Updated on 2022/04/12

写真a

 
ONOUE Takeshi
 
Organization
Nagoya University Hospital Center for Postgraduate Clinical Training and Career Development Lecturer of hospital
Title
Lecturer of hospital
External link

Degree 2

  1. 博士(医学) ( 2016.6   名古屋大学 ) 

  2. 学士(医学) ( 2007.3   名古屋大学 ) 

Research Interests 10

  1. 糖尿病

  2. 肥満症

  3. Education for patients

  4. Medical education

  5. 中枢神経系におけるインスリンシグナル

  6. 中枢神経系におけるエネルギー代謝機構

  7. 中枢神経系におけるインスリンシグナル

  8. 中枢神経系におけるエネルギー代謝機構

  9. 糖尿病

  10. 肥満症

Research Areas 3

  1. Life Science / Metabolism and endocrinology

  2. Humanities & Social Sciences / Tertiary education

  3. Life Science / General internal medicine

Research History 2

  1. Nagoya University   Nagoya University Hospital Center for Postgraduate Clinical Training and Career Development   Lecturer of hospital

    2022.4

  2. Nagoya University   Nagoya University Hospital Center for Postgraduate Clinical Training and Career Development   Assistant professor of hospital

    2017.4 - 2022.3

Education 3

  1. Nagoya University   Graduate School, Division of Medical Sciences

    - 2016

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    Country: Japan

  2. Nagoya University   Graduate School, Division of Medical Sciences

    - 2016

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    Country: Japan

  3. Nagoya University   Faculty of Medicine

    - 2007.3

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    Country: Japan

Professional Memberships 14

  1. 日本内分泌学会   評議員

  2. 日本糖尿病学会

  3. 日本肥満学会

  4. 日本神経内分泌学会

  5. 米国内分泌学会

  6. 米国糖尿病学会

  7. 日本内科学会

  8. Japan Society for Medical Education

  9. 日本内分泌学会

  10. 日本神経内分泌学会

  11. 日本糖尿病学会

  12. 日本肥満学会

  13. 米国内分泌学会

  14. 米国糖尿病学会

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Committee Memberships 3

  1.   Institutional Research (IR) WG  

    2019.4   

  2.   Diabetes support team  

    2016.4   

  3.   Nutrition Support Team  

    2016.4   

 

Papers 41

  1. Increased Risk of Thyroid Dysfunction by PD-1 and CTLA-4 Blockade in Patients Without Thyroid Autoantibodies at Baseline Reviewed

    Iwama Shintaro, Kobayashi Tomoko, Yasuda Yoshinori, Okuji Takayuki, Ito Masaaki, Ando Masahiko, Zhou Xin, Yamagami Ayana, Onoue Takeshi, Kawaguchi Yohei, Miyata Takashi, Sugiyama Mariko, Takagi Hiroshi, Hagiwara Daisuke, Suga Hidetaka, Banno Ryoichi, Hase Tetsunari, Morise Masahiro, Wakahara Keiko, Yokota Kenji, Kato Masashi, Nishio Naoki, Tanaka Chie, Miyata Kazushi, Ogura Atsushi, Ito Takanori, Sawada Tsunaki, Shimokata Tomoya, Niimi Kaoru, Ohka Fumiharu, Ishigami Masatoshi, Gotoh Momokazu, Hashimoto Naozumi, Saito Ryuta, Kiyoi Hitoshi, Kajiyama Hiroaki, Ando Yuichi, Hibi Hideharu, Sone Michihiko, Akiyama Masashi, Kodera Yasuhiro, Arima Hiroshi

    JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM   Vol. 107 ( 4 ) page: E1620 - E1630   2022.3

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    DOI: 10.1210/clinem/dgab829

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  2. Functional Lactotrophs in Induced Adenohypophysis Differentiated From Human iPS Cells Reviewed

    Miyake Natsuki, Nagai Takashi, Suga Hidetaka, Osuka Satoko, Kasai Takatoshi, Sakakibara Mayu, Soen Mika, Ozaki Hajime, Miwata Tsutomu, Asano Tomoyoshi, Kano Mayuko, Muraoka Ayako, Nakanishi Natsuki, Nakamura Tomoko, Goto Maki, Yasuda Yoshinori, Kawaguchi Yohei, Miyata Takashi, Kobayashi Tomoko, Sugiyama Mariko, Onoue Takeshi, Hagiwara Daisuke, Iwama Shintaro, Iwase Akira, Inoshita Naoko, Arima Hiroshi, Kajiyama Hiroaki

    ENDOCRINOLOGY   Vol. 163 ( 3 )   2022.3

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    DOI: 10.1210/endocr/bqac004

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  3. Predicting non-insulin-dependent state in patients with slowly progressive insulin-dependent (type 1) diabetes mellitus or latent autoimmune diabetes in adults. Reply to Sugiyama K and Saisho Y [letter] Reviewed

    Wada Eri, Onoue Takeshi, Kinoshita Tamaki, Hayase Ayaka, Handa Tomoko, Ito Masaaki, Furukawa Mariko, Okuji Takayuki, Kobayashi Tomoko, Iwama Shintaro, Sugiyama Mariko, Takagi Hiroshi, Hagiwara Daisuke, Suga Hidetaka, Banno Ryoichi, Goto Motomitsu, Arima Hiroshi

    DIABETOLOGIA   Vol. 65 ( 1 ) page: 252 - 253   2022.1

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

    DOI: 10.1007/s00125-021-05610-4

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  4. Adult-onset autoimmune diabetes identified by glutamic acid decarboxylase autoantibodies: a retrospective cohort study Reviewed

    Wada Eri, Onoue Takeshi, Kinoshita Tamaki, Hayase Ayaka, Handa Tomoko, Ito Masaaki, Furukawa Mariko, Okuji Takayuki, Kobayashi Tomoko, Iwama Shintaro, Sugiyama Mariko, Takagi Hiroshi, Hagiwara Daisuke, Suga Hidetaka, Banno Ryoichi, Goto Motomitsu, Arima Hiroshi

    DIABETOLOGIA   Vol. 64 ( 10 ) page: 2183 - 2192   2021.10

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    DOI: 10.1007/s00125-021-05516-1

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  5. GABA(B) receptor signaling in the caudate putamen is involved in binge-like consumption during a high fat diet in mice Reviewed

    Sun Runan, Tsunekawa Taku, Hirose Tomonori, Yaginuma Hiroshi, Taki Keigo, Mizoguchi Akira, Miyata Takashi, Kobayashi Tomoko, Sugiyama Mariko, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Suga Hidetaka, Banno Ryoichi, Bettler Bernhard, Arima Hiroshi

    SCIENTIFIC REPORTS   Vol. 11 ( 1 ) page: 19296   2021.9

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    DOI: 10.1038/s41598-021-98590-9

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  6. Deficiency of WFS1 leads to the impairment of AVP secretion under dehydration in male mice Reviewed

    Kurimoto Junki, Takagi Hiroshi, Miyata Takashi, Hodai Yuichi, Kawaguchi Yohei, Hagiwara Daisuke, Suga Hidetaka, Kobayashi Tomoko, Sugiyama Mariko, Onoue Takeshi, Ito Yoshihiro, Iwama Shintaro, Banno Ryoichi, Tanabe Katsuya, Tanizawa Yukio, Arima Hiroshi

    PITUITARY   Vol. 24 ( 4 ) page: 582 - 588   2021.8

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    DOI: 10.1007/s11102-021-01135-6

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  7. Prediabetes is associated with proteinuria development but not with glomerular filtration rate decline: A longitudinal observational study Reviewed

