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Redistribution of substrates to adipose tissue promotes obesity in mice with selective insulin resistance in muscle
Jason K. Kim, … , C. Ronald Kahn, Gerald I. Shulman
Jason K. Kim, … , C. Ronald Kahn, Gerald I. Shulman
Published June 15, 2000
Citation Information: J Clin Invest. 2000;105(12):1791-1797. https://doi.org/10.1172/JCI8305.
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Article

Redistribution of substrates to adipose tissue promotes obesity in mice with selective insulin resistance in muscle

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Abstract

Obesity and insulin resistance in skeletal muscle are two major factors in the pathogenesis of type 2 diabetes. Mice with muscle-specific inactivation of the insulin receptor gene (MIRKO) are normoglycemic but have increased fat mass. To identify the potential mechanism for this important association, we examined insulin action in specific tissues of MIRKO and control mice under hyperinsulinemic-euglycemic conditions. We found that insulin-stimulated muscle glucose transport and glycogen synthesis were decreased by about 80% in MIRKO mice, whereas insulin-stimulated fat glucose transport was increased threefold in MIRKO mice. These data demonstrate that selective insulin resistance in muscle promotes redistribution of substrates to adipose tissue thereby contributing to increased adiposity and development of the prediabetic syndrome.

Authors

Jason K. Kim, M. Dodson Michael, Stephen F. Previs, Odile D. Peroni, Franck Mauvais-Jarvis, Susanne Neschen, Barbara B. Kahn, C. Ronald Kahn, Gerald I. Shulman

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Figure 1

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(a) Steady-state glucose infusion rate, obtained from averaged rates of ...
(a) Steady-state glucose infusion rate, obtained from averaged rates of 90–120 minutes of hyperinsulinemic-euglycemic clamps, in the control group and MIRKO group. (b) Hepatic glucose production during the insulin-stimulated state in the control group and MIRKO group. Values are means ± SE for eight or nine experiments. AP < 0.05 versus control group.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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