Kentaro Ikemura, Gabriel Opoku, Ryosuke Ando, Shintaro Kodama, Takashi Ohtsuki, Hirosuke Yamaji, Shusei Yamamoto, Eri Katsuyama, Shogo Watanabe, Satoshi Hirohata

    International journal of molecular sciences   23 ( 5 )   2022.2

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    Osteoarthritis is a progressive disease characterized by cartilage destruction in the joints. Matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs) play key roles in osteoarthritis progression. In this study, we screened a chemical compound library to identify new drug candidates that target MMP and ADAMTS using a cytokine-stimulated OUMS-27 chondrosarcoma cells. By screening PCR-based mRNA expression, we selected 2-(8-methoxy-2-methyl-4-oxoquinolin-1(4H)-yl)-N-(3-methoxyphenyl) acetamide as a potential candidate. We found that 2-(8-methoxy-2-methyl-4-oxoquinolin-1(4H)-yl)-N-(3-methoxyphenyl) acetamide attenuated IL-1β-induced MMP13 mRNA expression in a dose-dependent manner, without causing serious cytotoxicity. Signaling pathway analysis revealed that 2-(8-methoxy-2-methyl-4-oxoquinolin-1(4H)-yl)-N-(3-methoxyphenyl) acetamide attenuated ERK- and p-38-phosphorylation as well as JNK phosphorylation. We then examined the additive effect of 2-(8-methoxy-2-methyl-4-oxoquinolin-1(4H)-yl)-N-(3-methoxyphenyl) acetamide in combination with low-dose betamethasone on IL-1β-stimulated cells. Combined treatment with 2-(8-methoxy-2-methyl-4-oxoquinolin-1(4H)-yl)-N-(3-methoxyphenyl) acetamide and betamethasone significantly attenuated MMP13 and ADAMTS9 mRNA expression. In conclusion, we identified a potential compound of interest that may help attenuate matrix-degrading enzymes in the early osteoarthritis-affected joints.

    DOI： 10.3390/ijms23052681

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  • Basic characteristics between mechanomyogram and muscle force during twitch and tetanic contractions in rat skeletal muscles. Reviewed International journal

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Shota Kumazaki, Mami Matsui, Hinako Nakayama, Sora Kirihara, Shang Ran, Satoshi Hirohata, Shogo Watanabe

    Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology   62   102627   2022.2

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    The mechanomyogram (MMG) is a signal measured by various vibration sensors for slight vibrations induced by muscle contraction, and it reflects the muscle force during electrically induced-contraction or until 60%-70% maximum voluntary contraction, so the MMG is considered an alternative and novel measurement tool for muscle strength. We simultaneously measured the MMG and muscle force in the gastrocnemius (GC), vastus intermedius (VI), and soleus (SOL) muscles of rats. The muscle force was measured by attaching a hook to the tendon using a load cell, and the MMG was measured using a charged-coupled device-type displacement sensor at the middle of the target muscle. The MMG-twitch waveform was very similar to that of the muscle force; however, the half relaxation time and relaxation time (10%), which are relaxation parameters, were prolonged compared to those of the muscle force. The MMG amplitude correlated with the muscle force. Since stimulation frequencies that are necessary to evoke tetanic progression have a significant correlation with the twitch parameter, there is a close relationship between twitch and tetanus in the MMG signal. Therefore, we suggest that the MMG, which is electrically induced and detected by a laser displacement sensor, may be an alternative tool for measuring muscle strength.

    DOI： 10.1016/j.jelekin.2021.102627

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  • Bile acids aggravate nonalcoholic steatohepatitis and cardiovascular disease in SHRSP5/Dmcr rat model. Reviewed International journal

    Shusei Yamamoto, Ikumi Sato, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shota Kumazaki, Shang Ran, Satoshi Hirohata, Kazuya Kitamori, Yukio Yamori, Shogo Watanabe

    Experimental and molecular pathology   114   104437   2020.6

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND AND AIMS: Nonalcoholic steatohepatitis (NASH) is linked to an increased risk of cardiovascular disease, regardless of the risk factors in metabolic syndrome. However, the intermediary factors between NASH and cardiovascular disease are still unknown. A previous study revealed that serum and hepatic bile acid (BA) levels are increased in some NASH patients. We aimed to examine whether NASH and cardiovascular disease were aggravated by BA using an animal model. METHOD AND RESULTS: From 10 to 18 weeks of age, SHRSP5/Dmcr rats divided into 3 groups were fed 3 types of high-fat and high-cholesterol (HFC) diets which were changed in the cholic acid (CA) concentration (0%, 2%, or 4%). The nitro oxide synthase inhibition (L-NAME) was administered intraperitoneally from 16 to 18 weeks of age. The 4% CA groups showed the worst LV dysfunction and myocardial fibrosis, and demonstrated severe hepatic fibrosis and lipid depositions. In addition, a large amount of lipid accumulation was observed in the aortas of the 4% CA group, and NFκB and VCAM-1 gene expression levels were increased. These findings were not seen in the 0% CA group. CONCLUSION: In the SHRSP5/Dmcr rat model, NASH and cardiovascular disease were aggravated with increasing BAs concentrations in an HFC diet.

