K. Teoman Uysal

TL;DR: It is shown that JNK activity is abnormally elevated in obesity and an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity.

TL;DR: Through its distinct actions in adipocytes and macrophages, aP2 provides a link between features of the metabolic syndrome and could be a new therapeutic target for the prevention of atherosclerosis.

TL;DR: It is shown 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, and decreases in Resistin expression are not required for the antidiabetic actions of peroxisome proliferator-activated receptor γ agonists.

TL;DR: The data indicate that in obesity, aP2-deficiency not only improves peripheral insulin resistance but also preserves pancreatic b cell function and has beneficial effects on lipid metabolism.

TL;DR: In obese (ob/ob) mice, neutralization of TNF-α or deletion of both TNF receptors (TNFRs) results in significantly reduced levels of plasma PAI-1 antigen, plasma insulin, and adipose tissue PAi-1 and TGF-β mRNAs.