scispace - formally typeset
G

Gökhan S. Hotamisligil

Researcher at Harvard University

Publications -  241
Citations -  88513

Gökhan S. Hotamisligil is an academic researcher from Harvard University. The author has contributed to research in topics: Insulin resistance & Adipose tissue. The author has an hindex of 105, co-authored 232 publications receiving 80085 citations. Previous affiliations of Gökhan S. Hotamisligil include Broad Institute & Pacific Northwest Diabetes Research Institute.

Papers
More filters
Journal ArticleDOI

Inflammation and metabolic disorders

Gökhan S. Hotamisligil
- 14 Dec 2006 - 
TL;DR: Dysfunction of the immune response and metabolic regulation interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease.
Journal ArticleDOI

Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

Gökhan S. Hotamisligil, +2 more
- 01 Jan 1993 - 
TL;DR: A role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity is indicated.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Inflammation, stress, and diabetes

Kathryn E. Wellen, +1 more
- 02 May 2005 - 
TL;DR: The molecular and cellular underpinnings of obesity-induced inflammation and the signaling pathways at the intersection of metabolism and inflammation that contribute to diabetes are discussed.
Journal ArticleDOI

Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes

Umut Ozcan, +9 more
- 15 Oct 2004 - 
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).