伊藤 裕 (イトウ ヒロシ)

Ito, Hiroshi



医学部 内科学教室(腎臓・内分泌・代謝) (信濃町)




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  • [職 歴] 昭和58年  京都大学医学部附属病院内科医員 平成 元年  米国ハーバード大学医学部 Brigham and Women's Hospital Molecular and Cellular Research Laboratory博士研究員 平成 2年  米国スタンフォード大学医学部循環器内科 Falk Cardiovascular Research Center 博士研究員 平成12年  京都大学大学院医学研究科臨床病態医科学 第二内科病棟医長 平成13年  京都大学大学院医学研究科臨床病態医科学講座 講師 平成13年  京都大学大学院医学研究科臨床病態医科学講座 助教授 平成18年  慶應義塾大学医学部内科学講座 教授 平成20年  京都大学医学部 非常勤講師(兼任) 平成20年  慶應義塾大学医学部総合医科学研究センター 副センター長(兼任) 平成27年  日本学術振興会 学術システム研究センター 主任研究員 平成27年  日本内分泌学会 代表理事 平成27年  慶應義塾大学医学部百寿総合研究センター 副センター長(兼任)

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  • 医学部, 内科学(腎臓・内分泌・代謝), 教授

学歴 【 表示 / 非表示

  • 1983年03月

    京都大学, 医学部, 医学科

    大学, 卒業

  • 1989年03月

    京都大学, 医学研究科

    大学院, 修了, 博士

免許・資格 【 表示 / 非表示

  • 第1種放射線取扱主任者, 1980年

  • ECFMG免許, 1983年

  • 医師免許, 1983年

  • 日本内分泌学会内分泌代謝科専門医, 1995年

  • 日本糖尿病専門医, 2003年

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研究分野 【 表示 / 非表示

  • 腎臓内科学

  • 代謝学

  • 内分泌学

研究キーワード 【 表示 / 非表示

  • 代謝

  • 内分泌

  • 糖尿病

  • 高血圧


論文 【 表示 / 非表示

  • Home-based Aerobic Exercise and Resistance Training in Peritoneal Dialysis Patients: A Randomized Controlled Trial

    Uchiyama K., Washida N., Morimoto K., Muraoka K., Kasai T., Yamaki K., Miyashita K., Wakino S., Itoh H.

    Scientific Reports (Scientific Reports)  9 ( 1 )  2019年12月


    © 2019, The Author(s). Potential effects of aerobic and resistance training in peritoneal dialysis (PD) patients have been partially elucidated. We investigated effects of a home-based exercise program on physical functioning and health-related quality of life (HRQOL) in PD patients. Patients were randomly assigned to exercise (n = 24) and usual care (n = 23) groups. The exercise patients performed aerobic exercise thrice weekly and resistance training twice weekly at home for 12 weeks. The usual care patients received no specific intervention. The distance in incremental shuttle walking test significantly improved in the exercise group compared with the usual care group (P = 0.02). Among the HRQOL subscales assessed using the Kidney Disease Quality of Life-Short Form questionnaire, kidney disease component summary (P = 0.03), physical role functioning (P = 0.01), emotional role functioning (P < 0.01), and role/social component summary (P < 0.01) significantly improved in the exercise group. Moreover, serum albumin was significantly maintained in the exercise group (P = 0.03). There were no reported adverse events associated with the intervention. To our knowledge, this is the first randomized controlled trial to indicate the beneficial effects of a 12-week home-based exercise program exclusively in PD patients.

  • Induction of human pluripotent stem cells into kidney tissues by synthetic mRNAs encoding transcription factors

    Hiratsuka K., Monkawa T., Akiyama T., Nakatake Y., Oda M., Goparaju S., Kimura H., Chikazawa-Nohtomi N., Sato S., Ishiguro K., Yamaguchi S., Suzuki S., Morizane R., Ko S., Itoh H., Ko M.

    Scientific Reports (Scientific Reports)  9 ( 1 )  2019年12月


    © 2019, The Author(s). The derivation of kidney tissues from human pluripotent stem cells (hPSCs) and its application for replacement therapy in end-stage renal disease have been widely discussed. Here we report that consecutive transfections of two sets of synthetic mRNAs encoding transcription factors can induce rapid and efficient differentiation of hPSCs into kidney tissues, termed induced nephron-like organoids (iNephLOs). The first set - FIGLA, PITX2, ASCL1 and TFAP2C, differentiated hPSCs into SIX2 + SALL1 + nephron progenitor cells with 92% efficiency within 2 days. Subsequently, the second set - HNF1A, GATA3, GATA1 and EMX2, differentiated these cells into PAX8 + LHX1 + pretubular aggregates in another 2 days. Further culture in both 2-dimensional and 3-dimensional conditions produced iNephLOs containing cells characterized as podocytes, proximal tubules, and distal tubules in an additional 10 days. Global gene expression profiles showed similarities between iNephLOs and the human adult kidney, suggesting possible uses of iNephLOs as in vitro models for kidneys.

  • Hypertension as a Metabolic Disorder and the Novel Role of the Gut

    Tanaka M., Itoh H.

