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Online Letters to the Editor

Response to Comment on: Takeda et al. Loss of ACE2 Exaggerates High-Calorie Diet–Induced Insulin Resistance by Reduction of GLUT4 in Mice. Diabetes 2013;62:223–233

  1. Koichi Yamamoto,
  2. Masao Takeda,
  3. Mitsuru Ohishi and
  4. Hiromi Rakugi
  1. Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Osaka, Japan
  1. Corresponding author: Mitsuru Ohishi, ohishi{at}geriat.med.osaka-u.ac.jp.
Diabetes 2013 Jul; 62(7): e10-e10. https://doi.org/10.2337/db13-0505
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We thank Dr. Chhabra and Dr. Lazartigues for their thoughtful comments on the role of ACE type 2 (ACE2) in glycemic control (1). In db/db mice or in C57Bl/6J mice infused with angiotensin II, their group has shown that ACE2 can help protect against hyperglycemia by promoting pancreatic insulin secretion (2,3). We found that deficiency of ACE2 causes impaired insulin sensitivity of mice treated with angiotensin II infusion or a high-calorie diet (4). Thus, ACE2 appears to play a multifunctional role in maintaining glucose homeostasis by regulating both insulin secretion and insulin sensitivity.

The counterregulating …

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Diabetes: 62 (7)

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July 2013, 62(7)
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Response to Comment on: Takeda et al. Loss of ACE2 Exaggerates High-Calorie Diet–Induced Insulin Resistance by Reduction of GLUT4 in Mice. Diabetes 2013;62:223–233
Koichi Yamamoto, Masao Takeda, Mitsuru Ohishi, Hiromi Rakugi
Diabetes Jul 2013, 62 (7) e10; DOI: 10.2337/db13-0505

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Response to Comment on: Takeda et al. Loss of ACE2 Exaggerates High-Calorie Diet–Induced Insulin Resistance by Reduction of GLUT4 in Mice. Diabetes 2013;62:223–233
Koichi Yamamoto, Masao Takeda, Mitsuru Ohishi, Hiromi Rakugi
Diabetes Jul 2013, 62 (7) e10; DOI: 10.2337/db13-0505
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  • Comment on: Sitnick et al. Skeletal Muscle Triacylglycerol Hydrolysis Does Not Influence Metabolic Complications of Obesity. Diabetes 2013;62:3350–3361
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