Michael F. Hirshman

TL;DR: The cold-induced 12-LOX product 12-HEPE was found to be a batokine that improves glucose metabolism by promoting glucose uptake into adipocytes and skeletal muscle through activation of an insulin-like intracellular signaling pathway.

TL;DR: It is demonstrated that the IRS2 protein in muscle is not necessary for insulin- or exercise-stimulated glucose transport, suggesting that the onset of diabetes in the taxonomic mice is not due to a defect in skeletal muscle glucose transport; hyperglycemia may cause insulin resistance in the muscle of IRS2−/− mice.

TL;DR: It is found that aberrant high activity of AMPK in the absence of energy deficit caused extensive remodeling of the substrate metabolism pathways to accommodate increases in both glucose uptake and fatty acid oxidation in the hearts of gamma2 mutant mice via distinct, yet synergistic mechanisms resulting in selective fuel storage as glycogen.

TL;DR: Findings show that the C2C12 cell contraction system reproduces the muscle phenotypes that arise in vivo, in situ (hindlimb muscles in an anesthetized animal), and in vitro (dissected muscle tissues in incubation buffer) by acute muscle contraction, demonstrating that the system is applicable for the analysis of intracellular events evoked by acute Muscle contraction.

TL;DR: It is shown that transforming growth factor-β2 is secreted from adipose tissue in response to exercise and improves glucose tolerance in mice, and exercise training improves systemic metabolism through inter-organ communication with fat via a lactate–TGF- β2 signaling cycle.