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Michael F. Hirshman

Researcher at Harvard University

Publications -  143
Citations -  22282

Michael F. Hirshman is an academic researcher from Harvard University. The author has contributed to research in topics: Skeletal muscle & Glucose uptake. The author has an hindex of 65, co-authored 131 publications receiving 20279 citations. Previous affiliations of Michael F. Hirshman include Merck & Co. & Joslin Diabetes Center.

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Calmodulin-binding domain of AS160 regulates contraction- but not insulin-stimulated glucose uptake in skeletal muscle.

TL;DR: The results suggest that the AS160 CBD directly regulates contraction-induced glucose uptake in mouse muscle and that calmodulin provides an additional means of modulating AS160 Rab-GAP function independent of phosphorylation.
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Exercise increases TBC1D1 phosphorylation in human skeletal muscle.

TL;DR: Exercise and weight loss are cornerstones in the treatment and prevention of type 2 diabetes, and both interventions function to increase insulin sensitivity and glucose uptake into skeletal muscle, but surprisingly, there was no effect on expression or phosphorylation of any of the muscle-signaling proteins.
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Glucose Ingestion Causes GLUT4 Translocation in Human Skeletal Muscle

TL;DR: It is demonstrated that oral ingestion of glucose increases the rate of glucose transport across the plasma membrane and causes GLUT4 translocation in human skeletal muscle, which suggests that under physiological conditions the translocation ofGLUT4 is an important mechanism for the stimulation of glucose uptake inhuman skeletal muscle.
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Contraction and AICAR Stimulate IL-6 Vesicle Depletion From Skeletal Muscle Fibers In Vivo

TL;DR: In this article, the authors used confocal imaging to visualize endogenous interleukin 6 (IL-6) protein in fixed muscle fibers and found IL-6 in small vesicle structures distributed throughout the fibers under basal conditions.
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Ablation of LKB1 in the heart leads to energy deprivation and impaired cardiac function

TL;DR: A critical role is established for LKB1 for normal cardiac function under both aerobic conditions and during recovery after ischemia in mice generated using the Cre-Lox system.