    Current Hypertension Reports (Current Hypertension Reports)  21 ( 8 )  2019年08月

    ISSN  15226417


    © 2019, The Author(s). Purpose of Review: Hypertension is related to impaired metabolic homeostasis and can be regarded as a metabolic disorder. This review presents possible mechanisms by which metabolic disorders increase blood pressure (BP) and discusses the importance of the gut as a novel modulator of BP. Recent Findings: Obesity and high salt intake are major risk factors for hypertension. There is a hypothesis of “salt-induced obesity”; i.e., high salt intake may tie to obesity. Heightened sympathetic nervous system (SNS) activity, especially in the kidney and brain, increases BP in obese patients. Adipokines, including adiponectin and leptin, and renin-angiotensin-aldosterone system (RAAS) contribute to hypertension. Adiponectin induced by a high-salt diet may decrease sodium/glucose cotransporter (SGLT) 2 expression in the kidney, which results in reducing BP. High salt can change secretions of adipokines and RAAS-related components. Evidence has been accumulating linking the gastrointestinal tract to BP. Glucagon-like peptide-1 (GLP-1) and ghrelin decrease BP in both rodents and humans. The sweet taste receptor in enteroendocrine cells increases SGLT1 expression and stimulates sodium/glucose absorption. Roux-en-Y gastric bypass improves glycemic and BP control due to reducing the activity of SGLT1. Na/H exchanger isoform 3 (NHE3) increases BP by stimulating the intestinal absorption of sodium. Gastrin functions as an intestinal sodium taste sensor and inhibits NHE3 activity. Intestinal mineralocorticoid receptors also regulate sodium absorption and BP due to changing ENaC activity. Gastric sensing of sodium induces natriuresis, and gastric distension increases BP. Changes in the composition and function of gut microbiota contribute to hypertension. A high-salt/fat diet may disrupt the gut barrier, which results in systemic inflammation, insulin resistance, and increased BP. Gut microbiota regulates BP by secreting vasoactive hormones and short-chain fatty acids. BP-lowering effects of probiotics and antibiotics have been reported. Bariatric surgery improves metabolic disorders and hypertension due to increasing GLP-1 secretion, decreasing leptin secretion and SNS activity, and changing gut microbiome composition. Strategies targeting the gastrointestinal system may be therapeutic options for improving metabolic abnormalities and reducing BP in humans. Summary: SNS, brain, adipocytes, RAAS, the kidney, the gastrointestinal tract, and microbiota play important roles in regulating BP. Most notably, the gut could be a novel target for treatment of hypertension as a metabolic disorder.

  • DNA Damage Repair and DNA Methylation in the Kidney

    Hayashi K., Hishikawa A., Itoh H.

    American Journal of Nephrology (American Journal of Nephrology)  50 ( 2 ) 81 - 91 2019年07月

    ISSN  02508095


    © 2019 © 2019 S. Karger AG, Basel. Copyright: All rights reserved. The DNA repair system is essential for the maintenance of genome integrity and is mainly investigated in the areas of aging and cancer. The DNA repair system is strikingly cell-type specific, depending on the expression of DNA repair factors; therefore, different DNA repair systems may exist in each type of kidney cell. Importance of DNA repair in the kidney is suggested by renal phenotypes caused by both genetic mutations in the DNA repair pathway and increased stimuli of DNA damage. Recently, we reported the importance of DNA double-strand break repair in glomerular podocytes and its involvement in the alteration of DNA methylation status, which regulates podocyte phenotypes. In this review, we summarize the roles of the DNA repair system in the kidneys and possible associations with altered kidney DNA methylation, which have been infrequently reported together. Investigations of DNA damage repair and epigenetic changes in the kidneys may achieve a profound understanding of kidney aging and diseases.

  • Influence of antihypertensive drugs in the subtype diagnosis of primary aldosteronism by adrenal venous sampling

    Nagasawa M., Yamamoto K., Rakugi H., Takeda M., Akasaka H., Umakoshi H., Tsuiki M., Takeda Y., Kurihara I., Itoh H., Ichijo T., Katabami T., Wada N., Shibayama Y., Yoshimoto T., Ogawa Y., Kawashima J., Sone M., Inagaki N., Takahashi K., Fujita M., Watanabe M., Matsuda Y., Kobayashi H., Shibata H., Kamemura K., Otsuki M., Fujii Y., Ogo A., Okamura S., Miyauchi S., Yanase T., Suzuki T., Kawamura T., Naruse M.