    DOI： 10.1016/j.yexmp.2020.104437

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  • Bile Acid Metabolism is an Intermediary Factor between Non-Alcoholic Steatohepatitis and Ischemic Heart Disease in SHRSP5/Dmcr Rats Reviewed

    Shota Kumazaki, Mayu Nakamura, Shun Sasaki, Rina Tagashira, Nozomi Maruyama, Ikumi Sato, Shusei Yamamoto, Shang Ran, Shinichi Usui, Ryoko Shinohata, Takashi Ohtsuki, Satoshi Hirohata, Kazuya Kitamori, Mari Mori, Yukio Yamori, Shogo Watanabe

    Journal of Nutrition & Food Sciences   09 ( 04 )   2019

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Longdom Group  

    DOI： 10.35248/2155-9600.19.9.763

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  • Non-alcoholic steatohepatitis aggravates nitric oxide synthase inhibition-induced arteriosclerosis in SHRSP5/Dmcr rat model. Reviewed International journal

    Shogo Watanabe, Shota Kumazaki, Shusei Yamamoto, Ikumi Sato, Kazuya Kitamori, Mari Mori, Yukio Yamori, Satoshi Hirohata

    International journal of experimental pathology   99 ( 6 )   282 - 294   2018.12

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    Non-alcoholic steatohepatitis (NASH) is linked to increased cardiovascular risk, independent of the broad spectrum of metabolic syndrome risk factors. Stroke-prone (SP) spontaneously hypertensive rats (SHRSP5/Dmcr) fed a high-fat and high-cholesterol (HFC) diet developed hepatic lesions similar to those in human NASH pathology. These rats simultaneously developed lipid deposits in the mesenteric arteries, cardiac fibrosis, endothelial dysfunction and left ventricle (LV) diastolic dysfunction. However, the intermediary factors between NASH and cardiovascular disease are still unknown. We investigated whether NASH aggravates nitric oxide (NO) synthase inhibition-induced arteriosclerosis in SHRSP5/Dmcr rats. Wistar Kyoto and SHRSP5/Dmcr rats were divided into 4 groups of 5 and fed the stroke-prone (SP) or HFC diets for 8 weeks. To induce NO synthase inhibition, Nω -nitro-L-arginine methyl ester hydrochloride (L-NAME) mixed with drinking water was administered in the final 2 weeks. The NASH+L-NAME group demonstrated the following characteristics related to arteriosclerosis and myocardial ischaemia: (a) LV systolic dysfunction with asynergy, (b) replacement fibrosis caused by the shedding of cardiomyocytes and (c) arterial lipid deposition and coronary occlusion secondary to endothelial dysfunction. These characteristics were not observed in the NASH or non-NASH+L-NAME groups. The SHRSP5/Dmcr rat model demonstrates that NASH significantly aggravates cardiovascular risk.

    DOI： 10.1111/iep.12301

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MISC

  • 北海道撮影・採集珍道中～「大屋図鑑」の完成に向けて～

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    季刊ゆずりは   ( 100 )   72 - 76   2024.1

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    Butterfly Science   ( 27 )   53 - 54   2023.11

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    季刊ゆずりは   ( 99 )   2023.10

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  • ベタメタゾン添加OUMS-27による細胞外小胞のマトリックス分解酵素抑制効果

    井口 和香, 佐藤 生弥, 安達 嘉奈子, 岩本 結衣, 中村 早希, 中野 愛梨, ハシブ・ファルハナ, 池村 健太郎, オッポク・ガブリエル, 山元 修成, 渡辺 彰吾, 廣畑 聡

    日本生化学会大会プログラム・講演要旨集   96回   [2P - 525]   2023.10

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    Language：Japanese   Publisher：(公社)日本生化学会  

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  • 隠岐諸島・島後でのサカハチチョウ新亜種採集・撮影記

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    季刊ゆずりは   ( 97 )   2023.4

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  • 高脂肪食誘導性NASH動物モデルにおける腸内細菌叢とLeaky gutの評価

    桐原 空, 中山 日菜子, 福岡 威人, 本間 宏基, 藤井 萌, 廣畑 聡, 山元 修成, 渡辺 彰吾

    腸内細菌学雑誌   37 ( 2 )   103 - 103   2023.4

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    Language：Japanese   Publisher：(公財)腸内細菌学会  

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  • 高脂肪食が腸内細菌叢および肝臓NLRP3インフラマソームに与える影響

