Jan 01, 2013; Rwanda Medical Journal. http://www.bioline.org.br/abstract?id=rw13021&lang=en

Abstract

Mitochondrial dysfunction contributes significantly to the pathogenesis and progression of diabetes. This study assessed the role of mitochondrial dysfunction in diabetes onset and progression, identified the proteins that interact with UCP2 and evaluated their suitability as targets for novel antidiabetic drugs. Proteins interacting with UCP2 were predicted using STRING 9.0. Among the proteins identified as veritable targets for novel antidiabetic drugs are leptin (LEP), peroxisome proliferator-activated receptor gamma (PPARG), ghrelin/obestatinprepropeptide (GHRL), Neuropeptide Y (NPY), peroxisome proliferator-activated receptor gamma (PPARA), Adiponectin (ADIPOQ), peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PPARGCIA), ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP50), and forkhead box A2 (FOXA2). The E values were predicted using STRING version 9.0. The predicted interactions are satisfactory and are supported by text mining, occurrence, neighborhood, database, fusion, experimental, and co-expression data. Development of lead compounds against these targets will help to address the burden of diabetes and provide more effective and safer anti-diabetic medicines.
In summary, our findings indicate that molecules that interact with UCP2 are leptin (LEP), PPARG, GHRL, Neuropeptide Y, PPARA, ADIPOQ, PPARGCIA, ATP50, and FOXA2. Validation of these targets and development of lead compounds against the targets will give rise to novel anti-diabetic drugs that will be much more effective help to address the burden of diabetes and provide more effective and safer anti-diabetic medicines.