    Journal of Hypertension (Journal of Hypertension)  37 ( 7 ) 1493 - 1499 2019年07月

    ISSN  02636352


    © 2019 Wolters Kluwer Health, Inc. All rights reserved. Objectives:Because of the influence on the renin-angiotensin-aldosterone system, it is recommended to avoid, if possible, the use of angiotensin-converting-enzyme inhibitors, angiotensin II type 1 receptor blockers, diuretics, β-blockers, and mineralocorticoid receptor antagonists during the diagnostic period of primary aldosteronism. A laterality index more than 4 in adrenocorticotropic hormone (ACTH)-stimulated adrenal venous sampling (ACTH-AVS) is a widely used classification of the unilateral subtype that can benefit from adrenalectomy. Here, we revealed clinical features of patients taking drugs that could affect the primary aldosteronism diagnosis (DAPD) and investigated whether the classification with laterality index more than 4 in ACTH-AVS is applicable to these patients.Patients and methods:Using a large database of primary aldosteronism patients in Japan, we analyzed 2122 patients with successful ACTH-AVS.Results:Patients who received any DAPD (n = 209) showed higher prevalence of comorbidity burdens and took more antihypertensive drugs compared with patients without DAPD. In patients taking DAPD, those with laterality index more than 4 had a higher prevalence of hypokalemia, a higher aldosterone-to-renin ratio and a higher prevalence of adrenal mass than those with laterality index of 4 or less. Adrenalectomy was performed in 76% patients with laterality index more than 4 and 20% with laterality index of 4 or less. Patients who underwent adrenalectomy showed biochemical cure in 89% with laterality index more than 4 and 50% with laterality index of 4 or less (P = 0.001). Multivariate regression analysis showed that laterality index more than 4 was an independent predictor of a biochemical cure. Biochemical cure rate in patients with laterality index more than 4 was consistently high, irrespective of the potential effect of individual DAPD on laterality index.Conclusion:Our findings suggest that in primary aldosteronism patients to whom DAPD were administrated due to severe clinical features, laterality index more than 4 in ACTH-AVS could accurately predict a biochemical cure after adrenalectomy.

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研究発表 【 表示 / 非表示

  • Obesity-associated gut inflammation and gut microbiota

    伊藤 裕

    International Congress on Obesity and Metabolic Syndrome (Seoul, Korea) , 2017年09月, シンポジウム・ワークショップ パネル(指名)

  • Does intensive treat-to-target LDL-C lowering therapy using statin in patients of diabetic retinopathy reduce cardiovascular events?:the EMPATHY study

    伊藤 裕

    European Society of Cardiology Congress 2017, 2017年08月, 口頭(一般)

  • 4. Diabetic hypertensives in Asia; Are we different from Westerners?

    伊藤 裕

    APSH/ISH Summer School,2017 (Shanghai, China) , 2017年08月, 公開講演,セミナー,チュートリアル,講習,講義等

  • "Organ memory" and Pre-emptive medicine for hypertension

    伊藤 裕

    APSH/ISH Summer School,2017 (Shanghai, China) , 2017年08月, 公開講演,セミナー,チュートリアル,講習,講義等

  • “メタボエイジング”と“イムノエイジング”を結ぶもの

    伊藤 裕

    第17回日本抗加齢医学会総会, 2017年06月, 公開講演,セミナー,チュートリアル,講習,講義等

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競争的資金等の研究課題 【 表示 / 非表示

  • 代謝産物を介した多細胞間ネットワークの統合的解析による臓器機能in toto把握


    文部科学省・日本学術振興会, 科学研究費助成事業, 伊藤 裕, 挑戦的研究(開拓), 補助金,  代表

  • エネルギー代謝維持多臓器間サーキットのハブ臓器としての腎臓の意義と代謝性腎症


    文部科学省・日本学術振興会, 科学研究費助成事業, 伊藤 裕, 基盤研究(A), 補助金,  代表

  • 質量分析イメージングによる腎代謝小分子の可視化と虚血腎の病態解明


    文部科学省・日本学術振興会, 科学研究費助成事業, 伊藤 裕, 挑戦的萌芽研究, 補助金,  代表



  • 尿細管糸球体代謝連関とMetabolic Kidney Diseaseの病態解明


    文部科学省・日本学術振興会, 科学研究費助成事業, 伊藤 裕, 基盤研究(A), 補助金,  代表


    生活習慣病の重積を基盤とするCKDを新たにMetabolic Kidney Dis easeと捉えた。近位尿細管におけるiNAMPTの意義について、iNAMPTはTGFβにより発現が低下することを明らかにした。iNAMPTプロモータ解析を行いこの発現調節の詳細を明らかにした。さらに糖尿病性腎症ではiNAMPTの発現低下によるSirt6の発現低下が組織線維化へ寄与する。NNMTの線維化に関わるメカニズムの検討を遂行した。NMMT過剰発現マウスの肝臓線維化は肝臓のメチオニン代謝反応の低下のためのメチル基の欠乏がCTGF遺伝子の発現をepigeneticに増加させて、線維化が亢進したと考えられた。

受賞 【 表示 / 非表示

  • 平成29年度井村臨床研究賞


  • 平成28年度日本糖尿病合併症学会Expert Investigator Award


  • 第18回日本心血管内分泌代謝学会 高峰譲吉賞


  • 第3回抗加齢研究奨励賞(臨床の部)


  • 上原記念生命科学財団 研究助成金


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担当授業科目 【 表示 / 非表示

  • 内科学(腎臓・内分泌・代謝)講義


  • 内科学講義


  • 内科学演習


  • 内科学実習


  • 内科学


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所属学協会 【 表示 / 非表示

  • 日本内分泌学会

  • 日本高血圧学会, 

  • 日本内科学会

  • 日本肥満学会, 

  • 日本心血管内分泌代謝学会


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