Abstract
Obesity is a strong modifiable risk factor for type 2 diabetes (T2D). Although the association between the 2 conditions is well established, the interplay of organ-specific adiposity, hepatic and peripheral insulin resistance, pancreatic beta-cell mass and function, and onset and severity of T2D varies enormously between individuals. Importantly, variations in adiposity patterns between individuals of different races/ethnicities and baseline, and possible subsequent changes of pancreatic beta-cell mass and function point to a genetic predisposition in the pathophysiology of T2D [1,2].
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