Updated on 2023/09/08


Research Institute of Environmental Medicine Designated assistant professor
Designated assistant professor

Degree 1

  1. 博士(医学) ( 2021.3   群馬大学 ) 

Research Areas 2

  1. Life Science / Nutrition science and health science

  2. Life Science / Metabolism and endocrinology

Awards 6

  1. 第43回日本肥満学会/第40回日本肥満症治療学会学術集会 JASSO/JSTO in OKINAWA 会長表彰


  2. 第95回 日本生化学会 若手優秀発表賞


  3. 第11回若手研究奨励賞 日本糖尿病学会

    2021.5   日本糖尿病学会  

  4. JSAAS Award 2020 for Outstanding Young Investigator

    2020.11   Japanese Society for Amino Acid Sciences  

  5. ホープ賞


  6. 若手研究会長賞

    2020.1   Japan Society of Metabolism and Clinical Nutrition  

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Papers 5

  1. Protein Kinase C (Pkc)-δ Mediates Arginine-Induced Glucagon Secretion in Pancreatic α-Cells Reviewed International journal

    Norikiyo Honzawa, Kei Fujimoto, Masaki Kobayashi, Daisuke Kohno, Osamu Kikuchi, Hiromi Yokota-Hashimoto, Eri Wada, Yuichi Ikeuchi, Yoko Tabei, Gerald W. Dorn, Kazunori Utsunomiya, Rimei Nishimura, Tadahiro Kitamura

    International Journal of Molecular Sciences   Vol. 23 ( 7 ) page: 4003 - 4003   2022.4

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:MDPI AG  

    The pathophysiology of type 2 diabetes involves insulin and glucagon. Protein kinase C (Pkc)-δ, a serine–threonine kinase, is ubiquitously expressed and involved in regulating cell death and proliferation. However, the role of Pkcδ in regulating glucagon secretion in pancreatic α-cells remains unclear. Therefore, this study aimed to elucidate the physiological role of Pkcδ in glucagon secretion from pancreatic α-cells. Glucagon secretions were investigated in Pkcδ-knockdown InR1G9 cells and pancreatic α-cell-specific Pkcδ-knockout (αPkcδKO) mice. Knockdown of Pkcδ in the glucagon-secreting cell line InR1G9 cells reduced glucagon secretion. The basic amino acid arginine enhances glucagon secretion via voltage-dependent calcium channels (VDCC). Furthermore, we showed that arginine increased Pkcδ phosphorylation at Thr505, which is critical for Pkcδ activation. Interestingly, the knockdown of Pkcδ in InR1G9 cells reduced arginine-induced glucagon secretion. Moreover, arginine-induced glucagon secretions were decreased in αPkcδKO mice and islets from αPkcδKO mice. Pkcδ is essential for arginine-induced glucagon secretion in pancreatic α-cells. Therefore, this study may contribute to the elucidation of the molecular mechanism of amino acid-induced glucagon secretion and the development of novel antidiabetic drugs targeting Pkcδ and glucagon.

    DOI: 10.3390/ijms23074003

    Web of Science



  2. Disordered branched chain amino acid catabolism in pancreatic islets is associated with postprandial hypersecretion of glucagon in diabetic mice.

    Wada E, Kobayashi M, Kohno D, Kikuchi O, Suga T, Matsui S, Yokota-Hashimoto H, Honzawa N, Ikeuchi Y, Tsuneoka H, Hirano T, Obinata H, Sasaki T, Kitamura T

    The Journal of nutritional biochemistry   Vol. 97   page: 108811   2021.11

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    DOI: 10.1016/j.jnutbio.2021.108811


  3. 糖尿病病態において分岐鎖アミノ酸の摂取が高グルカゴン血症を惹起する機序の解明

    和田 恵梨

    アミノ酸研究 = Amino acid research   Vol. 15 ( 1 ) page: 7 - 14   2021

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    CiNii Research

  4. Higher estimated net endogenous acid production with lower intake of fruits and vegetables based on a dietary survey is associated with the progression of chronic kidney disease. International journal

    Koji Toba, Michihiro Hosojima, Hideyuki Kabasawa, Shoji Kuwahara, Toshiko Murayama, Keiko Yamamoto-Kabasawa, Ryohei Kaseda, Eri Wada, Reiko Watanabe, Naohito Tanabe, Yoshiki Suzuki, Ichiei Narita, Akihiko Saito

    BMC nephrology   Vol. 20 ( 1 ) page: 421 - 421   2019.11

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

    BACKGROUND: Dietary acid load has been suggested to mediate the progression of chronic kidney disease (CKD). However, it is unclear what kinds of foods are actually associated with dietary acid load in patients with CKD. The self-administered diet history questionnaire (DHQ), which semi-quantitatively assesses the dietary habits of Japanese individuals through 150 question items, can estimate average daily intake of various foods and nutrients during the previous month. Using the DHQ, we investigated the association of dietary acid load with CKD progression. We also analyzed the kinds of food that significantly affect dietary acid load. METHODS: Subjects were 96 outpatients with CKD (average estimated glomerular filtration rate [eGFR], 53.0 ± 18.1 ml/min/1.73 m2) at Niigata University Hospital, who had completed the DHQ in 2011. We calculated net endogenous acid production (NEAP) from potassium and protein intake evaluated by the DHQ in order to assess dietary acid load. CKD progression was assessed by comparing eGFR between 2008 and 2014. RESULTS: NEAP was not correlated with protein intake (r = 0.088, p = 0.398), but was negatively correlated with potassium intake (r = - 0.748, p < 0.001). Reduction in eGFR from 2008 to 2014 was estimated to be significantly greater in patients with higher NEAP (NEAP > 50.1 mEq/day, n = 45) than in those with lower NEAP (NEAP ≤50.1 mEq/day, n = 50) by 5.9 (95% confidence interval [95%CI], 0.1 to 11.6) ml/min/1.73 m2. According to multiple logistic regression analysis, higher NEAP was significantly associated with lower intake of fruits (odds ratio [OR], 6.454; 95%CI, 2.19 to 19.00), green and yellow vegetables (OR, 5.18; 95%CI, 1.83 to14.66), and other vegetables (OR, 3.87; 95%CI, 1.29 to 11.62). CONCLUSIONS: Elevated NEAP could be a risk factor for CKD progression. Low intake of fruits and vegetables would increase dietary acid load and might affect the progression of renal dysfunction in Japanese CKD patients.