    Furukawa Mariko, Onoue Takeshi, Kato Kiminori, Wada Takashi, Shinohara Yukito, Kinoshita Fumie, Goto Motomitsu, Arima Hiroshi, Tsushita Kazuyo

    DIABETIC MEDICINE   Vol. 38 ( 8 ) page: e14607   2021.8

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    DOI: 10.1111/dme.14607

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  8. Glucocorticoid receptor signaling in ventral tegmental area neurons increases the rewarding value of a high-fat diet in mice Reviewed

    Mizoguchi Akira, Banno Ryoichi, Sun Runan, Yaginuma Hiroshi, Taki Keigo, Kobayashi Tomoko, Sugiyama Mariko, Tsunekawa Taku, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Suga Hidetaka, Nagai Taku, Yamada Kiyofumi, Arima Hiroshi

    SCIENTIFIC REPORTS   Vol. 11 ( 1 ) page: 12873   2021.6

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    DOI: 10.1038/s41598-021-92386-7

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  9. Comparison of High-Resolution Manometry in Patients Complaining of Dysphagia among Patients with or without Diabetes Mellitus Reviewed

    Muroi Koichi, Miyahara Ryoji, Funasaka Kohei, Furukawa Kazuhiro, Sawada Tsunaki, Maeda Keiko, Yamamura Takeshi, Ishikawa Takuya, Ohno Eizaburo, Nakamura Masanao, Kawashima Hiroki, Onoue Takeshi, Arima Hiroshi, Hirooka Yoshiki, Fujishiro Mitsuhiro

    DIGESTION   Vol. 102 ( 4 ) page: 554 - 562   2021.6

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    DOI: 10.1159/000510081

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  10. CD4(+) T cells are essential for the development of destructive thyroiditis induced by anti-PD-1 antibody in thyroglobulin-immunized mice Reviewed

    Yasuda Yoshinori, Iwama Shintaro, Sugiyama Daisuke, Okuji Takayuki, Kobayashi Tomoko, Ito Masaaki, Okada Norio, Enomoto Atsushi, Ito Sachiko, Yan Yue, Sugiyama Mariko, Onoue Takeshi, Tsunekawa Taku, Ito Yoshihiro, Takagi Hiroshi, Hagiwara Daisuke, Goto Motomitsu, Suga Hidetaka, Banno Ryoichi, Takahashi Masahide, Nishikawa Hiroyoshi, Arima Hiroshi

    SCIENCE TRANSLATIONAL MEDICINE   Vol. 13 ( 593 )   2021.5

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    DOI: 10.1126/scitranslmed.abb7495

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  11. High-fat Feeding Causes Inflammation and Insulin Resistance in the Ventral Tegmental Area in Mice Reviewed

    Mizoguchi Akira, Banno Ryoichi, Sun Runan, Yaginuma Hiroshi, Taki Keigo, Kobayashi Tomoko, Sugiyama Mariko, Tsunekawa Taku, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Suga Hidetaka, Arima Hiroshi

    NEUROSCIENCE   Vol. 461   page: 72 - 79   2021.5

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    DOI: 10.1016/j.neuroscience.2021.02.009

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  12. Arginine vasopressin-Venus reporter mice as a tool for studying magnocellular arginine vasopressin neurons Reviewed

    Hagiwara Daisuke, Tochiya Masayoshi, Azuma Yoshinori, Tsumura Tetsuro, Hodai Yuichi, Kawaguchi Yohei, Miyata Takashi, Kobayashi Tomoko, Sugiyama Mariko, Onoue Takeshi, Takagi Hiroshi, Ito Yoshihiro, Iwama Shintaro, Suga Hidetaka, Banno Ryoichi, Arima Hiroshi

    PEPTIDES   Vol. 139   page: 170517   2021.5

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    DOI: 10.1016/j.peptides.2021.170517

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  13. Anti-pituitary antibodies and susceptible human leukocyte antigen alleles as predictive biomarkers for pituitary dysfunction induced by immune checkpoint inhibitors. Reviewed

    Kobayashi T, Iwama S, Sugiyama D, Yasuda Y, Okuji T, Ito M, Ito S, Sugiyama M, Onoue T, Takagi H, Hagiwara D, Ito Y, Suga H, Banno R, Nishikawa H, Arima H

    Journal for immunotherapy of cancer   Vol. 9 ( 5 )   2021.5

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    DOI: 10.1136/jitc-2021-002493

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  14. Dietary sodium chloride attenuates increased beta-cell mass to cause glucose intolerance in mice under a high-fat diet Reviewed

    Taki Keigo, Takagi Hiroshi, Hirose Tomonori, Sun Runan, Yaginuma Hiroshi, Mizoguchi Akira, Kobayashi Tomoko, Sugiyama Mariko, Tsunekawa Taku, Onoue Takeshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Suga Hidetaka, Banno Ryoichi, Sakano Daisuke, Kume Shoen, Arima Hiroshi

    PLOS ONE   Vol. 16 ( 3 ) page: e0248065   2021.3

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    DOI: 10.1371/journal.pone.0248065

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  15. Peripheral combination treatment of leptin and an SGLT2 inhibitor improved glucose metabolism in insulin-dependent diabetes mellitus mice Reviewed

    Yaginuma Hiroshi, Banno Ryoichi, Sun Runan, Taki Keigo, Mizoguchi Akira, Kobayashi Tomoko, Sugiyama Mariko, Tsunekawa Taku, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Suga Hidetaka, Arima Hiroshi

    JOURNAL OF PHARMACOLOGICAL SCIENCES   Vol. 147 ( 4 ) page: 340 - 347   2021

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    DOI: 10.1016/j.jphs.2021.08.010

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  16. Endoplasmic reticulum chaperone BiP/GRP78 knockdown leads to autophagy and cell death of arginine vasopressin neurons in mice

    Kawaguchi Yohei, Hagiwara Daisuke, Miyata Takashi, Hodai Yuichi, Kurimoto Junki, Takagi Hiroshi, Suga Hidetaka, Kobayashi Tomoko, Sugiyama Mariko, Onoue Takeshi, Ito Yoshihiro, Iwama Shintaro, Banno Ryoichi, Grinevich Valery, Arima Hiroshi

    SCIENTIFIC REPORTS   Vol. 10 ( 1 ) page: 19730   2020.11

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    DOI: 10.1038/s41598-020-76839-z

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  17. Degradation of Mutant Protein Aggregates within the Endoplasmic Reticulum of Vasopressin Neurons

    Miyata Takashi, Hagiwara Daisuke, Hodai Yuichi, Miwata Tsutomu, Kawaguchi Yohei, Kurimoto Junki, Ozaki Hajime, Mitsumoto Kazuki, Takagi Hiroshi, Suga Hidetaka, Kobayashi Tomoko, Sugiyama Mariko, Onoue Takeshi, Ito Yoshihiro, Iwama Shintaro, Banno Ryoichi, Matsumoto Mami, Kawakami Natsuko, Ohno Nobuhiko, Sakamoto Hirotaka, Arima Hiroshi

    ISCIENCE   Vol. 23 ( 10 ) page: 101648   2020.10

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    DOI: 10.1016/j.isci.2020.101648

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  18. Higher level of body mass index (>= 22 kg/m(2)) is a useful predictor of non-insulin requirement in Slowly Progressive Insulin-Dependent (Type 1) Diabetes Mellitus (SPIDDM)

    Onoue T., Wada E., Hayase A., Handa T., Furukawa M., Kobayashi T., Goto M., Arima H.