    中山 日菜子, 桐原 空, 福岡 威人, 本間 宏基, 藤井 萌, 廣畑 聡, 山元 修成, 渡辺 彰吾

    腸内細菌学雑誌   37 ( 2 )   104 - 104   2023.4

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    Language：Japanese   Publisher：(公財)腸内細菌学会  

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  • 島嶼の蝶 サカハチチョウ隠岐諸島亜種の春型の生態と幼生期の飼育観察—Ecology and Observation of Araschnia burejana tojiroi Ohya, 2022 Based on Field Work and Rearing

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    Butterfly science = バタフライ・サイエンス   ( 25 )   83 - 87   2023

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    Language：Japanese   Publisher：日本蝶類科学学会  

    CiNii Books

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  • 疾患併発性サルコペニアモデルSHRSP5/Dmcrラットにおける腸内細菌叢の変化

    山元修成, 福岡威人, 後藤和義, 中山日菜子, 桐原空, 藤井萌, 藤井萌, 渡辺彰吾

    日本サルコペニア・フレイル学会誌   7 ( Supplement )   2023

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  • 非アルコール性脂肪肝炎モデル動物であるSHRSP5/Dmcrラットは二次性サルコペニアを発症する

    山元 修成, 本間 宏基, 藤井 萌, 柿本 麻衣, 桐原 空, 中山 日菜子, 佐藤 生弥, 廣畑 聡, 渡辺 彰吾

    日本サルコペニア・フレイル学会雑誌   6 ( Suppl. )   180 - 180   2022.10

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    Language：Japanese   Publisher：(一社)日本サルコペニア・フレイル学会  

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  • ヒメウラナミジャノメの異常型を採集

    山元修成

    季刊ゆずりは   ( 94 )   2022.7

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  • Personal View on the Classification of the High Brown Fritillary-A Problem Found Based on the Mating Results in the Field-

    山元修成

    Butterfly Science   ( 22 )   2022

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  • 鉄代謝はNASHと動脈硬化を結ぶ新たなリスク因子になりうるか

    本間宏基, 桐原空, 中山日菜子, 柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集   54th   2022

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  • 沖縄県多良間島におけるキタキチョウの記録

    山元修成

    季刊ゆずりは   ( 90 )   2021.7

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  • カバマダラの飼育にインゲンマメ・エンドウは使用可能か？

    山元修成

    季刊ゆずりは   ( 89 )   2021.4

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  • 鹿久居島でのミヤマカラスアゲハの記録と調査

    山元修成

    季刊ゆずりは   ( 88 )   2021.1

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  • 強心配糖体ウアバインの非糖部ウアバゲニンが示したウアバインに相反する生物活性

    田村理, 岡田麻衣子, 加藤茂明, 篠田康晴, 塩田倫史, 福永浩司, 渡辺彰吾, 山元修成, 程久美子, 上田実

    日本生薬学会年会講演要旨集   67th   2021

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  • フルクトース負荷による尿酸上昇がNASHと動脈硬化に及ぼす影響

    藤井萌, 柿本麻衣, 山元修成, 佐藤生弥, 本間宏基, 小松千尋, 奥川友葉, 柴田桃里, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   53rd   2021

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  • XO阻害薬フェブキソスタットによる抗酸化作用は肝臓・血管系を保護する

    柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 本間宏基, 奥川友葉, 柴田桃里, 小松千尋, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   53rd   2021

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  • Expression of Osteopontin in non-alcoholic steatohepatitis (NASH) fibrosis

    安藤亮典, 畑本早紀子, 中野愛梨, 池村健太郎, 兒玉慎太郎, OPOKU Gabriel, 山元修成, 稲垣純子, 今重之, HATIPOGLU Omer Faruk, 渡辺彰吾, 廣畑聡

    日本結合組織学会学術大会抄録集   53rd   2021

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  • メスアカムラサキ♀へのツマグロヒョウモン♂の誤求愛に関する実験

    山元修成

    Butterfly Science   ( 19 )   2021

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  • New Insights About Courtship Behavior of the Dryad Butterfly [Minois dryas (Scopoli, 1763)]-Field Observations and Experiments-

    山元修成

    Butterfly Science   ( 21 )   2021

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  • モンキチョウの雌雄型を採集

    山元修成

    季刊ゆずりは   ( 86 )   2020.7

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  • キタキチョウとミナミキチョウの斑紋差異を探る(2)

    山元 修成

    月刊むし : a monthly journal of entomology   ( 588 )   9 - 15   2020.2

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    Language：Japanese   Publisher：むし社  

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  • 新規LXRβアゴニストであるウアバゲニンを用いた動脈脂質沈着に対する改善効果の検討

