Here are couple interesting articles. The web address is a third very long article.
Dunger D, Yuen K, Ong K.
University Department of Paediatrics, University of Cambridge, Cambridge, UK.
The effects of circulating insulin-like growth factor I (IGF-I) on glucose metabolism are well recognized. IGF-I is also important in maintaining beta-cell mass and regulating endogenous growth hormone (GH) levels. Low IGF-I levels could explain links between small birth size and the risk of developing type 2 diabetes mellitus in short, obese adults. In a recent prospective study, childhood insulin secretion was related to IGF-I levels and statural growth, whereas insulin sensitivity was related to early post-natal weight gain. Common genetic polymorphisms in the IGF1 gene have been linked to small birth size, post-natal growth and future diabetes risk, but these results have been inconsistent. Recent adult studies have demonstrated that lower baseline IGF-I levels predict the subsequent development of impaired glucose tolerance (IGT), type 2 diabetes and cardiovascular disease. Administration of low-dose GH therapy, at a dose that minimizes the lipolytic effects of GH and has the ability to increase IGF-I levels, enhances insulin sensitivity in young healthy adults and in GH-deficient adults and increases insulin secretion in individuals with IGT. Whether the administration of low-dose GH, recombinant " IGF-I or combined IGF-I/IGF-binding protein 3 therapy prevents future development of IGT or type 2 diabetes in high-risk normoglycaemic and GH-deficient individuals merits further long-term studies. Copyright 2004 S. Karger AG, Basel.
PMID: 15761241 [PubMed - in process]
Department of Medicine, UNC School of Medicine, Chapel Hill, NC 27599, USA.
[email protected]
Insulin-like growth factor I (IGF-I) has significant structural homology with insulin. IGF-I has been shown to bind to insulin receptors to stimulate glucose transport in fat and muscle, to inhibit hepatic glucose output and to lower blood glucose while simultaneously suppressing insulin secretion. However, the precise role of IGF-I in maintaining normal glucose homeostasis and insulin sensitivity is not well defined. Studies in patients with diabetes have shown that in insulin-deficient states, serum IGF-I concentrations are low and increase with insulin therapy. Similarly, administration of insulin via the portal vein results in optimization of plasma IGF-I concentrations. A patient with an IGF1 gene deletion was shown to have severe insulin resistance that improved with IGF-I therapy. Studies conducted in experimental animals have shown that if IGF-I synthesis by the liver is deleted, the animals become insulin-resistant, and this is improved when IGF-I is administered. Likewise, deletion of the IGF-I receptor in muscle in mice induces severe insulin resistance. Administration of IGF-I to patients with type 2 diabetes mellitus has been shown to result in an improvement in insulin sensitivity and a reduction in the requirement for exogenously administered insulin to maintain glucose homeostasis. A polymorphism in the IGF1 gene that has been shown to reduce serum IGF-I results in an increased prevalence of type 2 diabetes. Taken together, these findings support the conclusion that IGF-I is necessary for normal insulin sensitivity, and impairment of IGF-I synthesis results in a worsening state of insulin resistance. Copyright 2004 S. Karger AG, Basel.
PMID: 15761237 [PubMed - in process]
Hepatocyte Nuclear Factor-1{alpha} Modulates Pancreatic {beta}-Cell Growth by Regulating the Expression of Insulin-Like Growth Factor-1 in INS-1 Cells -- Yang et al. 51 (6): 1785 -- Diabetes
