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New hope in the control of type 2 diabetes

New hope in the control of type 2 diabetes

In an article entitle, “Targeting VEGF-B as a novel treatment for insulin resistance and type 2 diabetes” published in Nature (490:426-4300 on 18th October, 2012, the results of the investigation by 15 authors headed by Ulf Eriksson reveal that the type 2 diabetes is caused by the excess lipid deposition in peripheral tissues impairing  insulin sensitivity and glucose uptake. Of relevance here is that a massive number of Type 2 diabetic patients are present in the population. A recent critical survey of the patients shows that VEGF-B controls endothelial uptake and transport of fatty acids in heart and skeletal muscle. The study has shown that reduced “VEGF-B signaling in mouse models of type 2 diabetes restores insulin sensitivity and improves glucose tolerance.” The investigators have further demonstrated that if  Genetic deletion of Vegfb in diabetic db/db mice prevented ectopic lipid deposition thereby enhancing uptake of muscle glucose and maintaining normoglycaemia.  Furthermore, they showed administration to db/db mice a) enhanced glucose tolerance, b) preserved pancreatic islet architecture, c) improved β-cell function and d) ameliorated dyslipidaemia, key elements of type 2 diabetes and the metabolic syndrome. The potential use of VEGF-B neutralization in type 2 diabetes was further elucidated in rats fed a high-fat diet, in which it normalized insulin sensitivity and increased glucose uptake in skeletal muscle and heart. The  results reported by the above group  have demonstrated that the VEGF-B can function as an efficient barrier to excess muscle lipid uptake even under conditions of severe obesity and type 2 diabetes, and that this barrier can be maintained by inhibition of VEGF-B signalling.  The authors propose that VEGF-B antagonism represents   a novel pharmacological approach for type 2 diabetes, targeting the lipid-transport properties of the endothelium to improve muscle insulin sensitivity and glucose disposal.

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