    山元修成, 佐藤生弥, 柿本麻衣, 藤井萌, 松井麻実, 高橋侑子, 弥勒院佳奈, RAN Shang, 田村理, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   52nd   2020

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  • オベチコール酸はSHRSP5/Dmcrラットにおける非アルコール性脂肪肝炎とアテローム性動脈硬化症を改善する

    佐藤生弥, 山元修成, 柿本麻衣, 藤井萌, 松井麻実, 高橋侑子, 弥勒院佳奈, RAN Shang, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   52nd   2020

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  • キタキチョウとミナミキチョウの斑紋差異を探る(1)

    山元 修成

    月刊むし : a monthly journal of entomology   ( 577 )   36 - 41   2019.3

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    Language：Japanese   Publisher：むし社  

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  • 非アルコール性脂肪肝炎において心血管疾患を増悪する仲介因子となり得る胆汁酸代謝

    山元修成, 佐藤生弥, 秋山菜摘, 酒井美玖, 福濱那月, SHANG Ran, 廣畑聡, 渡邊彰吾

    日本循環薬理学会口演要旨集   29th   2019

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  • 非アルコール性脂肪肝炎と心血管疾患を増悪させる仲介因子としての胆汁酸の役割

    佐藤弥生, 熊崎章太, 山元修成, 福濱那月, 秋山菜摘, 酒井美玖, シャン ラン, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   51st   2019

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  • 越年したキアゲハの幼虫の記録~幼虫越冬の可能性について~

    山元修成

    Butterfly Science   ( 15 )   2019

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  • 奄美大島のミカドアゲハ♀を10月に採集

    山元修成

    Butterfly Science   ( 13 )   2019

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  • 北諸県郡三股町宮村でミカドアゲハを採集

    小牧浩幸, 山元修成

    タテハモドキ   55   2018.12

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  • 地方からアサギマダラを考える

    山元修成

    季刊ゆずりは   ( 79 )   2018.10

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  • ベニモンカラスシジミにおけるインゲンマメの代用食としての有効性

    山元修成

    INSECTA MIYAZAKI   6   2018.5

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  • アカマダラの雌雄型の記録

    山元修成

    季刊ゆずりは   ( 77 )   2018.4

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  • リュウキュウムラサキの寿命

    山元修成

    大昆Crude   62   2018.2

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  • 鱗粉減退個体はどのようにして産まれるのか～異常型？羽化不全？それとも祖型？～

    山元修成

    大昆Crude   62   2018.2

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  • Existence of the Seasonal Dimorphism in The Rustic (Cupha erymanthis)

    山元修成

    Butterfly Science   ( 12 )   2018

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  • キチョウの秋型の出現要因は?

    山元修成

    Butterfly Science   ( 12 )   2018

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  • クジャクチョウは成虫でも集合性を示すか

    山元修成

    Butterfly Science   ( 10 )   2018

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  • センチコガネとオオセンチコガネの鑑別点

    山元修成

    タテハモドキ   53   2017.12

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  • 石垣島でメスアカムラサキを採集

    山元修成

    季刊ゆずりは   ( 74 )   2017.7

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  • 灯火に飛来したヤエヤマムラサキ♂

    山田守, 山元修成

    季刊ゆずりは   ( 73 )   2017.1

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  • Field Observations on Oviposition and Larval Behaviors of 3 Species of Butterflies Occurring in Okinawa

    山元修成

    Butterfly Science   ( 7 )   2017

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  • クロボシセセリの蛹化前後の生態

    山元修成

    Butterfly Science   ( 7 )   2017

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  • Bionomical Observations on 5 Butterfly Species Occurring in the Yaeyama Islands

    山元修成

    Butterfly Science   ( 9 )   2017

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  • ウラナミアカシジミ南紀亜種,最大産卵数の更新

    山元修成

    Butterfly Science   ( 9 )   2017

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  • ヒロオビミドリシジミの水浴びを観察

    山元修成

    Butterfly Science   ( 7 )   2017

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  • ミヤマクワガタ♂の奇形

    山元修成

    タテハモドキ   52   2016.12

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  • 都井岬でリュウキュウムラサキに導かれ、ホシボシキチョウを採集

    山元修成

    季刊ゆずりは   ( 70 )   2016.7

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  • 2016年3月の宮崎県南部の状況

    山元修成

    月刊ゆずりはクラブ   205   2016.4

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  • 8年前に再捕獲されていたアサギマダラ

    山元修成

    タテハモドキ   51   2015.12

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  • 都城市・北諸県郡の蝶の記録

    山元修成

    タテハモドキ   51   2015.12

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  • 都城市・串間市でのアサギマダラの再捕獲記録

    山元修成

    タテハモドキ   51   2015.12

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  • 曽於市末吉町高之峯でメスアカムラサキとウスキシロチョウを採集

