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Originally published In Press as doi:10.1074/jbc.M000764200 on March 9, 2000
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J Biol Chem, Vol. 275, Issue 19, 14173-14181, May 12, 2000

Increased Insulin Receptor Substrate-1 and Enhanced Skeletal Muscle Insulin Sensitivity in Mice Lacking CCAAT/Enhancer-binding Protein beta *

LiQin WangDagger , Jianhua ShaoDagger , Peggy MuhlenkampDagger , Sha LiuDagger , Patrick KlepcykDagger , Jianming Ren§, and Jacob E. FriedmanDagger

From the Dagger  Department of Nutrition, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4935 and the § Division of Metabolic Diseases, Bristol-Myers Squibb Company, Princeton, New Jersey 08543

CCAAT/enhancer-binding protein beta  (C/EBPbeta ) controls gene transcription and metabolic processes in a variety of insulin-sensitive tissues; however, its role in regulating insulin responsiveness in vivo has not been investigated. We performed hyperinsulinemic-euglycemic clamps in awake, non-stressed, chronically catheterized adult mice homozygous for a deletion in the gene for C/EBPbeta (C/EBPbeta -/-). Fasting plasma insulin, glucose, and free fatty acid (FFA) levels were significantly lower in C/EBPbeta -/- mice compared with wild-type (WT) controls. Acute hyperinsulinemia (4 h) suppressed hepatic glucose production, phosphoenolpyruvate carboxykinase mRNA, and plasma FFA to a similar extent in WT and C/EBPbeta -/- mice, suggesting that C/EBPbeta deletion does not alter the metabolic and gene regulatory response to insulin in liver and adipose tissue. In contrast, using submaximal (5 milliunits/kg/min) and maximal (20 milliunits/kg/min) insulin infusions, whole-body glucose disposal was 77% (p < 0.01) and 33% (p < 0.05) higher in C/EBPbeta -/- mice, respectively, compared with WT mice. Maximal insulin-stimulated 3-O-methylglucose uptake in isolated soleus muscle was 54% greater in C/EBPbeta -/- mice (p < 0.05). Furthermore, insulin-stimulated insulin receptor and Akt Ser473 phosphorylation and phosphatidylinositol 3-kinase activity were 1.6-2.5-fold greater in skeletal muscle from C/EBPbeta -/- mice compared with WT mice. The level of insulin receptor substrate-1 protein was increased 2-fold in skeletal muscle from C/EBPbeta -/- mice. These results demonstrate that C/EBPbeta deletion decreases plasma FFA levels and increases insulin signal transduction specifically in skeletal muscle, and both contribute to increased whole-body insulin sensitivity.

* This work was supported by Grant DK-50272 from the National Institutes of Health and by a grant from the American Diabetes Association (to J. E. F.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Nutrition, Case Western Reserve University School of Medicine, 10900 Euclid Ave., Cleveland, OH 44106-4935. Tel.: 216-368-1616; Fax: 216-368-6644; E-mail: jef8@po.cwru.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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