入江 潤一郎 (イリエ ジュンイチロウ)

Irie, Junichiro

写真a

所属(所属キャンパス)

医学部 内科学教室(腎臓・内分泌・代謝) (信濃町)

職名

准教授

外部リンク

学位 【 表示 / 非表示

  • 医学博士, 慶應義塾, 2005年02月

 

研究分野 【 表示 / 非表示

  • 代謝学 (Metabolism Studies)

研究キーワード 【 表示 / 非表示

  • 代謝学

  • 糖尿病

  • 肥満

 

論文 【 表示 / 非表示

  • 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年04月

    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年03月

    ISSN  0012186X

     概要を見る

    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年06月

    ISSN  0931-0509

     概要を見る

    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年03月

    ISSN  20401116

     概要を見る

    © 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年03月

    ISSN  2040-1116

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KOARA(リポジトリ)収録論文等 【 表示 / 非表示

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総説・解説等 【 表示 / 非表示

  • 【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年04月

    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年04月

    ISSN  0915-6607

     概要を見る

    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年12月

     概要を見る

    © 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年12月

    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年11月

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研究発表 【 表示 / 非表示

  • 腸内細菌による腸内環境整備と個体の代謝制御

    入江 潤一郎

    第14回日本抗加齢医学会総会 (大阪国際会議場) , 2014年06月, シンポジウム・ワークショップ パネル(指名)

  • 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

    入江 潤一郎

    第 47 回日本無菌生物ノートバイオロジー学会総会, 2014年01月, シンポジウム・ワークショップ パネル(指名)

  • 代謝異常症と腸内細菌

    入江 潤一郎

    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年01月, シンポジウム・ワークショップ パネル(指名)

  • 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

    津村和大,島田朗,及川洋一,入江潤一郎,中川佳則,猿田享男

    第32回日本免疫学会総会, 2002年12月, 口頭(一般)

  • 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

    山田悟,島田朗,及川洋一,入江潤一郎,中川佳則,丸山太郎,猿田享男

    第32回日本免疫学会総会, 2002年12月, 口頭(一般)

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競争的資金等の研究課題 【 表示 / 非表示

  • 腸管内胆汁酸代謝制御による新規肥満・糖尿病治療法の開発

    2018年04月
    -
    2021年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 入江 潤一郎, 基盤研究(C), 補助金,  代表

  • 腸管ホルモンによる腸内環境を標的とした新規代謝異常症治療法の開発

    2015年04月
    -
    2018年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 入江 潤一郎, 基盤研究(C), 補助金,  代表

 

担当授業科目 【 表示 / 非表示

  • 健康栄養科学

    2021年度

  • 内科学(腎臓・内分泌・代謝)講義

    2021年度

  • 内科学講義

    2021年度

  • 健康スポーツ栄養科学

    2021年度

  • 健康栄養科学

    2020年度

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担当経験のある授業科目 【 表示 / 非表示

  • 内科学(腎臓内分泌代謝内科)

    慶應義塾, 2017年度, 春学期, 専門科目, 講義

  • 内科学(腎臓内分泌代謝内科)

    慶應義塾, 2016年度, 春学期, 専門科目, 講義

  • 内科学(腎臓内分泌代謝内科)

    慶應義塾, 2015年度, 春学期, 専門科目, 講義

 

社会活動 【 表示 / 非表示

  • 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年11月
    -
    継続中

所属学協会 【 表示 / 非表示

  • 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