    山元修成

    SATSUMA   155   2015.11

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  • ヒメヒカゲの異常型

    山元修成

    季刊ゆずりは   ( 67 )   2015.10

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  • 日南海岸から屋久島へのアサギマダラの移動記録

    山元修成

    INSECTA MIYAZAKI   3   2015.9

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  • 三股町大八重でシータテハを採集

    山元修成

    INSECTA MIYAZAKI   3   2015.9

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  • タイワンツバメシジミの異常型

    山元修成

    Butterfly Science   ( 1 )   2015

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  • 西表島でのコモンマダラの記録

    山元修成

    Butterfly Science   ( 1 )   2015

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  • ツマグロヒョウモンの雌雄型を採集

    山元修成

    季刊ゆずりは   ( 63 )   2014.10

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  • サツマシジミのキリシマミズキへの産卵記録

    山元修成

    タテハモドキ   45   2009.12

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  • 都城盆地でクロマダラソテツシジミを探索 (4)

    山元修成

    宮崎むし情報 (総合版) 2008   21   2009

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  • 日南海岸のクロマダラソテツシジミとその他のチョウとガ

    山元修成

    宮崎むし情報 (総合版) 2008   76   2009

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  • 都城盆地でクロマダラソテツシジミを探索 (5)

    山元修成

    宮崎むし情報 (総合版) 2008   22   2009

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  • 都城市のクロマダラソテツシジミ調査記録 (1)

    山元修成

    宮崎むし情報 (総合版) 2008   83   2009

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  • 三股町でスギタニルリシジミ及びクロマダラソテツシジミの探索

    山元修成

    宮崎むし情報 (総合版) 2008   34 - 35   2009

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  • 都城市のクロマダラソテツシジミ調査記録 (2)

    山元修成

    宮崎むし情報 (総合版) 2008   83 - 84   2009

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  • クロマダラソテツシジミの春の調査

    山元修成

    宮崎むし情報 (総合版) 2008   34   2009

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  • 姫城中及びその周辺のチョウ (14)

    山元修成

    宮崎むし情報 (総合版) 2008   102   2009

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  • ヤクシマルリシジミのウマノスズクサへの産卵記録

    山元修成

    タテハモドキ   45   2008.12

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  • ベニシジミの異常型

    山元修成

    季刊ゆずりは   ( 39 )   2008.10

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  • 都城・北諸県郡の蝶

    山元修成

    タテハモドキ   43   61 - 71   2007.12

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  • コツバメの異常型

    山元修成

    季刊ゆずりは   ( 34 )   2007.7

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  • カラスアゲハの異常型

    山元修成

    季刊ゆずりは   ( 32 )   2007.1

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    Language：Japanese  

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  • 都城盆地でクロマダラソテツシジミを探索 (1)

    山元修成

    宮崎むし情報 (総合版) 2007   91   2007

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  • 都城盆地でクロマダラソテツシジミを探索 (2)

    山元修成

    宮崎むし情報 (総合版) 2007   92   2007

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  • 都城盆地でクロマダラソテツシジミを探索 (3)

    山元修成

    宮崎むし情報 (総合版) 2007   96   2007

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Presentations

  • 肺線維化を伴う特発性間質性肺炎急性増悪とS100A8/A9の関連の検討

    中村尚季, 肥後寿夫, 妹尾賢, 尾関太一, 角南良太, 山元修成, 板野純子, 谷口暁彦, 田中彩加, 木下理恵, 阪口政清, 前田嘉信, 宮原信明

    第20回合同地方会  2024.2.18 

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    Event date： 2024.2.17 - 2024.2.18

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  • NASH動物モデルにおける肝臓遊離コレステロール蓄積に関連する遺伝子変異解析

    福岡威人, 中山日菜子, 桐原空, 河野有華, 山元修成, 廣畑聡, 渡辺彰吾

    第59回高血圧関連疾患モデル学会学術総会  2023.11.25 

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    Event date： 2023.11.24 - 2023.11.25

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • 疾患併発性サルコペニアモデルSHRSP5/Dmcrラットにおける腸内細菌叢の変化

    山元修成, 福岡威人, 後藤和義, 中山日菜子, 桐原空, 藤井萌, 渡辺彰吾

    第10回日本サルコペニア・フレイル学会大会  2023.11.5 

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    Event date： 2023.11.4 - 2023.11.5

    Presentation type：Poster presentation  

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  • ベタメタゾン添加OUMS-27による細胞外小胞のマトリックス分解酵素抑制効果

    井口和香, 佐藤生弥, 安達嘉奈子, 岩本結衣, 中村早希, 中野愛梨, ハシブ ファルハナ, 池村健太郎, オッポク ガブリエル, 山元修成, 渡辺彰吾, 廣畑聡

    第96回日本性科学学会大会 

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    Event date： 2023.10.31 - 2023.11.2

