ER Stress and Lipid Metabolism in Adipocytes
The role of endoplasmic reticulum (ER) stress is a rapidly emerging field of interest in the pathogenesis of metabolic diseases. Recent studies have shown that chronic activation of ER stress is closely linked to dysregulation of lipid metabolism in several metabolically important cells including he...
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Series: | Biochemistry Research International |
Online Access: | http://dx.doi.org/10.1155/2012/312943 |
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doaj-3749489ef64740649de70623195931d02020-11-24T23:53:21ZengHindawi LimitedBiochemistry Research International2090-22472090-22552012-01-01201210.1155/2012/312943312943ER Stress and Lipid Metabolism in AdipocytesBeth S. Zha0Huiping Zhou1Department of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, 1217 East Marshall Street, MSB no. 533, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, 1217 East Marshall Street, MSB no. 533, Richmond, VA 23298, USAThe role of endoplasmic reticulum (ER) stress is a rapidly emerging field of interest in the pathogenesis of metabolic diseases. Recent studies have shown that chronic activation of ER stress is closely linked to dysregulation of lipid metabolism in several metabolically important cells including hepatocytes, macrophages, β-cells, and adipocytes. Adipocytes are one of the major cell types involved in the pathogenesis of the metabolic syndrome. Recent advances in dissecting the cellular and molecular mechanisms involved in the regulation of adipogenesis and lipid metabolism indicate that activation of ER stress plays a central role in regulating adipocyte function. In this paper, we discuss the current understanding of the potential role of ER stress in lipid metabolism in adipocytes. In addition, we touch upon the interaction of ER stress and autophagy as well as inflammation. Inhibition of ER stress has the potential of decreasing the pathology in adipose tissue that is seen with energy overbalance.http://dx.doi.org/10.1155/2012/312943 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Beth S. Zha Huiping Zhou |
spellingShingle |
Beth S. Zha Huiping Zhou ER Stress and Lipid Metabolism in Adipocytes Biochemistry Research International |
author_facet |
Beth S. Zha Huiping Zhou |
author_sort |
Beth S. Zha |
title |
ER Stress and Lipid Metabolism in Adipocytes |
title_short |
ER Stress and Lipid Metabolism in Adipocytes |
title_full |
ER Stress and Lipid Metabolism in Adipocytes |
title_fullStr |
ER Stress and Lipid Metabolism in Adipocytes |
title_full_unstemmed |
ER Stress and Lipid Metabolism in Adipocytes |
title_sort |
er stress and lipid metabolism in adipocytes |
publisher |
Hindawi Limited |
series |
Biochemistry Research International |
issn |
2090-2247 2090-2255 |
publishDate |
2012-01-01 |
description |
The role of endoplasmic reticulum (ER) stress is a rapidly emerging field of interest in the pathogenesis of metabolic diseases. Recent studies have shown that chronic activation of ER stress is closely linked to dysregulation of lipid metabolism in several metabolically important cells including hepatocytes, macrophages, β-cells, and adipocytes. Adipocytes are one of the major cell types involved in the pathogenesis of the metabolic syndrome. Recent advances in dissecting the cellular and molecular mechanisms involved in the regulation of adipogenesis and lipid metabolism indicate that activation of ER stress plays a central role in regulating adipocyte function. In this paper, we discuss the current understanding of the potential role of ER stress in lipid metabolism in adipocytes. In addition, we touch upon the interaction of ER stress and autophagy as well as inflammation. Inhibition of ER stress has the potential of decreasing the pathology in adipose tissue that is seen with energy overbalance. |
url |
http://dx.doi.org/10.1155/2012/312943 |
work_keys_str_mv |
AT bethszha erstressandlipidmetabolisminadipocytes AT huipingzhou erstressandlipidmetabolisminadipocytes |
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1725470258433622016 |