Jerrold M. Olefsky

TL;DR: The results show that CD11c+ cell depletion results in rapid normalization of insulin sensitivity and a marked decrease in inflammatory markers, both locally and systemically, as reflected by gene expression and protein levels, indicate that these CD11C+ cells are a potential therapeutic target for treatment of obesity-related insulin resistance and type II diabetes.

TL;DR: In summary, insulin does not stimulate leptin production acutely; however, a long-term effect of insulin on leptin production could be demonstrated both in vivo and in vitro, suggesting that insulin regulates OB gene expression and leptin production indirectly, probably through its trophic effect on adipocytes.

TL;DR: The findings show that TZD treatment increased adiponectin levels in all subjects, including normal subjects in which no other effects of TZDs are observed, and it may play a physiologic role in enhancing insulin sensitivity.

TL;DR: These studies show that ATMs in obese mice secrete exosomes containing miRNA cargo, which can be transferred to insulin target cell types through mechanisms of paracrine or endocrine regulation with robust effects on cellular insulin action, in vivo insulin sensitivity, and overall glucose homeostasis.

TL;DR: Recent findings related to this interconnected network of eicosanoids and inositol phospholipids are reviewed from the perspective of immunity and metabolic disease.