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

Biomed Pharmacother

Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Brazil. Electronic address:

Published: January 2019

AI Article Synopsis

  • The local renin-angiotensin system (RAS) in the pancreas plays a significant role in regulating insulin secretion and sensitivity, which is important for managing conditions like obesity and diabetes.
  • Insulin resistance can negatively impact pancreatic beta cells, leading to increased stress and reduced function, making these cells less effective over time.
  • Research suggests that modifying RAS can help preserve insulin-producing cells and prevent or treat type 2 diabetes, highlighting the potential benefits of using medications like angiotensin receptor blockers.

Article Abstract

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.

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Source
http://dx.doi.org/10.1016/j.biopha.2018.10.191DOI Listing

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