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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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AS160 regulates insulin- and contraction-stimulated glucose uptake in mouse skeletal muscle.

TL;DR: The data suggest that AS160 regulates both insulin- and contraction-stimulated glucose metabolism in mouse skeletal muscle in vivo and that the effects of mutant AS160 on the actions of insulin and contraction are not identical.
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The cold-induced lipokine 12,13-diHOME promotes fatty acid transport into brown adipose tissue

TL;DR: It is shown that the lipid 12, 13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) is a stimulator of BAT activity, and that its levels are negatively correlated with body-mass index and insulin sensitivity, and this data suggest that 12,13 -diHOME, or a functional analog, could be developed as a treatment for metabolic disorders.
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Nitric oxide increases glucose uptake through a mechanism that is distinct from the insulin and contraction pathways in rat skeletal muscle.

TL;DR: No stimulates glucose uptake through a mechanism that is distinct from both the insulin and contraction signaling pathways, suggesting that NO is a critical mediator of insulin- and/or contraction-stimulated transport.
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Reduced expression of the murine p85α subunit of phosphoinositide 3-kinase improves insulin signaling and ameliorates diabetes

TL;DR: Despite the decrease in p85alpha, PI 3-kinase activation is normal, insulin-stimulated Akt activity is increased, and glucose tolerance and insulin sensitivity are improved, and data suggest that regulation of p85 alpha levels may provide a novel therapeutic target for the treatment of type 2 diabetes.
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A Novel Role for Subcutaneous Adipose Tissue in Exercise-Induced Improvements in Glucose Homeostasis

TL;DR: Exercise training causes adaptations to scWAT that elicit metabolic improvements in other tissues, demonstrating a previously unrecognized role for adipose tissue in the beneficial effects of exercise on systemic glucose homeostasis.