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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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Identification of an intracellular pool of glucose transporters from basal and insulin-stimulated rat skeletal muscle

TL;DR: Western blot analysis using the monoclonal antibody mAb 1F8 (specific for the insulin-regulatable glucose transporter) demonstrated increased glucose transporter densities in plasma membranes from insulin-treated hind limb skeletal muscle compared with untreated tissues, while microsomal membranes from the diabetes-treated hamstring skeletal muscle had a concomitant decrease in transporter density.
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Discovery of TBC1D1 as an Insulin-, AICAR-, and Contraction-stimulated Signaling Nexus in Mouse Skeletal Muscle

TL;DR: A dissociation between AS160 protein expression and apparent AS160 PAS phosphorylation among soleus, tibialis anterior, and extensor digitorum longus muscles is discovered and is identified as the AS160 paralog TBC1D1, an obesity candidate gene regulating GLUT4 translocation in adipocytes.
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Exercise modulates postreceptor insulin signaling and glucose transport in muscle-specific insulin receptor knockout mice.

TL;DR: Normal expression of muscle insulin receptors is not needed for the exercise-mediated increase in glucose uptake and glycogen synthase activity in vivo, and the synergistic activation of glucose transport with exercise plus insulin is retained in MIRKO mice, suggesting a phenomenon mediated by nonmuscle cells or by downstream signaling events.
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Akt signaling in skeletal muscle: regulation by exercise and passive stretch.

TL;DR: It is demonstrated that treadmill running exercise of rats using two different protocols (intermediate high or high-intensity exhaustive exercise) significantly increases Akt activity and phosphorylation in skeletal muscle composed of various fiber types and that mechanical tension may be a part of the mechanism by which contraction activates Akt in fast-twitch muscles.
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Glucose Metabolism and Energy Homeostasis in Mouse Hearts Overexpressing Dominant Negative α2 Subunit of AMP-activated Protein Kinase

TL;DR: It is found that ATP depletion was accelerated in transgenic mice with cardiac-specific overexpression of a dominant negative mutant of the AMPK α2 catalytic subunit during no-flow ischemia, and these hearts developed left ventricular dysfunction manifested by an early and more rapid increase inleft ventricular end-diastolic pressure.