Antioxidant effect of angiotensin (1-7) in the protection of pancreatic ß cell function

Zhang, Fen; Liu, Chang; Wang, Lei; Cao, Xi; Wang, Ying Ying; Yang, Jin Kui

Diabetes is a chronic metabolic syndrome caused by insulin deficiency and resistance. There are 200 million diabetic individuals in the world, with only approximately one-half being diagnosed, and these numbers are expected to double by 2030. The disease often results in long-term microvascular, neurological, and macrovascular complications, including retinopathy, nephropathy, neuropathy, and increased risk of cardiovascular disease. Excessive activation of angiotensin II (AngII) is an important underlying mechanism for the development of diabetes, and Ang (1) (2) (3) (4) (5) (6) (7) is hypothesized to counteract it. Furthermore, the reninangiotensin system (RAS) is significantly involved in the development of diabetes and its complications. The activation of RAS causes pancreatic β cell dysfunction by suppressing pro-insulin biosynthesis, glucose-stimulated insulin secretion (GSIS) and first phase insulin secretion (1) (2) , as well as by increasing islet fibrosis (3) and oxidative stress (4) . The angiotensin-converting enzyme 2 (ACE2)-angiotensin (1) (2) (3) (4) (5) (6) (7) [Ang (1) (2) (3) (4) (5) (6) (7) ]-Mas axis is suggested to have an antagonistic effect on the RAS, while Ang (1-7) is the main antagonist of AngII. Angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor antagonist (ARB) can alleviate these pathological changes (3, (5) (6) (7) . Also, several clinical experiments have demonstrated the effectiveness of RAS blockade in reducing the onset of diabetes (8) (9) (10) (11) .