+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ PDF Full Text
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Translate
+ Recently Requested

Thematic review series: Adipocyte Biology. Adipocyte stress: the endoplasmic reticulum and metabolic disease



Thematic review series: Adipocyte Biology. Adipocyte stress: the endoplasmic reticulum and metabolic disease



Journal of Lipid Research 48(9): 1905-1914



In the context of obesity and its related maladies, the adipocyte plays a central role in the balance, or imbalance, of metabolic homeostasis. An obese, hypertrophic adipocyte is challenged by many insults, including surplus energy, inflammation, insulin resistance, and considerable stress to various organelles. The endoplasmic reticulum (ER) is one such vital organelle that demonstrates significant signs of stress and dysfunction in obesity and insulin resistance. Under normal conditions, the ER must function in the unique and trying environment of the adipocyte, adapting to meet the demands of increased protein synthesis and secretion, energy storage in the form of triglyceride droplet formation, and nutrient sensing that are particular to the differentiated fat cell. When nutrients are in pathological excess, the ER is overwhelmed and the unfolded protein response (UPR) is activated. Remarkably, the consequences of UPR activation have been causally linked to the development of insulin resistance through a multitude of possible mechanisms, including c-jun N-terminal kinase activation, inflammation, and oxidative stress. This review will focus on the function of the ER under normal conditions in the adipocyte and the pathological effects of a stressed ER contributing to adipocyte dysfunction and a thwarted metabolic homeostasis.

(PDF emailed within 0-6 h: $19.90)

Accession: 017509014

Download citation: RISBibTeXText

PMID: 17699733

DOI: 10.1194/jlr.R700007-JLR200


Related references

Thematic review series: Adipocyte Biology. Lipodystrophies: windows on adipose biology and metabolism. Journal of Lipid Research 48(7): 1433-1444, 2007

Thematic review series: adipocyte biology. Sympathetic and sensory innervation of white adipose tissue. Journal of Lipid Research 48(8): 1655-1672, 2007

Thematic review series: adipocyte biology. Adipose tissue function and plasticity orchestrate nutritional adaptation. Journal of Lipid Research 48(6): 1253-1262, 2007

Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet proteins: stabilization of lipid droplets and control of lipolysis. Journal of Lipid Research 48(12): 2547-2559, 2007

Endoplasmic reticulum stress regulates adipocyte resistin expression. Diabetes 58(8): 1879-1886, 2009

GLP-1 Improves Adipocyte Insulin Sensitivity Following Induction of Endoplasmic Reticulum Stress. Frontiers in Pharmacology 9: 1168, 2018

Succination of Protein Disulfide Isomerase Links Mitochondrial Stress and Endoplasmic Reticulum Stress in the Adipocyte During Diabetes. Antioxidants and Redox Signaling 27(16): 1281-1296, 2017

Succination of Protein Disulfide Isomerase (PDI) Links Mitochondrial Stress to Endoplasmic Reticulum Stress in the Adipocyte during Diabetes. Free Radical Biology and Medicine 76: S114-S115, 2014

Unexpected blockade of adipocyte differentiation by K-7174: implication for endoplasmic reticulum stress. Biochemical and Biophysical Research Communications 363(2): 355-360, 2007

Endoplasmic reticulum stress regulates inflammation in adipocyte of obese rats via toll-like receptors 4 signaling. Iranian Journal of Basic Medical Sciences 21(5): 502-507, 2018

Autophagy inhibition by biotin elicits endoplasmic reticulum stress to differentially regulate adipocyte lipid and protein synthesis. Cell Stress & Chaperones 2019, 2019

Pathologic endoplasmic reticulum stress induced by glucotoxic insults inhibits adipocyte differentiation and induces an inflammatory phenotype. Biochimica et Biophysica Acta 1863(6 Pt A): 1146-1156, 2016

Characterization of Mg2+- and (Ca2+ + Mg2+)-ATPase activity in adipocyte endoplasmic reticulum. Archives of Biochemistry and Biophysics 199(1): 92-102, 1980

Stim1, an endoplasmic reticulum Ca2+ sensor, negatively regulates 3T3-L1 pre-adipocyte differentiation. Differentiation; Research in Biological Diversity 77(3): 239-247, 2009

Relationship between calcium ion transport and (Ca2+ + Mg2+)-atpase activity in adipocyte endoplasmic reticulum. Biochimica et Biophysica Acta 596(3): 359-371, 1980