    DIABETOLOGIA   Vol. 63 ( SUPPL 1 ) page: S176 - S176   2020.9

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  19. Pituitary dysfunction induced by immune checkpoint inhibitors is associated with better overall survival in both malignant melanoma and non-small cell lung carcinoma: a prospective study Reviewed

    Kobayashi Tomoko, Iwama Shintaro, Yasuda Yoshinori, Okada Norio, Okuji Takayuki, Ito Masaaki, Onoue Takeshi, Goto Motomitsu, Sugiyama Mariko, Tsunekawa Taku, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Suga Hidetaka, Banno Ryoichi, Yokota Kenji, Hase Tetsunari, Morise Masahiro, Hashimoto Naozumi, Ando Masahiko, Fujimoto Yasushi, Hibi Hideharu, Sone Michihiko, Ando Yuichi, Akiyama Masashi, Hasegawa Yoshinori, Arima Hiroshi

    JOURNAL FOR IMMUNOTHERAPY OF CANCER   Vol. 8 ( 2 )   2020.6

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    DOI: 10.1136/jitc-2020-000779

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  20. Hypothalamic glial cells isolated by MACS reveal that microglia and astrocytes induce hypothalamic inflammation via different processes under high-fat diet conditions

    Sugiyama Mariko, Banno Ryoichi, Yaginuma Hiroshi, Taki Keigo, Mizoguchi Akira, Tsunekawa Taku, Onoue Takeshi, Takagi Hiroshi, Ito Yoshihiro, Iwama Shintaro, Goto Motomitsu, Suga Hidetaka, Komine Okiru, Yamanaka Koji, Arima Hiroshi

    NEUROCHEMISTRY INTERNATIONAL   Vol. 136   page: 104733   2020.6

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    DOI: 10.1016/j.neuint.2020.104733

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  21. Anti-thyroid antibodies and thyroid echo pattern at baseline as risk factors for thyroid dysfunction induced by anti-programmed cell death-1 antibodies: a prospective study

    Okada Norio, Iwama Shintaro, Okuji Takayuki, Kobayashi Tomoko, Yasuda Yoshinori, Wada Eri, Onoue Takeshi, Goto Motomitsu, Sugiyama Mariko, Tsunekawa Taku, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Suga Hidetaka, Banno Ryoichi, Hase Tetsunari, Morise Masahiro, Kanda Mitsuro, Yokota Kenji, Hashimoto Naozumi, Ando Masahiko, Fujimoto Yasushi, Nagino Masato, Kodera Yasuhiro, Fujishiro Mitsuhiro, Hibi Hideharu, Sone Michihiko, Kiyoi Hitoshi, Gotoh Momokazu, Ando Yuichi, Akiyama Masashi, Hasegawa Yoshinori, Arima Hiroshi

    BRITISH JOURNAL OF CANCER   Vol. 122 ( 6 ) page: 771 - 777   2020.3

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    DOI: 10.1038/s41416-020-0736-7

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  22. Dipeptidyl peptidase-4 inhibitor anagliptin reduces fasting apolipoprotein B-48 levels in patients with type 2 diabetes: A randomized controlled

    Onoue Takeshi, Goto Motomitsu, Wada Eri, Furukawa Mariko, Okuji Takayuki, Okada Norio, Kobayashi Tomoko, Iwama Shintaro, Sugiyama Mariko, Tsunekawa Taku, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Morishita Yoshiaki, Seino Yusuke, Suga Hidetaka, Banno Ryoichi, Hamada Yoji, Ando Masahiko, Yamamori Etsuko, Arima Hiroshi

    PLOS ONE   Vol. 15 ( 1 ) page: e0228004   2020.1

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    DOI: 10.1371/journal.pone.0228004

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  23. Hypothalamic Contribution to Pituitary Functions Is Recapitulated In Vitro Using 3D-Cultured Human iPS Cells

    Kasai Takatoshi, Suga Hidetaka, Sakakibara Mayu, Ozone Chikafumi, Matsumoto Ryusaku, Kano Mayuko, Mitsumoto Kazuki, Ogawa Koichiro, Kodani Yu, Nagasaki Hiroshi, Inoshita Naoko, Sugiyama Mariko, Onoue Takeshi, Tsunekawa Taku, Ito Yoshihiro, Takagi Hiroshi, Hagiwara Daisuke, Iwama Shintaro, Goto Motomitsu, Banno Ryoichi, Takahashi Jun, Arima Hiroshi

    CELL REPORTS   Vol. 30 ( 1 ) page: 18 - +   2020.1

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    DOI: 10.1016/j.celrep.2019.12.009

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  24. Flash glucose monitoring helps achieve better glycemic control than conventional self-monitoring of blood glucose in non-insulin-treated type 2 diabetes: a randomized controlled trial.

    Wada E, Onoue T, Kobayashi T, Handa T, Hayase A, Ito M, Furukawa M, Okuji T, Okada N, Iwama S, Sugiyama M, Tsunekawa T, Takagi H, Hagiwara D, Ito Y, Suga H, Banno R, Kuwatsuka Y, Ando M, Goto M, Arima H

    BMJ open diabetes research & care   Vol. 8 ( 1 )   2020.1

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    DOI: 10.1136/bmjdrc-2019-001115

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  25. Diagnosis of central diabetes insipidus using a vasopressin radioimmunoassay during hypertonic saline infusion

    Takagi Hiroshi, Hagiwara Daisuke, Handa Tomoko, Sugiyama Mariko, Onoue Takeshi, Tsunekawa Taku, Ito Yoshihiro, Iwama Shintaro, Goto Motomitsu, Suga Hidetaka, Banno Ryoichi, Takahashi Kunihiko, Matsui Shigeyuki, Arima Hiroshi

    ENDOCRINE JOURNAL   Vol. 67 ( 3 ) page: 267 - 274   2020

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    DOI: 10.1507/endocrj.EJ19-0224

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  26. GABA(B) Receptor Signaling in the Mesolimbic System Suppresses Binge-like Consumption of a High-Fat Diet

    Tsunekawa Taku, Banno Ryoichi, Yaginuma Hiroshi, Taki Keigo, Mizoguchi Akira, Sugiyama Mariko, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Goto Motomitsu, Suga Hidetaka, Bettler Bernhard, Arima Hiroshi

    ISCIENCE   Vol. 20   page: 337-+   2019.10

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    DOI: 10.1016/j.isci.2019.09.032

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  27. Improved methods for the differentiation of hypothalamic vasopressin neurons using mouse induced pluripotent stem cells

    Mitsumoto Kazuki, Suga Hidetaka, Sakakibara Mayu, Soen Mika, Yamada Tomiko, Ozaki Hajime, Nagai Takashi, Kano Mayuko, Kasai Takatoshi, Ozone Chikafumi, Ogawa Koichiro, Sugiyama Mariko, Onoue Takeshi, Tsunekawa Taku, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Goto Motomitsu, Banno Ryoichi, Arima Hiroshi

    STEM CELL RESEARCH   Vol. 40   page: 101572   2019.10

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    DOI: 10.1016/j.scr.2019.101572

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  28. Automated Feedback Messages With Shichifukujin Characters Using IoT System-Improved Glycemic Control in People With Diabetes: A Prospective, Multicenter Randomized Controlled Trial.

