E
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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Journal ArticleDOI
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.
David B. Ring,Kirk W. Johnson,Erik J. Henriksen,John M. Nuss,John M. Nuss,Dane Goff,Tyson R. Kinnick,Sylvia Ma,John W. Reeder,Isa Samuels,Isa Samuels,Trina Slabiak,Allan S. Wagman,Mary Ellen Wernette Hammond,Stephen D. Harrison +14 more
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
Erik J. Henriksen,Raymond E. Bourey,Kenneth J. Rodnick,László Korányi,M. A. Permutt,John O. Holloszy +5 more
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.