    DOI: 10.1186/s12882-019-1591-8

    Web of Science



  5. SGLT1 in pancreatic α cells regulates glucagon secretion in mice, possibly explaining the distinct effects of SGLT2 inhibitors on plasma glucagon levels. International journal

    Takayoshi Suga, Osamu Kikuchi, Masaki Kobayashi, Sho Matsui, Hiromi Yokota-Hashimoto, Eri Wada, Daisuke Kohno, Tsutomu Sasaki, Kazusane Takeuchi, Satoru Kakizaki, Masanobu Yamada, Tadahiro Kitamura

    Molecular metabolism   Vol. 19   page: 1 - 12   2019.1

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

    OBJECTIVES: It is controversial whether sodium glucose transporter (SGLT) 2 inhibitors increase glucagon secretion via direct inhibition of SGLT2 in pancreatic α cells. The role of SGLT1 in α cells is also unclear. We aimed to elucidate these points that are important not only for basic research but also for clinical insight. METHODS: Plasma glucagon levels were assessed in the high-fat, high-sucrose diet (HFHSD) fed C57BL/6J mice treated with dapagliflozin or canagliflozin. RT-PCR, RNA sequence, and immunohistochemistry were conducted to test the expression of SGLT1 and SGLT2 in α cells. We also used αTC1 cells and mouse islets to investigate the molecular mechanism by which SGLT1 modulates glucagon secretion. RESULTS: Dapagliflozin, but not canagliflozin, increased plasma glucagon levels in HFHSD fed mice. SGLT1 and glucose transporter 1 (GLUT1), but not SGLT2, were expressed in αTC1 cells, mouse islets and human islets. A glucose clamp study revealed that the plasma glucagon increase associated with dapagliflozin could be explained as a response to acute declines in blood glucose. Canagliflozin suppressed glucagon secretion by inhibiting SGLT1 in α cells; consequently, plasma glucagon did not increase with canagliflozin, even though blood glucose declined. SGLT1 effect on glucagon secretion depended on glucose transport, but not glucose metabolism. Islets from HFHSD and db/db mice displayed higher SGLT1 mRNA levels and lower GLUT1 mRNA levels than the islets from control mice. These expression levels were associated with higher glucagon secretion. Furthermore, SGLT1 inhibitor and siRNA against SGLT1 suppressed glucagon secretion in isolated islets. CONCLUSIONS: These data suggested that a novel mechanism regulated glucagon secretion through SGLT1 in α cells. This finding possibly explained the distinct effects of dapagliflozin and canagliflozin on plasma glucagon levels in mice.

    DOI: 10.1016/j.molmet.2018.10.009

    Web of Science




  1. 【栄養・代謝物シグナルと食品機能 転写、エピゲノムの制御から代謝性疾患の治療・予防に向けて】(第3章)栄養・代謝物シグナル修飾および破綻と疾患 糖尿病病態における高グルカゴン血症と分岐鎖アミノ酸の関連

    和田 恵梨, 北村 忠弘

    実験医学   Vol. 40 ( 7 ) page: 1168 - 1174   2022.5

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    Language:Japanese   Publisher:(株)羊土社  


  2. 栄養と感覚(嗅覚/味覚を中心とした)の新しい融合研究領域 グルカゴンによるアミノ酸・糖代謝調節と糖尿病・肥満

    北村 忠弘, 和田 恵梨, 小林 雅樹

    日本栄養・食糧学会大会講演要旨集   Vol. 73回   page: 156 - 156   2019.4

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    Language:Japanese   Publisher:(公社)日本栄養・食糧学会  

  3. グルカゴンは糖代謝よりもアミノ酸代謝に重要? 糖尿病・肥満に対する治療標的の可能性も含めて

    北村 忠弘, 和田 恵梨, 小林 雅樹

    アミノ酸研究   Vol. 12 ( 2 ) page: 81 - 87   2019.3

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    Language:Japanese   Publisher:日本アミノ酸学会  

KAKENHI (Grants-in-Aid for Scientific Research) 2

  1. Effect of Weight-Cycling on adipose tissue inflammation; A novel mechanism of inflammation regulation by BCAA catabolism

    Grant number:23K16815  2023.4 - 2025.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

  2. 糖尿病における分岐鎖アミノ酸代謝とグルカゴン分泌の関連の解明

    Grant number:21K21213  2021.8 - 2023.3

    科学研究費助成事業  研究活動スタート支援

    和田 恵梨

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    Authorship:Principal investigator 

    Grant amount:\3120000 ( Direct Cost: \2400000 、 Indirect Cost:\720000 )