    Kobayashi T, Tsushita K, Nomura E, Muramoto A, Kato A, Eguchi Y, Onoue T, Goto M, Muto S, Yatsuya H, Arima H

    Journal of diabetes science and technology   Vol. 13 ( 4 ) page: 796 - 798   2019.7

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    DOI: 10.1177/1932296819851785

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  29. Tanycyte-Like Cells Derived From Mouse Embryonic Stem Culture Show Hypothalamic Neural Stem/Progenitor Cell Functions

    Kano Mayuko, Suga Hidetaka, Ishihara Takeshi, Sakakibara Mayu, Soen Mika, Yamada Tomiko, Ozaki Hajime, Mitsumoto Kazuki, Kasai Takatoshi, Sugiyama Mariko, Onoue Takeshi, Tsunekawa Taku, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Iwama Shintaro, Goto Motomitsu, Banno Ryoichi, Arima Hiroshi

    ENDOCRINOLOGY   Vol. 160 ( 7 ) page: 1701 - 1718   2019.7

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    DOI: 10.1210/en.2019-00105

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  30. Chemical chaperone 4-phenylbutylate reduces mutant protein accumulation in the endoplasmic reticulum of arginine vasopressin neurons in a mouse model for familial neurohypophysial diabetes insipidus

    Masayoshi Tochiya, Daisuke Hagiwara, Yoshinori Azuma, Takashi Miyata, Yoshiaki Morishita, Hidetaka Suga, Takeshi Onoue, Taku Tsunekawa, Hiroshi Takagi, Yoshihiro Ito, Shintaro Iwama, Motomitsu Goto, Ryoichi Banno, Hiroshi Arima

    Neuroscience Letters   Vol. 682   page: 50 - 55   2018.8

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    Familial neurohypophysial diabetes insipidus (FNDI), characterized by progressive polyuria and loss of arginine vasopressin (AVP) neurons, is an autosomal dominant disorder caused by AVP gene mutations. Our previous studies with FNDI model mice demonstrated that mutant proteins accumulated in the endoplasmic reticulum (ER) of AVP neurons. Here, we examined therapeutic effects of the chemical chaperone 4-phenylbutylate (4-PBA) in FNDI mice. Treatment with 4-PBA reduced mutant protein accumulation in the ER of FNDI mice and increased AVP release, leading to reduced urine volumes. Furthermore, AVP neuron loss under salt loading was attenuated by 4-PBA treatment. These data suggest that 4-PBA ameliorated mutant protein accumulation in the ER of AVP neurons and thereby prevented FNDI phenotype progression.

    DOI: 10.1016/j.neulet.2018.06.013

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  31. Patients With Antithyroid Antibodies Are Prone To Develop Destructive Thyroiditis by Nivolumab: A Prospective Study International journal

    Kobayashi Tomoko, Iwama Shintaro, Yasuda Yoshinori, Okada Norio, Tsunekawa Taku, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Morishita Yoshiaki, Goto Motomitsu, Suga Hidetaka, Banno Ryoichi, Yokota Kenji, Hase Tetsunari, Morise Masahiro, Hashimoto Naozumi, Ando Masahiko, Kiyoi Hitoshi, Gotoh Momokazu, Ando Yuichi, Akiyama Masashi, Hasegawa Yoshinori, Arima Hiroshi

    JOURNAL OF THE ENDOCRINE SOCIETY   Vol. 2 ( 3 ) page: 241 - 251   2018.3

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

    Context: Immune checkpoint inhibitors, including anti-programmed cell death-1 (PD-1) antibodies, have become promising treatments for a variety of advanced malignancies. However, these medicines can cause immune-related adverse events (irAEs), including endocrinopathies. Objective: This study examined the incidence of endocrine irAEs induced by nivolumab. Patients and Main Outcome Measured: Sixty-six patients treated with nivolumab at Nagoya University Hospital were prospectively evaluated for pituitary hormones, thyroid function, antithyroid antibodies (Abs), and glucose levels every 6 weeks after the initiation of nivolumab for 24 weeks. Results: Four out of 66 patients developed destructive thyroiditis, and three patients developed hypothyroidism requiring levothyroxine replacement. The prevalence of positive anti-thyroglobulin Abs (TgAbs) and/or anti-thyroid peroxidase Abs (TPOAbs) at baseline was significantly higher in the group that developed destructive thyroiditis (3/4) compared with the group that did not develop thyroiditis (3/62; P = 0.002). There were no significant differences in other clinical variables between the groups. There were no endocrine irAEs other than destructive thyroiditis during the 24 weeks. The prevalence of TgAbs and/or TPOAbs at baseline was not associated with the development of other irAEs, including pneumonitis, colitis, or skin reactions. Conclusions: Our real-world data showed that destructive thyroiditis was an endocrine irAE that was frequently induced by nivolumab and was significantly associated with positive TgAbs and/or TPOAbs before treatment. Our findings indicate that evaluating these Abs before treatment may help identify patients with a high risk of thyroidal irAEs and may have important clinical benefit.

    DOI: 10.1210/js.2017-00432

    Web of Science

    PubMed

  32. Sequestosome 1 (SQSTMI/p62) maintains protein folding capacity under endoplasmic reticulum stress in mouse hypothalamic organotypic culture

    Takashi Tominaga, Motomitsu Goto, Takeshi Onoue, Akira Mizoguchi, Mariko Sugiyama, Taku Tsunekawa, Daisuke Hagiwara, Yoshiaki Morishita, Yoshihiro Ito, Shintaro Iwama, Hidetaka Suga, Ryoichi Banno, Hiroshi Arima

    NEUROSCIENCE LETTERS   Vol. 656   page: 103 - 107   2017.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ELSEVIER IRELAND LTD  

    Sequestosome 1 (SQSTM1) also known as ubiquitin-binding protein p62 (p62) is a cargo protein involved in the degradation of misfolded proteins via selective autophagy. Disruption of autophagy and resulting accumulation of misfolded proteins in the endoplasmic reticulum (ER) leads to ER stress. ER stress is implicated in several neurodegenerative diseases and obesity. As knockout of p62 (p62KO) reportedly induces obesity in mice, we examined how p62 contributes to ER stress and the ensuing unfolded protein response (UPR) in hypothalamus using mouse organotypic cultures in the present study. Cultures from p62KO mice showed significantly reduced formation of LC3-GFP puncta, an index of autophagosome formation, in response to the chemical ER stressor thapsigargin compared to wild-type (WT) cultures. Hypothalamic cultures from p62KO mice exhibited higher basal expression of the UPR/ER stress markers CHOP mRNA and ATF4 mRNA than WT cultures. Thapsigargin enhanced CHOP, ATF4, and BiP mRNA as well as p-elF2 alpha protein expression in both NWT and p62KO cultures, but all peak values were greater in p621(0 cultures. A proteasome inhibitor increased p62 expression in WT cultures and upregulated the UPR/ER stress markers CHOP mRNA and ATF4 mRNA in both genotypes, but to a greater extent in p62KO cultures. Therefore, p62 deficiency disturbed autophagosome formation and enhanced both basal and chemically induced ER stress, suggesting that p62 serves to prevent ER stress in mouse hypothalamus by maintaining protein folding capacity. (C) 2017 Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.neulet.2017.06.014

    Web of Science

    PubMed

  33. Randomized controlled trial for assessment of Internet of Things system to guide intensive glucose control in diabetes outpatients: Nagoya Health Navigator Study protocol

    Takeshi Onoue, Motomitsu Goto, Tomoko Kobayashi, Takashi Tominaga, Masahiko Ando, Hiroyuki Honda, Yasuko Yoshida, Takahiro Tosaki, Hisashi Yokoi, Sawako Kato, Shoichi Maruyama, Hiroshi Arima

    NAGOYA JOURNAL OF MEDICAL SCIENCE   Vol. 79 ( 3 ) page: 323 - 329   2017.8

     More details

    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NAGOYA UNIV, SCH MED  

    The Internet of Things (IoT) allows collecting vast amounts of health-relevant data such as daily activity, body weight (BW), and blood pressure (BP) automatically. The use of IoT devices to monitor diabetic patients has been studied, but could not evaluate IoT-dependent effects because health data were not measured in control groups. This multicenter, open-label, randomized, parallel group study will compare the impact of intensive health guidance using IoT and conventional medical guidance on glucose control. It will be conducted in outpatients with type 2 diabetes for a period of 6 months. IoT devices to measure amount of daily activity, BW, and BP will be provided to IoT group patients. Healthcare professionals (HCPs) will provide appropriate feedback according to the data. Non-IoT control, patients will be given measurement devices that do not have a feedback function. The primary outcome is glycated hemoglobin at 6 months. The study has already enrolled 101 patients, 50 in the IoT group and 51 in the non-IoT group, at the two participating outpatient clinics. The baseline characteristics of two groups did not differ, except for triglycerides. This will be the first randomized, controlled study to evaluate IoT-dependent effects of intensive feedback from HCPs. The results will validate a new method of health-data collection and provision of feedback suitable for diabetes support with increased effectiveness and low cost.

