Irie, Junichiro

写真a

Affiliation

School of Medicine, Department of Internal Medicine (Nephrology, Endocrinology and Metabolism) (Shinanomachi)

Position

Associate Professor

External Links

Academic Degrees 【 Display / hide

  • 医学博士, Keio University, 2005.02

 

Research Areas 【 Display / hide

  • Life Science / Metabolism and endocrinology (Metabolism Studies)

Research Keywords 【 Display / hide

  • 代謝学

  • 糖尿病

  • 肥満

 

Papers 【 Display / hide

  • RELATIONSHIP BETWEEN SERUM TOTAL BILIRUBIN CONCENTRATION AND MACROVASCULAR COMPLICATIONS IN PATIENTS WITH TYPE 2 DIABETES MELLITUS

    Tanaka Masami, Nishimura Takeshi, Meguro Shu, Irie Junichiro, Saisho Yoshifumi, Mitsuishi Masanori, Itoh Arata, Inaishi Jun, Nakajima Yuya, Itoh Hiroshi

    JOURNAL OF HYPERTENSION 39   E208 - E208 2021.04

    ISSN  0263-6352

  • C-C motif chemokine receptor 9 regulates obesity-induced insulin resistance via inflammation of the small intestine in mice

    Amiya T., Nakamoto N., Irie J., Taniki N., Chu P.S., Koda Y., Miyamoto K., Yamaguchi A., Shiba S., Morikawa R., Itoh H., Kanai T.

    Diabetologia (Diabetologia)  64 ( 3 ) 603 - 617 2021.03

    ISSN  0012186X

     View Summary

    Aims/hypothesis: Accumulation of adipose tissue macrophages is considered pivotal in the development of obesity-associated inflammation and insulin resistance. In addition, recent studies suggest an involvement of the intestine as the primary organ in inducing hyperglycaemia and insulin resistance. We have reported that the C-C motif chemokine receptor (CCR) CCR9 is associated with intestinal immunity and has a pathogenic role in various liver diseases. However, its contribution to type 2 diabetes is unknown. In the current study, we aimed to clarify the involvement of CCR9 in the pathology of type 2 diabetes and the potential underlying mechanisms. Methods: To elucidate how CCR9 affects the development of metabolic phenotypes, we examined the impact of CCR9 deficiency on the pathogenesis of type 2 diabetes using male C57BL/6J (wild-type [WT]) and CCR9-deficient (CCR9 knockout [KO]) mice fed a 60% high-fat diet (HFD) for 12 weeks. Results: WT and Ccr9KO mice fed an HFD exhibited a comparable weight gain; however, glucose tolerance and insulin resistance were significantly improved in Ccr9KO mice. Moreover, visceral adipose tissue (VAT) and the liver of Ccr9KO mice presented with less inflammation and increased expression of glucose metabolism-related genes than WT mice. Ccr9 and Ccl25 expression were specifically higher in the small intestine but was not altered by HFD feeding and type 2 diabetes development. Accumulation of IFN-γ-producing CD4 T lymphocytes and increased intestinal permeability in the small intestine was observed in WT mice following HFD feeding, but these changes were suppressed in HFD-fed Ccr9KO mice. Adoptive transfer of gut-tropic CCR9-expressing T lymphocytes partially reversed the favourable glucose tolerance found in Ccr9KO mice via exacerbated inflammation in the small intestine and VAT. Conclusions/interpretation: CCR9 plays a central role in the pathogenesis of type 2 diabetes by inducing an inflammatory shift in the small intestine. Our findings support CCR9 as a new therapeutic target for type 2 diabetes via the gut–VAT–liver axis. Graphical abstract: [Figure not available: see fulltext.] +

  • Contribution of uremic dysbiosis to insulin resistance and sarcopenia.

    Uchiyama K, Wakino S, Irie J, Miyamoto J, Matsui A, Tajima T, Itoh T, Oshima Y, Yoshifuji A, Kimura I, Itoh H

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (Nephrology Dialysis Transplantation)  35 ( 9 ) 1501 - 1517 2020.06

    ISSN  0931-0509

     View Summary

    Background. Chronic kidney disease (CKD) leads to insulin resistance (IR) and sarcopenia, which are associated with a high mortality risk in CKD patients; however, their pathophysiologies remain unclear. Recently, alterations in gut microbiota have been reported to be associated with CKD. We aimed to determine whether uremic dysbiosis contributes to CKD-associated IR and sarcopenia. Methods. CKD was induced in specific pathogen-free mice via an adenine-containing diet; control animals were fed a normal diet. Fecal microbiota transplantation (FMT) was performed by oral gavage in healthy germ-free mice using cecal bacterial samples obtained from either control mice (control-FMT) or CKD mice (CKD-FMT). Vehicle mice were gavaged with sterile phosphate-buffered saline. Two weeks after inoculation, mice phenotypes, including IR and sarcopenia, were evaluated. Results. IR and sarcopenia were evident in CKD mice compared with control mice. These features were reproduced in CKD-FMT mice compared with control-FMT and vehicle mice with attenuated insulin-induced signal transduction and mitochondrial dysfunction in skeletal muscles. Intestinal tight junction protein expression and adipocyte sizes were lower in CKD-FMT mice than in control-FMT mice. Furthermore, CKD-FMT mice showed systemic microinflammation, increased concentrations of serum uremic solutes, fecal bacterial fermentation products and elevated lipid content in skeletal muscle. The differences in gut microbiota between CKD and control mice were mostly consistent between CKD-FMT and control-FMT mice. Conclusions. Uremic dysbiosis induces IR and sarcopenia, leaky gut and lipodystrophy.