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  • Evaluation of gut microbiota and leaky gut in a high-fat diet-induced NASH animal model

    Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Koki Honma, Moe Fujii, Satoshi Hirohata, Shusei Yamamoto, Shogo Watanabe

    Asian Pacific Association for the Study of the Liver Single Topic Conference 2023 

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    Event date： 2023.9.21 - 2023.9.23

    Language：English   Presentation type：Poster presentation  

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  • Cholesterol crystals aggravates NASH by activating the NLRP3 inflammasome

    Hinako Nakayama, Sora Kirihara, Taketo Fukuoka, Koki Honma, Moe Fujii, Shusei Yamamoto, Satoshi Hirohata, Shogo Watanabe

    Asian Pacific Association for the Study of the Liver Single Topic Conference 2023 

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    Event date： 2023.9.21

    Language：English   Presentation type：Poster presentation  

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  • 高脂肪食が腸内細菌叢および肝臓NLRP3インフラマソームに与える影響

    中山日菜子, 桐原空, 福岡威人, 藤井萌, 山元修成, 廣畑聡, 渡辺彰吾

    第27回腸内細菌学会学術集会  2023.6.27 

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    Event date： 2023.6.27 - 2023.6.28

    Language：Japanese   Presentation type：Poster presentation  

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  • 高脂肪食誘導性NASH動物モデルにおける腸内細菌叢とLeaky gutの評価

    桐原空, 中山日菜子, 福岡威人, 本間宏基, 藤井萌, 廣畑聡, 山元修成, 渡辺彰吾

    第27回腸内細菌学会学術集会  2023.6.27 

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    Event date： 2023.6.27 - 2023.6.28

    Language：Japanese   Presentation type：Poster presentation  

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  • Suppression of the NO/AMPK Pathway Aggravates Non-Alcoholic Steatohepatitis and Cardiovascular Disease via Abnormal Lipid Metabolism in SHRSP5/Dmcr rat

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Hinako Nakayama, Sora Kirihara, Shinichi Usui, Ryoko Shinohata, Kazuya Kitamori, Satoshi Hirohata, Shogo Watanabe

    32nd Conference of the Asian Pacific Association for the Study of the Liver (APASL 2023) 

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    Event date： 2023.2.15 - 2023.2.19

    Language：English   Presentation type：Poster presentation  

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  • 非アルコール性脂肪肝炎モデル動物であるSHRSP5/Dmcrラットは二次性サルコペニアを発症する

    山元修成, 本間宏基, 藤井萌, 柿本麻衣, 桐原空, 中山日菜子, 佐藤生弥, 廣畑聡, 渡辺彰吾

    第９回日本サルコペニア・フレイル学会大会 

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    Event date： 2022.10.29 - 2022.10.30

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  • 鉄代謝は非アルコール性脂肪肝炎と動脈硬化を結ぶ新たなリスク因子になりうるか

    本間宏基, 桐原空, 中山日菜子, 柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 廣畑聡, 渡辺彰吾

    第54回日本動脈硬化学会総会・学術集会  2022.7.23 

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    Event date： 2022.7.23 - 2022.7.24

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  • フルクトース負荷による尿酸上昇がNASHと動脈硬化に及ぼす影響

    藤井萌, 柿本麻衣, 山元修成, 佐藤生弥, 本間宏基, 小松千尋, 奥川友葉, 柴田桃里, 廣畑聡, 渡辺彰吾

    第53回日本動脈硬化学会総会・学術集会 

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    Event date： 2021.10.23 - 2021.10.24

    Presentation type：Poster presentation  

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  • XO阻害薬フェブキソスタットによる抗酸化作用は肝臓・血管系を保護する

    柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 本間宏基, 奥川友葉, 柴田桃里, 小松千尋, 廣畑聡, 渡辺彰吾

    第53回日本動脈硬化学会総会・学術集会 

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    Event date： 2021.10.23 - 2021.10.24

    Language：Japanese   Presentation type：Poster presentation  

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  • 強心配糖体ウアバインの非糖部ウアバゲニンが示したウアバインに相反する生物活性

    田村理, 岡田麻衣子, 加藤茂明, 篠田康晴, 塩田倫史, 福永浩司, 渡辺彰吾, 山元修成, 程久美子, 上田実

    日本生薬学会第67回年会 

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    Event date： 2021.9.19 - 2021.9.20

    Language：Japanese   Presentation type：Poster presentation  

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  • Effect of Elevated Uric Acid by Fructose Overload on NASH and Atherosclerosis

    Moe Fujii, Mai Kakimoto, Shusei Yamamoto, Ikumi Sato, Koki Honma, Chihiro Komatsu, Tomoha Okugawa, Momori Shibata, Satoshi Hirohata, Shogo Watanabe

