Adipose Tissue Resistin Expression Is Severely Suppressed in Obesity and Stimulated by Peroxisome Proliferator-activated Receptor γ Agonists

• Published in: The Journal of biological chemistry Vol. 276; no. 28; pp. 25651 - 25653
• Main Authors: Way, James M., Görgün, Cem Z., Tong, Qiang, Uysal, K. Teoman, Brown, Kathleen K., Harrington, W. Wallace, Oliver, William R., Willson, Timothy M., Kliewer, Steven A., Hotamisligil, Gökhan S.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 13.07.2001
• Subjects: Adipocytes - metabolism; Animals; Benzophenones - pharmacology; Down-Regulation - drug effects; Hormones, Ectopic - biosynthesis; Hypoglycemic Agents - pharmacology; Intercellular Signaling Peptides and Proteins; Male; Mice; Nerve Growth Factor; Obesity - metabolism; peroxisome proliferator-activated receptors; Proteins; Rats; Receptors, Cytoplasmic and Nuclear - agonists; Receptors, Cytoplasmic and Nuclear - metabolism; Resistin; Rosiglitazone; Thiazoles - pharmacology; Thiazolidinediones; Transcription Factors - agonists; Transcription Factors - metabolism; Tyrosine - analogs & derivatives; Tyrosine - pharmacology
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1074/jbc.C100189200

Elevated levels of the hormone resistin, which is secreted by fat cells, are proposed to cause insulin resistance and to serve as a link between obesity and type 2 diabetes. In this report we show that resistin expression is significantly decreased in the white adipose tissue of several different models of obesity including the ob/ob, db/db, tub/tub, and KKAy mice compared with their lean counterparts. Furthermore, in response to several different classes of antidiabetic peroxisome proliferator-activated receptor γ agonists, adipose tissue resistin expression is increased in both ob/ob mice and Zucker diabetic fatty rats. These data demonstrate that experimental obesity in rodents is associated with severely defective resistin expression, and decreases in resistin expression are not required for the antidiabetic actions of peroxisome proliferator-activated receptor γ agonists.