ER Stress and Autophagy in Obesity and Nonalcoholic Fatty Liver Disease

ER Stress and Autophagy in Obesity and Nonalcoholic Fatty Liver Disease Curr Pathobiol Rep (2017) 5:289–299 DOI 10.1007/s40139-017-0145-7 AUTOPHAGY IN PATHOBIOLOGY (W-X DING AND H-M SHEN, SECTION EDITORS) ER Stress and Autophagy in Obesity and Nonalcoholic Fatty Liver Disease 1 1 1 Nicholas R. L. Lind & Qingwen Qian & Ling Yang Published online: 2 June 2017 Springer Science+Business Media New York 2017 Abstract epidemic. Obesity greatly increases the risk of developing a Purpose of review This review highlights the extent to which wide range of diseases including insulin resistance, type 2 dysfunction of the endoplasmic reticulum (ER) and autophagy diabetes, and fatty liver disease [1]. Obesity-associated insulin contribute to the pathogenesis of obesity-associated hepatic resistance promotes the progression of non-alcoholic fatty liv- steatosis and non-alcoholic fatty liver disease (NAFLD). We er disease (NAFLD). Whereas NAFLD is estimated to occur addressed the following questions: what is the role of the in only 20–30% of the general adult population, it occurs in unfolded protein response (UPR) and autophagy in the liver? 70–80% of individuals with obesity and diabetes [2, 3]. What interactions between the UPR and autophagy are present Conversely, NAFLD is thought to contribute to insulin resis- during the progression of obesity-associated NAFLD? What tance and type 2 diabetes [4–6]. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Pathobiology Reports Springer Journals

ER Stress and Autophagy in Obesity and Nonalcoholic Fatty Liver Disease

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Medicine & Public Health; Pathology
eISSN
2167-485X
D.O.I.
10.1007/s40139-017-0145-7
Publisher site
See Article on Publisher Site

Abstract

Curr Pathobiol Rep (2017) 5:289–299 DOI 10.1007/s40139-017-0145-7 AUTOPHAGY IN PATHOBIOLOGY (W-X DING AND H-M SHEN, SECTION EDITORS) ER Stress and Autophagy in Obesity and Nonalcoholic Fatty Liver Disease 1 1 1 Nicholas R. L. Lind & Qingwen Qian & Ling Yang Published online: 2 June 2017 Springer Science+Business Media New York 2017 Abstract epidemic. Obesity greatly increases the risk of developing a Purpose of review This review highlights the extent to which wide range of diseases including insulin resistance, type 2 dysfunction of the endoplasmic reticulum (ER) and autophagy diabetes, and fatty liver disease [1]. Obesity-associated insulin contribute to the pathogenesis of obesity-associated hepatic resistance promotes the progression of non-alcoholic fatty liv- steatosis and non-alcoholic fatty liver disease (NAFLD). We er disease (NAFLD). Whereas NAFLD is estimated to occur addressed the following questions: what is the role of the in only 20–30% of the general adult population, it occurs in unfolded protein response (UPR) and autophagy in the liver? 70–80% of individuals with obesity and diabetes [2, 3]. What interactions between the UPR and autophagy are present Conversely, NAFLD is thought to contribute to insulin resis- during the progression of obesity-associated NAFLD? What tance and type 2 diabetes [4–6].

Journal

Current Pathobiology ReportsSpringer Journals

Published: Jun 2, 2017

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