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Kenneth J. Rodnick

Researcher at Idaho State University

Publications -  78
Citations -  4112

Kenneth J. Rodnick is an academic researcher from Idaho State University. The author has contributed to research in topics: Glucose transporter & Rainbow trout. The author has an hindex of 32, co-authored 78 publications receiving 3895 citations. Previous affiliations of Kenneth J. Rodnick include Stanford University & University of Maine.

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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.

Contribution Of Impaired Myocardial InsulinSignaling To Mitochondrial Dysfunction AndOxidative Stress In The Heart

TL;DR: The hypothesis that perinatal loss of insulin signaling in the heart impairs mitochondrial function is tested and defects in fatty acid and pyruvate metabolism and tricarboxylic acid flux may explain the mitochondrial dysfunction observed.
Journal ArticleDOI

Contribution of Impaired Myocardial Insulin Signaling to Mitochondrial Dysfunction and Oxidative Stress in the Heart

TL;DR: In this paper, the authors tested the hypothesis that perinatal loss of insulin signaling in the heart impairs mitochondria function and found that the contribution of altered myocardial insulin action independent of associated changes in systemic metabolism is incompletely understood.
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Exercise training, glucose transporters, and glucose transport in rat skeletal muscles

TL;DR: It is concluded that an increase inGLUT4, but not of GLUT1 protein, is a component of the adaptive response of muscle to endurance exercise and that the increase in GLUT4 protein is associated with an increased capacity for glucose transport.
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Immunocytochemical and biochemical studies of GLUT4 in rat skeletal muscle.

TL;DR: The data suggest that translocation of GLUT4 from intracellular tubulo-vesicular structures is the major mechanism by which insulin and exercise regulate muscle glucose transport.