The renin-angiotensin system as a target to solve the riddle of endocrine pancreas homeostasis

被引：29
作者：
Graus-Nunes, Francielle [1 ]
Souza-Mello, Vanessa [1 ]
机构：
[1] Univ Estado Rio De Janeiro, Inst Biol, Biomed Ctr, Lab Morphometry Metab & Cardiovasc Dis, Av 28 Setembro 87 Fds, BR-20551030 Rio De Janeiro, RJ, Brazil
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2019年 / 109卷
关键词：
Pancreas; Islet; Local renin-angiotensin system; GSIS; AT1R; CONVERTING ENZYME 2; STIMULATED INSULIN-SECRETION; BETA-CELL DYSFUNCTION; HIGH-FAT DIET; MOUSE MODEL; METABOLIC SYNDROME; RESISTANCE; INHIBITION; BLOCKADE; ISLETS;
D O I：
10.1016/j.biopha.2018.10.191
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Local renin-angiotensin system (RAS) in the pancreas is linked to the modulation of glucose-stimulated insulin secretion (GSIS) in beta cells and insulin sensitivity in target tissues, emerging as a promising tool in the prevention and/or treatment of obesity, diabetes, and systemic arterial hypertension. Insulin resistance alters pancreatic islet cell distribution and morphology and hypertrophied islets exhibit upregulated angiotensin II type 1 receptor, which drives oxidative stress, apoptosis, and fibrosis, configuring beta cell dysfunction and diminishing islet lifespan. Pharmacological modulation of RAS has shown beneficial effects in diet-induced obesity model, mainly related to the translational potential that angiotensin receptor blockers and ECA2/ANG (1-7)/MAS receptor axis modulation have when it comes to islet preservation and type 2 diabetes prevention and/or treatment. This review describes the existing evidence for different approaches to blocking RAS elements in the management of insulin resistance and diabetes and focuses on islet remodeling and GSIS in rodents and humans.
引用
收藏
页码：639 / 645
页数：7
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