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Erik J. Henriksen

Researcher at University of Arizona

Publications -  142
Citations -  8832

Erik J. Henriksen is an academic researcher from University of Arizona. The author has contributed to research in topics: Insulin & Skeletal muscle. The author has an hindex of 50, co-authored 142 publications receiving 8391 citations. Previous affiliations of Erik J. Henriksen include Washington University in St. Louis & University of Tübingen.

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Invited review: Effects of acute exercise and exercise training on insulin resistance.

TL;DR: It is clear that further investigations are needed to further elucidate the specific molecular mechanisms underlying the beneficial effects of acute exercise and exercise training on the glucose transport system in insulin-resistant mammalian skeletal muscle.
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Oxidative Stress and the Etiology of Insulin Resistance and Type 2 Diabetes

TL;DR: The importance of oxidative stress in the development of insulin resistance in mammalian skeletal muscle tissue is highlighted, at least in part via a p38-MAPK-dependent mechanism, and interventions that reduce this oxidative stress and oxidative damage can improve insulin action in insulin-resistant animal models are indicated.
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Selective glycogen synthase kinase 3 inhibitors potentiate insulin activation of glucose transport and utilization in vitro and in vivo.

TL;DR: Novel substituted aminopyrimidine derivatives that inhibit human GSK-3 potently with at least 500-fold selectivity against 20 other protein kinases are described and suggested to be useful as acute-acting therapeutics for the treatment of the insulin resistance of type 2 diabetes.
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Glucose transporter protein content and glucose transport capacity in rat skeletal muscles

TL;DR: The results suggest that the differences in maximally stimulated glucose transport activity among the three fiber types may be related to differences in their content of GLUT-4 protein.
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Selective Angiotensin II Receptor Antagonism Reduces Insulin Resistance in Obese Zucker Rats

TL;DR: Angiotensin II receptor (AT1-subtype) antagonism, either acutely or chronically, improves glucose tolerance, at least in part because of an enhancement in skeletal-muscle glucose transport, and the effect of chronic angiotens in II receptor antagonism on type I skeletal-Muscle glucose uptake is associated with an increase in GLUT-4 protein expression.