The role of insulin‐like growth factor‐I and its binding proteins in glucose homeostasis and type 2 diabetes

SN Rajpathak, MJ Gunter… - Diabetes/metabolism …, 2009 - Wiley Online Library
SN Rajpathak, MJ Gunter, J Wylie‐Rosett, GYF Ho, RC Kaplan, R Muzumdar, TE Rohan…
Diabetes/metabolism research and reviews, 2009Wiley Online Library
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 …
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 β‐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.
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