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. 2017 May 30;66(8):2201–2212. doi: 10.2337/db16-1318

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© 2017 by the American Diabetes Association.

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ACE2 is localized to non–β-cells and contributes to angiotensin-(1–7)–mediated potentiation of insulin secretion. Pancreas sections from C57BL/6.NEP^+/+ mice (A) and humans (B) were immunostained for ACE2, insulin (INS), glucagon (GLU), somatostatin (SS), and PP. Merged images (MERGE) show colocalization (yellow) of ACE2 with glucagon, somatostatin, and PP, but not insulin. Islets are demarcated by the dashed line in panel B. Scale bars: 50 μm. C: Insulin secretion in response to 2.8 or 20 mmol/L glucose from C57BL/6.NEP^+/+ islets cultured for 48 h in the absence or presence of 1 nmol/L angiotensin-(1–7) with or without the ACE2 inhibitor DX600 (10 μmol/L). Data are the mean ± SEM; n = 5. *P < 0.05 vs. vehicle 20 mmol/L glucose.

ACE2 is localized to non–β-cells and contributes to angiotensin-(1–7)–mediated potentiation of insulin secretion. Pancreas sections from C57BL/6.NEP^+/+ mice (A) and humans (B) were immunostained for ACE2, insulin (INS), glucagon (GLU), somatostatin (SS), and PP. Merged images (MERGE) show colocalization (yellow) of ACE2 with glucagon, somatostatin, and PP, but not insulin. Islets are demarcated by the dashed line in panel B. Scale bars: 50 μm. C: Insulin secretion in response to 2.8 or 20 mmol/L glucose from C57BL/6.NEP^+/+ islets cultured for 48 h in the absence or presence of 1 nmol/L angiotensin-(1–7) with or without the ACE2 inhibitor DX600 (10 μmol/L). Data are the mean ± SEM; n = 5. *P < 0.05 vs. vehicle 20 mmol/L glucose.