    DOI: 10.18999/nagjms.79.3.323

    Web of Science

    PubMed

  34. PTP1B deficiency improves hypothalamic insulin sensitivity resulting in the attenuation of AgRP mRNA expression under high-fat diet conditions

    Mariko Sugiyama, Ryoichi Banno, Akira Mizoguchi, Takashi Tominaga, Taku Tsunekawa, Takeshi Onoue, Daisuke Hagiwara, Yoshihiro Ito, Yoshiaki Morishita, Shintaro Iwama, Motomitsu Goto, Hidetaka Suga, Hiroshi Arima

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   Vol. 488 ( 1 ) page: 116 - 121   2017.6

     More details

    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Hypothalamic insulin receptor signaling regulates energy balance and glucose homeostasis via agouti related protein (AgRP). While protein tyrosine phosphatase 1B (PTP1B) is classically known to be a negative regulator of peripheral insulin signaling by dephosphorylating both insulin receptor beta (IR beta) and insulin receptor substrate, the role of PTP1B in hypothalamic insulin signaling remains to be fully elucidated. In the present study, we investigated the role of PTP1B in hypothalamic insulin signaling using PTP1B deficient (KO) mice in vivo and ex vivo. For the in vivo study, hypothalamic insulin resistance induced by a high-fat diet (HFD) improved in KO mice compared to wild-type (WT) mice. Hypothalamic AgRP mRNA expression levels were also significantly decreased in KO mice independent of body weight changes. In an ex vivo study using hypothalamic organotypic cultures, insulin treatment significantly increased the phosphorylation of both IR beta and Akt in the hypothalamus of KO mice compared to WT mice, and also significantly decreased AgRP mRNA expression levels in KO mice. While incubation with inhibitors of phosphatidylinositol-3 kinase (PI3K) had no effect on basal levels of Akt phosphorylation, these suppressed insulin induction of Akt phosphorylation to almost basal levels in WT and KO mice. The inhibition of the PI3K-Akt pathway blocked the downregulation of AgRP mRNA expression in KO mice treated with insulin. These data suggest that PTP1B acts on the hypothalamic insulin signaling via the PI3K-Akt pathway. Together, our results suggest a deficiency of PTP1B improves hypothalamic insulin sensitivity resulting in the attenuation of AgRP mRNA expression under HFD conditions. (C) 2017 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2017.05.019

    Web of Science

    PubMed

  35. Deficiency of PTP1B Attenuates Hypothalamic Inflammation via Activation of the JAK2-STAT3 Pathway in Microglia

    Taku Tsunekawa, Ryoichi Banno, Akira Mizoguchi, Mariko Sugiyama, Takashi Tominaga, Takeshi Onoue, Daisuke Hagiwara, Yoshihiro Ito, Shintaro Iwama, Motomitsu Goto, Hidetaka Suga, Yoshihisa Sugimura, Hiroshi Arima

    EBIOMEDICINE   Vol. 16   page: 172 - 183   2017.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ELSEVIER SCIENCE BV  

    Protein tyrosine phosphatase 1B (PTP1B) regulates leptin signaling in hypothalamic neurons via the JAK2-STAT3 pathway. PTP1B has also been implicated in the regulation of inflammation in the periphery. However, the role of PTP1B in hypothalamic inflammation, which is induced by a high-fat diet (HFD), remains to be elucidated. Here, we showed that STAT3 phosphorylation (p-STAT3) was increased in microglia in the hypothalamic arcuate nucleus of PTP1B knock-out mice (KO) on a HFD, accompanied by decreased Tnf and increased Il10 mRNA expression in the hypothalamus compared to wild-type mice (WT). In hypothalamic organotypic cultures, incubation with TNF alpha led to increased p-STAT3, accompanied by decreased Tnf and increased Il10 mRNA expression, in KO compared to WT. Incubation with p-STAT3 inhibitors or microglial depletion eliminated the differences in inflammation between genotypes. These data indicate an important role of JAK2-STAT3 signaling negatively regulated by PTP1B in microglia, which attenuates hypothalamic inflammation under HFD conditions. (C) 2017 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

    DOI: 10.1016/j.ebiom.2017.01.007

    Web of Science

    PubMed

  36. Reactive oxygen species mediate insulin signal transduction in mouse hypothalamus

    Takeshi Onoue, Motomitsu Goto, Takashi Tominaga, Mariko Sugiyama, Taku Tsunekawa, Daisuke Hagiwara, Ryoichi Banno, Hidetaka Suga, Yoshihisa Sugimura, Hiroshi Arima

    NEUROSCIENCE LETTERS   Vol. 619   page: 1 - 7   2016.4

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:ELSEVIER IRELAND LTD  

    In the hypothalamus, several reports have implied that ROS mediate physiological effects of insulin. In this study, we investigated the mechanisms of insulin-induced ROS production and the effect of ROS on insulin signal transduction in mouse hypothalamic organotypic cultures. Insulin increased intracellular ROS, which were suppressed by NADPH oxidase inhibitor. H2O2 increased phospho-insulin receptor beta (p-IR beta) and phospho-Akt (p-Akt) levels. Insulin-induced increases in p-IR beta and p-Akt levels were attenuated by ROS scavenger or NADPH oxidase inhibitor. Our data suggest that insulin-induced phosphorylation of IR beta and Akt is mediated via ROS which are predominantly produced by NADPH oxidase in mouse hypothalamus. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/j.neulet.2016.03.011

    Web of Science

    PubMed

  37. AgRP Neuron-Specific Deletion of Glucocorticoid Receptor Leads to Increased Energy Expenditure and Decreased Body Weight in Female Mice on a High-Fat

    Miyuki Shibata, Ryoichi Banno, Mariko Sugiyama, Takashi Tominaga, Takeshi Onoue, Taku Tsunekawa, Yoshinori Azuma, Daisuke Hagiwara, Wenjun Lu, Yoshihiro Ito, Motomitsu Goto, Hidetaka Suga, Yoshihisa Sugimura, Yutaka Oiso, Hiroshi Arima

    ENDOCRINOLOGY   Vol. 157 ( 4 ) page: 1457 - 1466   2016.4

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:OXFORD UNIV PRESS INC  

    Agouti-related protein (AgRP) expressed in the arcuate nucleus is a potent orexigenic neuropeptide, which increases food intake and reduces energy expenditure resulting in increases in body weight (BW). Glucocorticoids, key hormones that regulate energy balance, have been shown in rodents to regulate the expression of AgRP. In this study, we generated AgRP-specific glucocorticoid receptor (GR)-deficient (knockout [KO]) mice. Female and male KO mice on a high-fat diet (HFD) showed decreases in BW at the age of 6 weeks compared with wild-type mice, and the differences remained significant until 16 weeks old. The degree of resistance to diet-induced obesity was more robust in female than in male mice. On a chow diet, the female KO mice showed slightly but significantly attenuated weight gain compared with wild-type mice after 11 weeks, whereas there were no significant differences in BW in males between genotypes. Visceral fat pad mass was significantly decreased in female KO mice on HFD, whereas there were no significant differences in lean body mass between genotypes. Although food intake was similar between genotypes, oxygen consumption was significantly increased in female KO mice on HFD. In addition, the uncoupling protein-1 expression in the brown adipose tissues was increased in KO mice. These data demonstrate that the absence of GR signaling in AgRP neurons resulted in increases in energy expenditure accompanied by decreases in adiposity in mice fed HFD, indicating that GR signaling in AgRP neurons suppresses energy expenditure under HFD conditions.