  • Efficacy and safety of once-weekly exenatide after switching from twice-daily exenatide in patients with type 2 diabetes

    Watanabe Y., Saisho Y., Inaishi J., Kou K., Yamauchi A., Kanazawa Y., Okubo Y., Tokui M., Imai T., Murakami R., Tsuchiya T., Sasaki H., Masaoka T., Irie J., Meguro S., Itoh H.

    Journal of Diabetes Investigation (Journal of Diabetes Investigation)  11 ( 2 ) 382 - 388 2020.03

    ISSN  20401116

     View Summary

    © 2019 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd Aims/Introduction: To evaluate the efficacy and safety of once-weekly (q.w.) extended-release exenatide after switching from twice-daily (b.i.d.) exenatide in patients with type 2 diabetes. Materials and Methods: This was an investigator-initiated, prospective, single-arm, multicenter study. Individuals with type 2 diabetes who had been treated with exenatide b.i.d. for at least 3 months were enrolled and switched to exenatide q.w. for 24 weeks. The primary end-point was change in HbA1c at week 24 to test the glucose-lowering effect of exenatide q.w. versus exenatide b.i.d. Results: A total of 58 Japanese individuals with type 2 diabetes completed the study. Glycated hemoglobin was reduced by 0.2% at week 24 (7.2 ± 1.2% vs 7.0 ± 1.2% [56 ± 13 vs 53 ± 13 mmol/mol], 95% confidence interval −0.4 to −0.03%, P < 0.005 for non-inferiority, P = 0.01 for superiority). Fasting plasma glucose was reduced by 12 mg/dL at week 24 (154 ± 46 vs 142 ± 46 mg/dL, P = 0.02). β-Cell function assessed by homeostasis model assessment of β-cell function and C-peptide index was significantly improved at week 24. The incidence of self-reported hypoglycemia was reduced, and treatment satisfaction assessed by the Diabetes Treatment Satisfaction Questionnaire and Diabetes Medication Satisfaction Questionnaire was improved at week 24, with no change in body weight. There was no serious adverse event related to the study drug. Conclusions: Switching from exenatide b.i.d. to exenatide q.w. resulted in a reduction in glycated hemoglobin, fasting plasma glucose and the incidence of hypoglycemia, and improvement in β-cell function and treatment satisfaction in patients with type 2 diabetes. These findings will be useful for selecting optimal treatment in individuals with type 2 diabetes.

  • Efficacy and safety of once-weekly exenatide after switching from twice-daily exenatide in patients with type 2 diabetes.

    Watanabe Y, Saisho Y, Inaishi J, Kou K, Yamauchi A, Kanazawa Y, Okubo Y, Tokui M, Imai T, Murakami R, Tsuchiya T, Sasaki H, Masaoka T, Irie J, Meguro S, Itoh H, Twin-exenatide Study Group.

    Journal of diabetes investigation 11 ( 2 ) 382 - 388 2020.03

    ISSN  2040-1116

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Papers, etc., Registered in KOARA 【 Display / hide

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Reviews, Commentaries, etc. 【 Display / hide

  • 【内科疾患の診断基準・病型分類・重症度】(第10章)代謝・内分泌 2型糖尿病

    入江 潤一郎

    内科 ((株)南江堂)  127 ( 4 ) 941 - 943 2021.04

    ISSN  0022-1961

  • 【食事療法と運動療法】食事療法の基礎と臨床 糖・脂質代謝異常症に対する食事療法と腸内細菌叢

    大友 佑介, 入江 潤一郎

    The Lipid ((株)メディカルレビュー社)  32 ( 1 ) 26 - 32 2021.04

    ISSN  0915-6607

     View Summary

    糖尿病や脂質異常症などを有する患者において、腸内細菌の構成と機能が健常者と異なることが明らかになってきた。患者の腸内細菌叢は、短鎖脂肪酸や胆汁酸、アミノ酸の代謝機能が健常者と異なっており、そのために腸管ホルモン分泌が低下し、また腸管バリア機能の低下によるエンドトキシン血症が生じ、宿主にインスリン抵抗性が惹起されている。経口摂取する食物繊維や脂質の量、摂取時間などを指示する食事療法は、腸内細菌の機能維持にきわめて重要であり、腸内細菌と宿主の代謝応答を視野に入れた食事処方が今後は必要である。(著者抄録)

  • Author Correction: CD44 variant inhibits insulin secretion in pancreatic β cells by attenuating LAT1-mediated amino acid uptake (Scientific Reports, (2018), 8, 1, (2785), 10.1038/s41598-018-20973-2)

    Kobayashi N., Okazaki S., Sampetrean O., Irie J., Itoh H., Saya H.