    The 10th International Congress on Lipid & Atherosclerosis (ICoLA)  2021.9.10 

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    Event date： 2021.9.10 - 2021.9.11

    Language：English   Presentation type：Oral presentation (general)  

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  • Antioxidant Action of Xanthine Oxidase Inhibitor Febuxostat Protects Liver and Blood Vascular System

    Mai Kakimoto, Moe Fujii, Ikumi Sato, Shusei Yamamoto, Koki Honma, Tomoha Okugawa, Momori Shibata, Chihiro Komatsu, Satoshi Hirohata, Shogo Watanabe

    The 10th International Congress on Lipid & Atherosclerosis (ICoLA) 

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    Event date： 2021.9.10 - 2021.9.11

    Language：English  

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  • The Novel Liver X Receptor beta Agonist, Ouabagenin, Prevent Arterial Lipid Deposition in SHRSP5/Dmcr Rat

    Shusei Yamamoto, Ikumi Satoh, Mai Kakimoto, Moe Fujii, Mami Matsui, Yuko Takahashi, Kana Mirokuin, Shang Ran, Satoru Tamura, Satoshi Hirohata, Shogo Watanabe

    The 88th European Atherosclerosis Society (EAS) Congress 

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    Event date： 2020.10.4 - 2020.10.7

    Language：English  

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  • Obeticholic acid ameliorates Non-alcoholic steatohepatitis and atherosclerosis in SHRSP5/Dmcr rats

    Ikumi Satoh, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Mami Matsui, Yuko Takahashi, Kana Mirokuin, Shang Ran, Satoshi Hirohata, Shogo Watanabe

    The 88th European Atherosclerosis Society (EAS) Congress 

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    Event date： 2020.10.4 - 2020.10.7

    Language：English  

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  • 新規LXRβアゴニストであるウアバゲニンを用いた動脈脂質沈着に対する改善効果の検討

    山元修成, 佐藤生弥, 柿本麻衣, 藤井萌, 松井麻実, 髙橋侑子, 弥勒院佳奈, Shang Ran, 田村理, 廣畑聡, 渡辺彰吾

    第52回日本動脈硬化学会総会・学術集会 

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    Event date： 2020.7.17 - 2020.7.31

    Language：Japanese  

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  • オベチコール酸はSHRSP5/Dmcrラットにおける非アルコール性脂肪肝炎とアテローム性動脈硬化症を改善する

    佐藤生弥, 山元修成, 柿本麻衣, 藤井萌, 松井麻実, 髙橋侑子, 弥勒院佳奈, Shang Ran, 廣畑聡, 渡辺彰吾

    第52回日本動脈硬化学会総会・学術集会 

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    Event date： 2020.7.17 - 2020.7.31

    Language：Japanese  

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  • 非アルコール性脂肪肝炎において心血管疾患を増悪する仲介因子となり得る胆汁酸代謝

    山元修成, 佐藤生弥, 秋山菜摘, 酒井美玖, 福濱那月, Shang Ran, 廣畑聡, 渡辺彰吾

    第55回高血圧関連疾患モデル学会  2019.11.29 

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    Event date： 2019.11.29 - 2019.11.30

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • Bile Acids Aggravate Non-alcoholic Steatohepatitis and Cardiovascular Disease in SHRSP5/Dmcr

    Ikumi Satoh, Shusei Yamamoto, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shang Ran, Shota Kumazaki, Satoshi Hirohata, Shogo Watanabe

    The 8th International Congress on Lipid & Atherosclerosis (ICoLA)  2019.9.6 

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    Event date： 2019.9.5 - 2019.9.7

    Language：English   Presentation type：Poster presentation  

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  • Bile Acid Metabolism Mediates between Nonalcoholic Steatohepatitis and Cardiovascular Disease

    Shusei Yamamoto, Ikumi Sato, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shota Kumazaki, Shang Ran, Satoshi Hirohata, Shogo Watanabe

    The 8th International Congress on Lipid & Atherosclerosis (ICoLA) 

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    Event date： 2019.9.5 - 2019.9.7

    Language：English   Presentation type：Poster presentation  

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  • 非アルコール性脂肪肝炎と心血管疾患を増悪させる仲介因子としての胆汁酸の役割

    佐藤生弥, 熊崎章太, 山元修成, 福濱那月, 秋山菜摘, 酒井美玖, Shang Ran, 廣畑聡, 渡辺彰吾

    第51回日本動脈硬化学会総会・学術集会  2019.7.11 

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    Event date： 2019.7.11 - 2019.7.12

    Presentation type：Poster presentation  

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  • Effect of ferroptosis by iron overload on non-alcoholic steatohepatitis and atherosclerosis

    Koki Honma, Hionako Nakayama, Sora Kirihara, Ikumi Sato, Eito Matsumoto, Sana Matsusita, Tomona Kaihara, Taketo Fukuoka, Shusei Yamamoto, Satoshi Hirohata, Shogo Watanabe