    DOI: 10.1210/en.2015-1430

    Web of Science

    PubMed

  38. Agrp Neuron-Specific Deletion of Glucocorticoid Receptor Leads to Decreased Body Weight and Adiposity in Mice

    Shibata Miyuki, Banno Ryoichi, Onoue Takeshi, Tsunekawa Taku, Adachi Koichi, Ito Yoshihiro, Goto Motomitsu, Arima Hiroshi, Oiso Yutaka

    ENDOCRINE REVIEWS   Vol. 35 ( 3 ) page: .   2014.6

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

    Web of Science

  39. Insulin-Induced Phosphorylation of Akt Is Mediated Via NADPH Oxidase-Derived Reactive Oxygen Species in the Mouse Hypothalamic Organotypic Cultures

    Onoue Takeshi, Goto Motomitsu, Tsunekawa Taku, Shibata Miyuki, Adachi Koichi, Ito Yoshihiro, Bonno Ryoichi, Arima Hiroshi, Oiso Yutaka

    ENDOCRINE REVIEWS   Vol. 35 ( 3 ) page: .   2014.6

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

    Web of Science

  40. MAPK Signaling Is Inhibited By Mitogen-Activated Protein Kinase Phosphatase 1 in Mouse Hypothalamus

    Adachi Koichi, Goto Motomitsu, Onoue Takeshi, Tsunekawa Taku, Shibata Miyuki, Hagimoto Shigeru, Ito Yoshihiro, Banno Ryoichi, Suga Hidetaka, Sugimura Yoshihisa, Arima Hiroshi, Oiso Yutaka

    ENDOCRINE REVIEWS   Vol. 35 ( 3 ) page: .   2014.6

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

    Web of Science

  41. Mitogen-activated protein kinase phosphatase 1 negatively regulates MAPK signaling in mouse hypothalamus

    Koichi Adachi, Motomitsu Goto, Takeshi Onoue, Taku Tsunekawa, Miyuki Shibata, Shigeru Hagimoto, Yoshihiro Ito, Ryoichi Banno, Hidetaka Suga, Yoshihisa Sugimura, Yutaka Oiso, Hiroshi Arima

    NEUROSCIENCE LETTERS   Vol. 569   page: 49 - 54   2014.5

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:ELSEVIER IRELAND LTD  

    Mitogen-activated protein kinase phosphatase 1 (MKP-1) is shown to negatively regulate MAPK signaling in various peripheral tissues as well as the central nervous system such as cortex, striatum and hippocampus. In this study, we examined whether MKP-1 regulates MAPK signaling in the mouse hypothalamus. Intraperitoneal injection of TNF alpha significantly increased MKP-1 mRNA expression in paraventricular and arcuate nuclei in the hypothalamus. TNF alpha treatment induced increases in MKP-1 expression at both mRNA and protein levels, accompanied by the inactivation of MAPK signaling in mouse hypothalamic explants. Inhibition of MKP-1 by its inhibitor or siRNA increased MAPK activity in the explants. Our data indicate that MKP-1 negatively regulates MAPK signaling in the mouse hypothalamus. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/j.neulet.2014.03.032

    Web of Science

    PubMed

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Books 4

  1. インスリンを使用していない2型糖尿病患者におけるflash glucose monitoring(FGM)による血糖コントロール

    ( Role: Joint author)

    Calm 8(1), 先端医学社  2021.1 

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    Responsible for pages:15-19  

  2. 高齢社会における人と自動車

    ( Role: Joint author)

    コロナ社  2021.1 

  3. 甲状腺クリーゼー妙に意識が悪い 心房細動と思ったら……

    近藤猛、尾上剛史( Role: Joint author)

    救急外来、ここだけの話、医学書院  2021 

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    Responsible for pages:201-208   Language:Japanese Book type:Scholarly book

  4. 肥満症に対する内科的治療

    尾上剛史、有馬寛( Role: Joint author)

    臨床外科、医学書院  2021 

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    Responsible for pages:412-416   Language:Japanese Book type:Scholarly book

MISC 6

  1. Chemical chaperone 4-phenylbutylate reduces mutant protein accumulation in the endoplasmic reticulum of arginine vasopressin neurons in a mouse model for familial neurohypophysial diabetes insipidus

    Masayoshi Tochiya, Daisuke Hagiwara, Yoshinori Azuma, Takashi Miyata, Yoshiaki Morishita, Hidetaka Suga, Takeshi Onoue, Taku Tsunekawa, Hiroshi Takagi, Yoshihiro Ito, Shintaro Iwama, Motomitsu Goto, Ryoichi Banno, Hiroshi Arima

    Neuroscience Letters   Vol. 682   page: 50 - 55   2018.8

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    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)   Publisher:Elsevier Ireland Ltd  

    Familial neurohypophysial diabetes insipidus (FNDI), characterized by progressive polyuria and loss of arginine vasopressin (AVP) neurons, is an autosomal dominant disorder caused by AVP gene mutations. Our previous studies with FNDI model mice demonstrated that mutant proteins accumulated in the endoplasmic reticulum (ER) of AVP neurons. Here, we examined therapeutic effects of the chemical chaperone 4-phenylbutylate (4-PBA) in FNDI mice. Treatment with 4-PBA reduced mutant protein accumulation in the ER of FNDI mice and increased AVP release, leading to reduced urine volumes. Furthermore, AVP neuron loss under salt loading was attenuated by 4-PBA treatment. These data suggest that 4-PBA ameliorated mutant protein accumulation in the ER of AVP neurons and thereby prevented FNDI phenotype progression.

    DOI: 10.1016/j.neulet.2018.06.013

    Scopus

    PubMed

  2. Patients With Antithyroid Antibodies Are Prone To Develop Destructive Thyroiditis by Nivolumab: A Prospective Study International journal

    Kobayashi Tomoko, Iwama Shintaro, Yasuda Yoshinori, Okada Norio, Tsunekawa Taku, Onoue Takeshi, Takagi Hiroshi, Hagiwara Daisuke, Ito Yoshihiro, Morishita Yoshiaki, Goto Motomitsu, Suga Hidetaka, Banno Ryoichi, Yokota Kenji, Hase Tetsunari, Morise Masahiro, Hashimoto Naozumi, Ando Masahiko, Kiyoi Hitoshi, Gotoh Momokazu, Ando Yuichi, Akiyama Masashi, Hasegawa Yoshinori, Arima Hiroshi

    JOURNAL OF THE ENDOCRINE SOCIETY   Vol. 2 ( 3 ) page: 241-251 - 251   2018.3

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    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)  

