(2005,二型糖尿病MKR小鼠模型).pdfVIP

0013-7227/06/$15.00/0 Endocrinology 147(6):2619–2630 Printed in U.S.A. Copyright © 2006 by The Endocrine Society doi: 10.1210/en.2005-1556 Recombinant Human Insulin-Like Growth Factor-I Treatment Inhibits Gluconeogenesis in a Transgenic Mouse Model of Type 2 Diabetes Mellitus Patricia Pennisi, Oksana Gavrilova, Jennifer Setser-Portas, William Jou, Stefania Santopietro, David Clemmons, Shoshana Yakar, and Derek LeRoith Diabetes Branch (P.P., J.S.-P., S.S., S.Y., D.L.) and Mouse Metabolism Core Laboratory (O.G., W.J.), National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892; and Division of Endocrinology (D.C.), University of North Carolina, Chapel Hill, North Carolina 27599 IGF-I and insulin are structurally related polypeptides that position such as a decrease in fat mass and an increase in lean mediate a similar pattern of biological effects via receptors body mass. Insulin, fatty acid, and triglyceride levels were not that display considerably homology. Administration of recom- affected by rhIGF-I, nor were insulin or glucose tolerance in binant human IGF-I (rhIGF-I) has been proven to improve MKR mice. Hyperinsulinemic-euglycemic clamp analysis glucose control and liver and muscle insulin sensitivity in demonstrated no improvement in overall insulin sensitivity. patients with type 2 diabetes mellitus (DM). The effect of Pyruvate and glutamine tolerance tests proved that there was rhIGF-I treatment was evaluated in a mouse model of type