@article {10.3844/ajbsp.2012.87.98, article_type = {journal}, title = {Bioinformatics Analysis of Some Functional Genes and Proteins Involved in Obesity-Induced Type 2 Diabetes}, author = {Abdella, Ehab M. and Ahmed, Rasha R. and Ashour, Mohamed B. and Ahmed, Osama M. and Abu Zid, Sameh F. and Mahmoud, Ayman M.}, volume = {1}, year = {2013}, month = {May}, pages = {87-98}, doi = {10.3844/ajbsp.2012.87.98}, url = {https://thescipub.com/abstract/ajbsp.2012.87.98}, abstract = {The incidence of type-2 diabetes is rising rapidly worldwide, mainly because of the increase in the incidence of obesity, which is an important risk factor for this condition. Both obesity and type-2 diabetes are complex genetic traits but they also share some nongenetic risk factors. Differences among individuals in their susceptibility to both these conditions probably reflect their genetic constitutions. The dramatic improvements in genomic and bioinformatic resources are accelerating the pace of gene discovery. It is tempting to speculate the key susceptible genes/proteins that bridges diabetes mellitus and obesity. In this regard, we evaluated the role of several genes/proteins that are believed to be involved in the evolution of obesity associated diabetes through thorough literature search. Also we analyzed the data pertaining to genes of these proteins extracted from the databases that are available online for free access. The functional cDNA sequences of these genes/proteins are extracted from National Center for Biotechnology Information (NCBI) and Ensembl Genome Browser. Our bioinformatic analysis reports 21 genes as ominous link with obesity associated diabetes. Also this study indicated that, adipose tissue is now known to express and secrete a variety of metabolites, hormones and cytokines that have been implicated in the development of insulin resistance.This bioinformatic study will be useful for future studies towards therapeutic inventions of obesity associated type-2 diabetes.}, journal = {Current Research in Bioinformatics}, publisher = {Science Publications} }