Diabetes and obesity are both increasing dramatically in the United States of America and other parts of the world. One third of the American population (34%) are obese (BMI >30 kg/m2). Eleven percent of the population over 20 years of age have type 2 diabetes. Significant increases are predicted by 2050, which is significant because both diabetes and obesity are independent risk factors for hosts of other diseases, as well as risk factors for each other. These conditions constitute major sources of morbidity and mortality, as well as financial loss through impairment of abilities to work, and by creating and exaggerating disease leading to increased expense of healthcare, and increased need in frequency of healthcare. T-Bet Transcription Factor is one mechanism linking both diabetes and obesity interaction. Particular T-Bet genotypes result in varied body-type (mass/obesity) to insulin sensitivity profiles. Lipotoxicity is another linking factor between obesity and type 2 diabetes mellitus. Visceral adiposity accelerates development of insulin resistance by causing chronic increase in fatty acids in circulation, causing reduction in usage of glucose as a cellular energy source. Central obesity is particularly disposing to this kind of insulin resistance development. Cytokine, adipokines including tumor necrosis factor, IL-6, resisitin, retinol binding protein 4 and others are linked in development of insulin resistance as well. Mitochondrial dysfunction has also been identified as a factor in the correlation between these 2 diseases. Causal genes such as PPARG, KCNJ11, melanocortin-4 gene, TCF7L2 variants and others are also implicated and are actively being investigated further to elucidate complexities of these mechanisms and allow for therapeutic interventional opportunities in the future.
Key words: Diabetes, Obesity, Lipotoxicity, Insulin Resistance
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