    Scientific Reports (Scientific Reports)  10 ( 1 ) 6084 2020.12

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    © 2020, The Author(s). An amendment to this paper has been published and can be accessed via a link at the top of the paper.

  • 【腸内細菌と全身疾患】腸内細菌と代謝疾患 腸内細菌と肥満症

    杉山 和俊, 入江 潤一郎, 伊藤 裕

    Pharma Medica ((株)メディカルレビュー社)  38 ( 12 ) 41 - 45 2020.12

    ISSN  0289-5803

  • 糖尿病および合併症治療の展望〜糖尿病患者の健康長寿への架け橋〜 NAD+合成系賦活化に基づく2型糖尿病およびその合併症予防・治療の試み

    山口 慎太郎, 吉野 純, 永久 太一, 小杉 将太郎, 三石 正憲, 長谷川 一宏, 入江 潤一郎, 脇野 修, 伊藤 裕

    糖尿病合併症 ((一社)日本糖尿病合併症学会)  34 ( Suppl.1 ) 107 - 107 2020.11

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Presentations 【 Display / hide

  • 腸内細菌による腸内環境整備と個体の代謝制御

    Irie Junichiro

    第14回日本抗加齢医学会総会 (大阪国際会議場) , 

    2014.06

    Symposium, workshop panel (nominated)

  • 腸内細菌の代謝異常症形成における意義とその治療応用の可能性

    Irie Junichiro

    第 47 回日本無菌生物ノートバイオロジー学会総会, 

    2014.01

    Symposium, workshop panel (nominated)

  • 代謝異常症と腸内細菌

    Irie Junichiro

    第17回日本病態栄養学会年次学術集会 (大阪国際会議場) , 

    2014.01

    Symposium, workshop panel (nominated)

  • 膵島関連自己抗体陰性1型糖尿病におけるGAD反応性T細胞の検討

    Tsumura Kazuhiro, Shimada Akira, Oikawa Youichi, Irie Junichirou, Nakagawa Yoshinori, Saruta Takao

    第32回日本免疫学会総会, 

    2002.12

    Oral presentation (general)

  • 1型糖尿病患者末梢血中におけるCXCR3陽性細胞ポピユレーションの検討

    Yamada Satoru, Shimada Akira, Oikawa Youichi, Irie Junichirou, Nakagawa Yoshinori, Maruyama Tarou, Saruta Takao

    第32回日本免疫学会総会, 

    2002.12

    Oral presentation (general)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 腸管内分泌細胞の発生・発達に対する短鎖脂肪酸の意義の検討

    2021.04
    -
    2024.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

  • Novel therapy for obesity and diabetes through intestinal bile acid metabolism

    2018.04
    -
    2021.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

  • Novel therapy for metabolic diseases through intestinal environment by intestinal hormone

    2015.04
    -
    2018.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

 

Courses Taught 【 Display / hide

  • LECTURE SERIES, INTERNAL MEDICINE (NEPHROLOGY, ENDOCRINOLOGY, AND METABOLISM)

    2022

  • LECTURE SERIES, INTERNAL MEDICINE

    2022

  • INTRODUCTORY NUTRITION FOR HEALTH AND SPORTS

    2022

  • CLINICAL CLERKSHIP IN NEPHROLOGY, ENDOCRINOLOGY, AND METABOLISM

    2022

  • CLINICAL CLERKSHIP IN INTERNAL MEDICINE (NEPHROLOGY, ENDOCRINOLOGY, AND METABOLISM)

    2022

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Courses Previously Taught 【 Display / hide

  • 内科学(腎臓内分泌代謝内科)

    Keio University

    2017.04
    -
    2018.03

    Spring Semester, Lecture

  • 内科学(腎臓内分泌代謝内科)

    Keio University

    2016.04
    -
    2017.03

    Spring Semester, Lecture

  • 内科学(腎臓内分泌代謝内科)

    Keio University

    2015.04
    -
    2016.03

    Spring Semester, Lecture

 

Social Activities 【 Display / hide

  • 第50回糖尿病週間講演会 「腸内環境をふまえた肥満・糖尿病治療の工夫」

    2014.11
    -
    Present

Memberships in Academic Societies 【 Display / hide

  • 日本内科学会

     
  • 日本糖尿病学会

     
  • 日本内分泌学会

     
  • 日本肥満学会

     
  • 日本肥満症治療学会