    Context: Immune checkpoint inhibitors, including anti-programmed cell death-1 (PD-1) antibodies, have become promising treatments for a variety of advanced malignancies. However, these medicines can cause immune-related adverse events (irAEs), including endocrinopathies. Objective: This study examined the incidence of endocrine irAEs induced by nivolumab. Patients and Main Outcome Measured: Sixty-six patients treated with nivolumab at Nagoya University Hospital were prospectively evaluated for pituitary hormones, thyroid function, antithyroid antibodies (Abs), and glucose levels every 6 weeks after the initiation of nivolumab for 24 weeks. Results: Four out of 66 patients developed destructive thyroiditis, and three patients developed hypothyroidism requiring levothyroxine replacement. The prevalence of positive anti-thyroglobulin Abs (TgAbs) and/or anti-thyroid peroxidase Abs (TPOAbs) at baseline was significantly higher in the group that developed destructive thyroiditis (3/4) compared with the group that did not develop thyroiditis (3/62; P = 0.002). There were no significant differences in other clinical variables between the groups. There were no endocrine irAEs other than destructive thyroiditis during the 24 weeks. The prevalence of TgAbs and/or TPOAbs at baseline was not associated with the development of other irAEs, including pneumonitis, colitis, or skin reactions. Conclusions: Our real-world data showed that destructive thyroiditis was an endocrine irAE that was frequently induced by nivolumab and was significantly associated with positive TgAbs and/or TPOAbs before treatment. Our findings indicate that evaluating these Abs before treatment may help identify patients with a high risk of thyroidal irAEs and may have important clinical benefit.

    DOI: 10.1210/js.2017-00432

    PubMed

  3. Sequestosome 1 (SQSTMI/p62) maintains protein folding capacity under endoplasmic reticulum stress in mouse hypothalamic organotypic culture

    Takashi Tominaga, Motomitsu Goto, Takeshi Onoue, Akira Mizoguchi, Mariko Sugiyama, Taku Tsunekawa, Daisuke Hagiwara, Yoshiaki Morishita, Yoshihiro Ito, Shintaro Iwama, Hidetaka Suga, Ryoichi Banno, Hiroshi Arima

    NEUROSCIENCE LETTERS   Vol. 656   page: 103 - 107   2017.8

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    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)   Publisher:ELSEVIER IRELAND LTD  

    Sequestosome 1 (SQSTM1) also known as ubiquitin-binding protein p62 (p62) is a cargo protein involved in the degradation of misfolded proteins via selective autophagy. Disruption of autophagy and resulting accumulation of misfolded proteins in the endoplasmic reticulum (ER) leads to ER stress. ER stress is implicated in several neurodegenerative diseases and obesity. As knockout of p62 (p62KO) reportedly induces obesity in mice, we examined how p62 contributes to ER stress and the ensuing unfolded protein response (UPR) in hypothalamus using mouse organotypic cultures in the present study. Cultures from p62KO mice showed significantly reduced formation of LC3-GFP puncta, an index of autophagosome formation, in response to the chemical ER stressor thapsigargin compared to wild-type (WT) cultures. Hypothalamic cultures from p62KO mice exhibited higher basal expression of the UPR/ER stress markers CHOP mRNA and ATF4 mRNA than WT cultures. Thapsigargin enhanced CHOP, ATF4, and BiP mRNA as well as p-elF2 alpha protein expression in both NWT and p62KO cultures, but all peak values were greater in p621(0 cultures. A proteasome inhibitor increased p62 expression in WT cultures and upregulated the UPR/ER stress markers CHOP mRNA and ATF4 mRNA in both genotypes, but to a greater extent in p62KO cultures. Therefore, p62 deficiency disturbed autophagosome formation and enhanced both basal and chemically induced ER stress, suggesting that p62 serves to prevent ER stress in mouse hypothalamus by maintaining protein folding capacity. (C) 2017 Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.neulet.2017.06.014

    Web of Science

    PubMed

  4. Randomized controlled trial for assessment of Internet of Things system to guide intensive glucose control in diabetes outpatients: Nagoya Health Navigator Study protocol

    Takeshi Onoue, Motomitsu Goto, Tomoko Kobayashi, Takashi Tominaga, Masahiko Ando, Hiroyuki Honda, Yasuko Yoshida, Takahiro Tosaki, Hisashi Yokoi, Sawako Kato, Shoichi Maruyama, Hiroshi Arima

    NAGOYA JOURNAL OF MEDICAL SCIENCE   Vol. 79 ( 3 ) page: 323 - 329   2017.8

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    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)   Publisher:NAGOYA UNIV, SCH MED  

    The Internet of Things (IoT) allows collecting vast amounts of health-relevant data such as daily activity, body weight (BW), and blood pressure (BP) automatically. The use of IoT devices to monitor diabetic patients has been studied, but could not evaluate IoT-dependent effects because health data were not measured in control groups. This multicenter, open-label, randomized, parallel group study will compare the impact of intensive health guidance using IoT and conventional medical guidance on glucose control. It will be conducted in outpatients with type 2 diabetes for a period of 6 months. IoT devices to measure amount of daily activity, BW, and BP will be provided to IoT group patients. Healthcare professionals (HCPs) will provide appropriate feedback according to the data. Non-IoT control, patients will be given measurement devices that do not have a feedback function. The primary outcome is glycated hemoglobin at 6 months. The study has already enrolled 101 patients, 50 in the IoT group and 51 in the non-IoT group, at the two participating outpatient clinics. The baseline characteristics of two groups did not differ, except for triglycerides. This will be the first randomized, controlled study to evaluate IoT-dependent effects of intensive feedback from HCPs. The results will validate a new method of health-data collection and provision of feedback suitable for diabetes support with increased effectiveness and low cost.

    DOI: 10.18999/nagjms.79.3.323

    Web of Science

    PubMed

  5. PTP1B deficiency improves hypothalamic insulin sensitivity resulting in the attenuation of AgRP mRNA expression under high-fat diet conditions

    Mariko Sugiyama, Ryoichi Banno, Akira Mizoguchi, Takashi Tominaga, Taku Tsunekawa, Takeshi Onoue, Daisuke Hagiwara, Yoshihiro Ito, Yoshiaki Morishita, Shintaro Iwama, Motomitsu Goto, Hidetaka Suga, Hiroshi Arima

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   Vol. 488 ( 1 ) page: 116 - 121   2017.6

     More details

    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)   Publisher:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Hypothalamic insulin receptor signaling regulates energy balance and glucose homeostasis via agouti related protein (AgRP). While protein tyrosine phosphatase 1B (PTP1B) is classically known to be a negative regulator of peripheral insulin signaling by dephosphorylating both insulin receptor beta (IR beta) and insulin receptor substrate, the role of PTP1B in hypothalamic insulin signaling remains to be fully elucidated. In the present study, we investigated the role of PTP1B in hypothalamic insulin signaling using PTP1B deficient (KO) mice in vivo and ex vivo. For the in vivo study, hypothalamic insulin resistance induced by a high-fat diet (HFD) improved in KO mice compared to wild-type (WT) mice. Hypothalamic AgRP mRNA expression levels were also significantly decreased in KO mice independent of body weight changes. In an ex vivo study using hypothalamic organotypic cultures, insulin treatment significantly increased the phosphorylation of both IR beta and Akt in the hypothalamus of KO mice compared to WT mice, and also significantly decreased AgRP mRNA expression levels in KO mice. While incubation with inhibitors of phosphatidylinositol-3 kinase (PI3K) had no effect on basal levels of Akt phosphorylation, these suppressed insulin induction of Akt phosphorylation to almost basal levels in WT and KO mice. The inhibition of the PI3K-Akt pathway blocked the downregulation of AgRP mRNA expression in KO mice treated with insulin. These data suggest that PTP1B acts on the hypothalamic insulin signaling via the PI3K-Akt pathway. Together, our results suggest a deficiency of PTP1B improves hypothalamic insulin sensitivity resulting in the attenuation of AgRP mRNA expression under HFD conditions. (C) 2017 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2017.05.019

