Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012:2012:312943.
doi: 10.1155/2012/312943. Epub 2012 Feb 12.

ER Stress and Lipid Metabolism in Adipocytes

Beth S Zha  1 , Huiping Zhou
Affiliations

ER Stress and Lipid Metabolism in Adipocytes

Beth S Zha et al. Biochem Res Int. 2012.

Abstract

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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Potential link between ER stress signaling pathways and lipid droplet formation in adipocytes.
Figure 2
Figure 2
ER-stress-induced inflammation in adipocytes and macrophages contributes to atherosclerosis and fatty liver diseases.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Bays HE, González-Campoy JM, Henry RR, et al. Is adiposopathy (sick fat) an endocrine disease? International Journal of Clinical Practice. 2008;62(10):1474–1483. - PMC - PubMed
    1. Surmi BK, Hasty AH. Macrophage infiltration into adipose tissue: initiation, propagation and remodeling. Future Lipidology. 2008;3(5):545–556. - PMC - PubMed
    1. Mittra S, Bansal VS, Bhatnagar PK. From a glucocentric to a lipocentric approach towards metabolic syndrome. Drug Discovery Today. 2008;13(5-6):211–218. - PubMed
    1. Kabir M, Catalano KJ, Ananthnarayan S, et al. Molecular evidence supporting the portal theory: a causative link between visceral adiposity and hepatic insulin resistance. American Journal of Physiology. 2005;288(2):E454–E461. - PubMed
    1. Yoshii H, Lam TKT, Gupta N, et al. Effects of portal free fatty acid elevation on insulin clearance and hepatic glucose flux. American Journal of Physiology. 2006;290(6):E1089–E1097. - PubMed

LinkOut - more resources

  NODES
INTERN 1
twitter 2