Endoplasmic Reticulum Stress Plays a Central Role in Development of Leptin Resistance
Lale Ozcan,Ayse Seda Ergin,Allen Lu,Jason Chung,Sumit Sarkar,Duyu Nie,Martin G. Myers,Umut Ozcan +7 more
TLDR
It is shown that increased endoplasmic reticulum stress and activation of the unfolded protein response in the hypothalamus of obese mice inhibits leptin receptor signaling and chemical chaperones, 4-phenyl butyric acid, and tauroursodeoxycholic acid, act as leptin-sensitizing agents, which may provide the basis for a novel treatment of obesity.About:
This article is published in Cell Metabolism.The article was published on 2009-01-07 and is currently open access. It has received 819 citations till now. The article focuses on the topics: Leptin receptor & Unfolded protein response.read more
Citations
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Adipose tissue as an endocrine organ.
TL;DR: These proteins commonly known as adipokines are central to the dynamic control of energy metabolism, communicating the nutrient status of the organism with the tissues responsible for controlling both energy intake and expenditure as well as insulin sensitivity.
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Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease
TL;DR: The endoplasmic reticulum is the major site in the cell for protein folding and trafficking and is central to many cellular functions and is emerging as a potential site for the intersection of inflammation and metabolic disease.
Journal ArticleDOI
Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress.
Ira Tabas,David Ron +1 more
TL;DR: The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress.
Journal ArticleDOI
Inflammatory links between obesity and metabolic disease.
Carey N. Lumeng,Alan R. Saltiel +1 more
TL;DR: This Review highlights the cellular and molecular mechanisms at play in the generation of obesity-induced inflammation and underscores how defining the immune regulation in metabolic tissues has broadened the understanding of the diversity of inflammatory responses.
Journal ArticleDOI
Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis†
TL;DR: Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.
References
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Central nervous system control of food intake
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Signal integration in the endoplasmic reticulum unfolded protein response
David Ron,Peter Walter +1 more
TL;DR: Together, at least three mechanistically distinct arms of the UPR regulate the expression of numerous genes that function within the secretory pathway but also affect broad aspects of cell fate and the metabolism of proteins, amino acids and lipids.
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Leptin and the regulation of body weight in mammals
TL;DR: The role of leptin in the control of body weight and its relevance to the pathogenesis of obesity are reviewed.
Journal ArticleDOI
Weight-Reducing Effects of the Plasma Protein Encoded by the obese Gene
Jeffrey L. Halaas,Gajiwala Ketan,Margherita Maffei,Steven L. Cohen,Brian T. Chait,Daniel Rabinowitz,Roger Lallone,Stephen K. Burley,Jeffrey M. Friedman +8 more
TL;DR: Injection of wild-type mice twice daily with the mouse protein resulted in a sustained 12 percent weight loss, decreased food intake, and a reduction of body fat from 12.2 to 0.7 percent, suggesting that the OB protein serves an endocrine function to regulate body fat stores.
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Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Umut Ozcan,Qiong Cao,Erkan Yilmaz,Ann-Hwee Lee,Neal N. Iwakoshi,Esra Özdelen,Gurol Tuncman,Cem Z. Görgün,Laurie H. Glimcher,Gökhan S. Hotamisligil +9 more
TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).