Open Access<p>Endoplasmic Reticulum (ER) Stress in Part Mediates Effects of Angiotensin II in Pancreatic Beta Cells</p>
Author(s) -
Latha Ramalingam,
Boontharick Sopontammarak,
Kalhara R. Menikdiwela,
Naima MoustaidMoussa
Publication year - 2020
Publication title -
diabetes, metabolic syndrome and obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.853
H-Index - 43
ISSN - 1178-7007
DOI - 10.2147/dmso.s257797
Subject(s) - unfolded protein response , endocrinology , medicine , endoplasmic reticulum , angiotensin ii , insulin , renin–angiotensin system , beta cell , secretion , biology , chemistry , receptor , microbiology and biotechnology , islet , blood pressure
The renin angiotensin aldosterone system (RAAS) is a hormone system known for its role in regulating blood pressure and fluid balance. Numerous RAAS inhibitors routinely prescribed for hypertension have also beneficial effects in type 2 diabetes (T2D) prevention. RAAS components are expressed locally in many tissues, including adipose tissue and pancreas, where they exert metabolic effects through RAAS bioactive hormone angiotensin II (Ang II). Pancreatic beta cells are specialized insulin-producing cells; they have also developed endoplasmic reticulum (ER), which contributes to beta cell dysfunction, when proteins are misfolded in disease states such as T2D. However, no studies have investigated the relationship between RAAS and ER stress in beta cells as a mechanism linking pancreatic RAAS to T2D. Hence, we hypothesized that Ang II treatment of beta cells increases ER stress and inflammation leading to reduced insulin secretion.