| Literature DB >> 19145587 |
Swapnil N Rajpathak1, Marc J Gunter, Judith Wylie-Rosett, Gloria Y F Ho, Robert C Kaplan, Radhika Muzumdar, Thomas E Rohan, Howard D Strickler.
Abstract
This review addresses the possible role of the insulin-like growth factor (IGF)-axis in normal glucose homoeostasis and in the etiopathogenesis of type 2 diabetes. IGF-I, a peptide hormone, shares amino acid sequence homology with insulin and has insulin-like activity; most notably, the promotion of glucose uptake by peripheral tissues. Type 2 diabetes as well as pre-diabetic states, including impaired fasting glucose and impaired glucose tolerance, are associated cross-sectionally with altered circulating levels of IGF-I and its binding proteins (IGFBPs). Administration of recombinant human IGF-I has been reported to improve insulin sensitivity in healthy individuals as well as in patients with insulin resistance and type 2 diabetes. Further, IGF-I may have beneficial effects on systemic inflammation, a risk factor for type 2 diabetes, and on pancreatic beta-cell mass and function. There is considerable inter-individual heterogeneity in endogenous levels of IGF-I and its binding proteins; however, the relationship between these variations and the risk of developing type 2 diabetes has not been extensively investigated. Large prospective studies are required to evaluate this association. Copyright 2009 John Wiley & Sons, Ltd.Entities:
Mesh:
Substances:
Year: 2009 PMID: 19145587 PMCID: PMC4153414 DOI: 10.1002/dmrr.919
Source DB: PubMed Journal: Diabetes Metab Res Rev ISSN: 1520-7552 Impact factor: 4.876