M
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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Journal ArticleDOI
Overexpression of TRB3 in muscle alters muscle fiber type and improves exercise capacity in mice
Ding An,Sarah J. Lessard,Taro Toyoda,Min-Young Lee,Ho-Jin Koh,Ling Qi,Michael F. Hirshman,Laurie J. Goodyear +7 more
TL;DR: The findings suggest that TRB3 regulates muscle fiber type via a peroxisome proliferator-activated receptor-α (PPAR-α)-regulated miR499/miR208b pathway, revealing a novel function for TRB 3 in the regulation of skeletal muscle fibertype and exercise capacity.
Journal ArticleDOI
Dissociation of AMP-activated protein kinase and p38 mitogen-activated protein kinase signaling in skeletal muscle.
Richard C. Ho,Nobuharu Fujii,Nobuharu Fujii,Lee A. Witters,Michael F. Hirshman,Laurie J. Goodyear,Laurie J. Goodyear +6 more
TL;DR: In this article, the p38 mitogen-activated protein kinase (MAPK) has been proposed to be a downstream intermediate of AMPK-mediated signaling in skeletal muscle, but it was shown that p38 MAPK is not a downstream component of AMP-mediated signalling.
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Akt2 influences glycogen synthase activity in human skeletal muscle through regulation of NH₂-terminal (sites 2 + 2a) phosphorylation.
Martin Friedrichsen,Jesper B. Birk,Erik A. Richter,Rasmus Ribel-Madsen,Christian Kirkegaard Pehmøller,Christian Kirkegaard Pehmøller,Bo Falck Hansen,Henning Beck-Nielsen,Michael F. Hirshman,Laurie J. Goodyear,Allan Vaag,Pernille Poulsen,Pernille Poulsen,Jørgen F. P. Wojtaszewski +13 more
TL;DR: Akt2-dependent NH₂-terminal dephosphorylation may be the site for "fine-tuning" insulin-mediated GS activation in humans, according to a study population of nondiabetic twins.
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Islet transplantation restores normal levels of insulin receptor and substrate tyrosine phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle and myocardium of streptozocin-induced diabetic rats.
Francesco Giorgino,Francesco Logoluso,Alberto M. Davalli,Raffaele Napoli,Luigi Laviola,Michael F. Hirshman,Edward S. Horton,Gordon C. Weir,Robert J. Smith +8 more
TL;DR: Islet transplantation fully corrected the diabetes-induced changes in protein tyrosine phosphorylation and PI 3-kinase activity and normalized IRS-1 and IRS-2 protein content in both skeletal muscle and myocardium, suggesting that insulin delivered into the systemic circulation by pancreatic islets transplanted under the kidney capsule can adequately correct altered insulin signaling mechanisms in insulinopenic diabetes.
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Chronic growth hormone treatment in normal rats reduces post-prandial skeletal muscle plasma membrane GLUT1 content, but not glucose transport or GLUT4 expression and localization.
Raffaele Napoli,Antonio Cittadini,Jesse C. Chow,Michael F. Hirshman,Robert J. Smith,Pamela S. Douglas,Edward S. Horton +6 more
TL;DR: High-dose hGH treatment for 4 weeks did not alter post-prandial skeletal muscle glucose transport activity and mRNA data suggest that this reduction might result from a decrease in the synthesis of GLUT1.