The general area of interest of our laboratory is the regulation of the glucose transport system in normal skeletal muscle and in insulin-resistant skeletal muscle, as exists in pre-diabetes and overt type 2 diabetes.
The insulin resistance syndrome is characterized by the clustering of several atherogenic risk factors in the same individual, including essential hypertension, glucose intolerance, insulin resistance of skeletal muscle glucose transport, hyperinsulinemia, dyslipidemia, and central obesity. We are interested in investigating interventions that can favorably impact upon this syndrome. More specifically, using genetically obese animal models of insulin resistance, such as the obese Zucker (fa/fa) rat, we use an integrative approach to study the underlying mechanisms whereby exercise training and certain pharmaceutical interventions, such as antihypertensive agents, antioxidants, and selective enzyme inhibitors, can enhance insulin action on the skeletal muscle glucose transport system and improve whole body glucose tolerance. Inherent to these studies is the examination of alterations in insulin signal transduction and GLUT-4 protein expression and trafficking. We are also investigating the role of a specific serine/threonine kinase, glycogen synthase kinase-3, in the etiology of insulin resistance in skeletal muscle.
We also have a long-standing interest in the adaptive responses of carbohydrate and protein metabolism in skeletal muscle to acute and chronic alterations in contractile activity, including not only exercise, but also muscle unweighting by real or simulated weightlessness and denervation. We have characterized how the expression and functionality of specific intracellular insulin signaling factors are changed with short-term and longer-term unweighting, and how these changes relate to insulin action in unweighted skeletal muscle.
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of the BMCB site and to an abstract of that particular paper.
Kim, J.S., V. Saengsirisuwan, J.A. Sloniger, M.K. Teachey, and E.J.
Henriksen. 2006. Oxidant stress and skeletal muscle glucose transport: Roles of insulin signaling and p38 MAPK. Free Radical Biology and Medicine 41: 818-824.
Dokken, B.B., and E.J. Henriksen. 2006. Chronic selective glycogen synthase kinase-3 inhibition enhances glucose disposal and muscle insulin action in prediabetic obese Zucker rats. American Journal of Physiology. Endocrinology and Metabolism 291: E207-E213.
Lemieux, A.M., C.J. Diehl, J.A. Sloniger, and E.J. Henriksen. 2005. Voluntary exercise training enhances glucose transport but not insulin signaling capacity in muscle of hypertensive TG(mREN2)27 rats. Journal of Applied Physiology 99: 357-362.
