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Diabetes 50:1134-1142, 2001
© 2001 by the American Diabetes Association, Inc.

Regulation by Insulin of Gene Expression in Human Skeletal Muscle and Adipose Tissue

Evidence for Specific Defects in Type 2 Diabetes

Pierre-Henri Ducluzeau1, Noël Perretti1, Martine Laville1,2,3, Fabrizio Andreelli1,3, Nathalie Vega1, Jean-Paul Riou1,2,3, and Hubert Vidal1,2

1 Institut National de la Santé et de la Recherche Médicale (INSERM) U.449 and
2 Human Nutrition Research Center of Lyon, Faculty of Medicine R. Laennec
3 Department of Endocrinology, Diabetology, and Nutrition, E. Herriot Hospital, Lyon, France

Defective regulation of gene expression may be involved in the pathogenesis of type 2 diabetes. We have characterized the concerted regulation by insulin (3-h hyperinsulinemic clamp) of the expression of 10 genes related to insulin action in skeletal muscle and in subcutaneous adipose tissue, and we have verified whether a defective regulation of some of them could be specifically encountered in tissues of type 2 diabetic patients. Basal mRNA levels (determined by reverse transcriptase–competitive polymerase chain reaction) of insulin receptor, insulin receptor substrate-1, p85{alpha} phosphatidylinositol 3-kinase (PI3K), p110{alpha}PI3K, p110ßPI3K, GLUT4, glycogen synthase, and sterol regulatory-element-binding protein-1c (SREBP-1c) were similar in muscle of control (n = 17), type 2 diabetic (n = 9), type 1 diabetic (n = 9), and nondiabetic obese (n = 9) subjects. In muscle, the expression of hexokinase II was decreased in type 2 diabetic patients (P < 0.01). In adipose tissue, SREBP-1c (P < 0.01) mRNA expression was reduced in obese (nondiabetic and type 2 diabetic) subjects and was negatively correlated with the BMI of the subjects (r = -0.63, P = 0.02). Insulin (±1,000 pmol/l) induced a two- to threefold increase (P < 0.05) in hexokinase II, p85{alpha}PI3K, and SREBP-1c mRNA levels in muscle and in adipose tissue in control subjects, in insulin-resistant nondiabetic obese patients, and in hyperglycemic type 1 diabetic subjects. Upregulation of these genes was completely blunted in type 2 diabetic patients. This study thus provides evidence for a specific defect in the regulation of a group of important genes in response to insulin in peripheral tissues of type 2 diabetic patients.


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