    Web of Science

    PubMed

  6. Deficiency of PTP1B Attenuates Hypothalamic Inflammation via Activation of the JAK2-STAT3 Pathway in Microglia

    Taku Tsunekawa, Ryoichi Banno, Akira Mizoguchi, Mariko Sugiyama, Takashi Tominaga, Takeshi Onoue, Daisuke Hagiwara, Yoshihiro Ito, Shintaro Iwama, Motomitsu Goto, Hidetaka Suga, Yoshihisa Sugimura, Hiroshi Arima

    EBIOMEDICINE   Vol. 16   page: 172 - 183   2017.2

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    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)   Publisher:ELSEVIER SCIENCE BV  

    Protein tyrosine phosphatase 1B (PTP1B) regulates leptin signaling in hypothalamic neurons via the JAK2-STAT3 pathway. PTP1B has also been implicated in the regulation of inflammation in the periphery. However, the role of PTP1B in hypothalamic inflammation, which is induced by a high-fat diet (HFD), remains to be elucidated. Here, we showed that STAT3 phosphorylation (p-STAT3) was increased in microglia in the hypothalamic arcuate nucleus of PTP1B knock-out mice (KO) on a HFD, accompanied by decreased Tnf and increased Il10 mRNA expression in the hypothalamus compared to wild-type mice (WT). In hypothalamic organotypic cultures, incubation with TNF alpha led to increased p-STAT3, accompanied by decreased Tnf and increased Il10 mRNA expression, in KO compared to WT. Incubation with p-STAT3 inhibitors or microglial depletion eliminated the differences in inflammation between genotypes. These data indicate an important role of JAK2-STAT3 signaling negatively regulated by PTP1B in microglia, which attenuates hypothalamic inflammation under HFD conditions. (C) 2017 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

    DOI: 10.1016/j.ebiom.2017.01.007

    Web of Science

    PubMed

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Presentations 10

  1. 原発性アルドステロン症術後に重度高カリウム血症を生じた1例

    浜田 雄大,尾上 剛史, 津村 哲郎, 有馬 寛

    第246回日本内科学会東海地方会  2022.2.20 

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    Event date: 2022.2

    Language:Japanese   Presentation type:Oral presentation (general)  

  2. IoTを活用した糖尿病生活習慣改善支援~七福神アプリ~ Invited

    第41回日本肥満学会 

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    Event date: 2021.3

  3. 安静時代謝の変動に対する摂取エネルギー/消費エネルギー比の影響の検討

    第41回日本肥満学会 

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    Event date: 2021.3

  4. 低血糖~予防可能な代謝障害~に起因する運転リスクとその対策 Invited

    第56回日本交通科学学会総 

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    Event date: 2020.11

  5. 入院患者の血糖管理 Invited

    第21回日本病院総合診療医学会学術総会 

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    Event date: 2020.9

  6. IoTを用いた生活習慣病へのアプローチ Invited

    尾上剛史 津下一代 有馬寛

    第40回 日本肥満学会 

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    Event date: 2019.11

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Country:Japan  

  7. Randomized controlled trial to evaluate the effects of anaglipitin, a DPP-4 inhibitor, on blood lipids in type 2 diabetic patients International conference

    Takeshi Onoue, Mariko Furukawa, Eri Wada, Norio Okada, Tomoko Kobayashi, Shintaro Iwama, Motomitsu Goto, Masahiko Ando, Hiroshi Arima

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    Event date: 2019.3

    Language:English   Presentation type:Poster presentation  

    Country:United States  

  8. Randomized controlled trial for assessment of Internet of Things system to guide intensive glucose control in diabetes outpatients: Nagoya Health Navigator Study International conference

    第100回米国内分泌学会 

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    Event date: 2018.3

    Language:English   Presentation type:Poster presentation  

    Country:United States  

  9. IoT(Internet of things)システムを用いた療養指導強化による糖代謝改善についての検討-クリニック通院患者を対象とした前向き研究-

    尾上剛史 他.

    第60回日本糖尿病学会年次学術集会 

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    Event date: 2017.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  10. NADPH oxidase-derived reactive oxygen species (ROS) enhance insulin signaling in mouse hypothalamus International conference

    第96回米国内分泌学会 

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    Event date: 2014.6

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

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Research Project for Joint Research, Competitive Funding, etc. 4

  1. 低血糖時アラート機能は糖尿病治療患者の運転中低血糖を予防できるか

    2021.9 - 2022.9

    交通事故医療・一般研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\800000 ( Direct Cost: \718000 、 Indirect Cost:\82000 )

  2. 「基礎代謝の変動を考慮した減量のための摂取カロリーの設定方法」を用いた減量プログラムの有効性に関する研究

    2020.12 - 2021.11

    医学研究・健康増進活動等助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\500000 ( Direct Cost: \500000 )

  3. 診療録直結型大規模糖尿病レジストリを用いた糖尿病合併症抑制のための治療法に関するエビデンス創出のための研究

    2020.8

    循環器疾患・糖尿病等生活習慣病対策実用化研究事業 

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    Grant amount:\5239520 ( Direct Cost: \4030400 、 Indirect Cost:\1209120 )

  4. 壮年期就労者を対象とした生活習慣病予防のための動機付け支援の技術開発に関する研究

    2019.4

    循環器疾患・糖尿病等生活習慣病対策実用化研究事業 

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    Grant amount:\2070900 ( Direct Cost: \1593000 、 Indirect Cost:\477900 )

KAKENHI (Grants-in-Aid for Scientific Research) 1

  1. 持続血糖測定機会提供と学習支援を併用した糖尿病患者への新しい体験型学習方法の開発

    Grant number:21K17659  2021.4 - 2024.3

    科学研究費助成事業  若手研究

    尾上 剛史

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    Authorship:Principal investigator 

    Grant amount:\3900000 ( Direct Cost: \3000000 、 Indirect Cost:\900000 )

    本研究では、持続血糖測定による体験型学習の効果を最大化できる糖尿病患者向け学習支援方法の開発を目指す。既存の持続血糖測定器を用いた介入研究データを分析し、対象者の特性による効果の違いや効果的な介入期間を検証した上で、併用する学習支援内容の検討を行い、最終的な体験型学習の効果を検証する。本研究の結果、持続血糖測定の学習効果(食事療法・運動療法の強化)が臨床応用されるとともに、体験型学習が糖尿病の新しい患者教育手段として開発されることが期待される。

 

Teaching Experience (On-campus) 14

  1. 臓器別講義 糖尿病・内分泌

    2021

  2. 選択特別講義(生活習慣病)

    2021

  3. 現代医療と生命科学

    2021

  4. 臨床実習II 糖尿病・内分泌内科

    2021

  5. 臨床実習 糖尿病・内分泌内科

    2021

  6. 現代医療と生命科学

    2020

  7. 臨床実習II 糖尿病・内分泌内科

    2020

  8. 臨床実習 糖尿病・内分泌内科

    2020

  9. 選択特別講義(生活習慣病)

    2020

  10. 選択特別講義(生活習慣病)

    2019

  11. 臨床実習II 糖尿病・内分泌内科

    2019

  12. 臨床実習 糖尿病・内分泌内科

    2019

  13. PBL

    2019

  14. PBL

    2018

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Social Contribution 3

  1. 世界糖尿病デー市民公開講座

    Role(s):Lecturer, Planner

    2021

  2. 世界糖尿病デー市民公開講座

    Role(s):Lecturer, Planner

    2020

  3. 世界糖尿病デー市民公開講座

    Role(s):Lecturer, Planner

    2019.11