    The 11th International Congress on Lipid & Atherosclerosis  2022.9.17 

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Awards

  • 第6回 金光賞

    2023.4   岡山大学  

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  • Travel Grant

    2020.10   European Atherosclerosis Society (EAS)   The Novel Liver X Receptor beta Agonist, Ouabagenin, Prevent Arterial Lipid Deposition in SHRSP5/Dmcr Rat

    Shusei Yamamoto, Ikumi Satoh, Mai Kakimoto, Moe Fujii, Mami Matsui, Yuko Takahashi, Kana Mirokuin, Shang Ran, Satoru Tamura, Satoshi Hirohata, Shogo Watanabe

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  • Travel Grant

    2019.9   International Congress on Lipid & Atherosclerosis (ICoLA)   Bile Acid Metabolism Mediates between Nonalcoholic Steatohepatitis and Cardiovascular Disease

    Shusei Yamamoto, Ikumi Sato, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shota Kumazaki, Shang Ran, Satoshi Hirohata, Shogo Watanabe

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  • Butterfly Science Award

    2018.3   The Butterfly Science Society of Japan  

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Research Projects

  • NAFLD併発性サルコペニアの発症メカニズムと胆汁酸抑制による予防効果検証

    Grant number：24K20705  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  若手研究

    山元 修成

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    Grant amount：\4550000 （ Direct expense: \3500000 、 Indirect expense：\1050000 ）

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  • Investigation of the mechanism of sarcopenia complications after the onset of nonalcoholic fatty liver disease

    2024.03 - 2025.03

    公益財団法人 中冨健康科学振興財団 

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    Authorship：Principal investigator 

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  • Therapeutic Effects of Xanthine Oxidoreductase Inhibitors on Lean NASH and Atherosclerosis

    2023.04 - 2024.03

    公益財団法人 痛風・尿酸財団 

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    Authorship：Coinvestigator(s) 

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  • The gut microbiota in nonalcoholic steatohepatitis with concomitant sarcopenia

    2022.09 - 2023.08

    公益財団法人 寺岡記念育英会 

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    Authorship：Principal investigator 

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  • 腸内細菌叢の変化は非アルコール性脂肪肝炎における心血管疾患の併発リスクを上昇させるか

    2021.12 - 2022.03

    岡山大学保健学研究科  外部資金獲得のための研究公募助成 

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    Authorship：Principal investigator 

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  • Role of bile acids in the development of sarcopenia

    2021.07 - 2022.07

    The Association for Fordays Self-Reliance Support in japan 

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    Authorship：Principal investigator 

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  • The novel intercurrent mechanism and treatment of sarcopenia with nonalcoholic steatohepatitis

    Grant number：21J23123  2021.04 - 2024.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for JSPS Fellows  Grant-in-Aid for JSPS Fellows

    山元 修成

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    Grant amount：\3100000 （ Direct expense: \3100000 ）

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Other research activities

 

Class subject in charge

  • Medical Safety Management science （2023academic year） 1st semester  - 水3～6

  • Automation Technology for Laboratory Medicine （2023academic year） Second semester  - 月4～5

  • Introduction to Physiology （2023academic year） Third semester  - 水1～2

  • Laboratory Exercise in Clinical Physiology （2023academic year） 3rd and 4th semester  - [第３学期]火1～8,水3～8, [第４学期]火1～8

  • Laboratory Exercise in Human Anatomy （2023academic year） Second semester  - 木3～8

  • Clinical Immunology （2023academic year） Second semester  - 木1～2

  • Laboratory Exercise in Clinical Microbiology （2023academic year） Fourth semester  - 水3～8,木3～8

  • Laboratory Science Exercise （2023academic year） 2nd and 3rd semester  - [第２学期]火7, [第３学期]月7

  • Human Anatomy （2023academic year） 1st semester  - 木1～2

  • Laboratory Exercise in Human Anatomy （2023academic year） Second semester  - 木3～8

  • Exercise of Team Medical Activities （2022academic year） 1st and 2nd semester  - その他

  • Laboratory Exercise in Laboratory Immunology （2022academic year） Second semester  - 水3～8,木3～8

  • Laboratory Exercise in Clinical Physiology （2022academic year） 3rd and 4th semester  - [第３学期]火1～8,水3～8, [第４学期]火1～8

  • Clinical Immunology （2022academic year） Second semester  - 木1～2

  • Laboratory Exercise in Clinical Microbiology （2022academic year） Fourth semester  - 水3～8,木3～8

  • Laboratory Science Exercise （2022academic year） 2nd and 3rd semester  - [第２学期]火7, [第３学期]月7

  • 生理検査学実習 （2021academic year） ３・４学期

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