Stuart M. Furler

TL;DR: It is concluded that the LCACoA content of muscle provides a direct index of intracellular lipid metabolism and its links to insulin action, which, unlike triglyceride content, is not subject to contamination by closely associated adipose tissue.

TL;DR: It is postulate that muscle cytosolic accumulation of the metabolically active long-chain fatty acyl CoAs (LCACoA) is involved, leading to insulin resistance and impaired insulin signalling or impaired enzyme activity, and the interactions described here are fundamental to optimizing therapy of insulin resistance based on alterations in muscle lipid metabolism.

TL;DR: It is demonstrated that the short-term exercise training increased circulating adiponectin levels with accompanied improved insulin sensitivity, and was an extension to a previously reported exercise intervention in sedentary males.

TL;DR: It is concluded that muscle insulin resistance induced by high-fat feeding is readily ameliorated by three independent, short-term physiological manipulations.

TL;DR: Insulin resistance induced by feeding rats a high-fat diet is associated with tissue-specific adaptations that enhance utilization of increased dietary lipid but could also contribute to the accumulation of intramuscular lipid with a detrimental effect on insulin action.