The quickening pace of genetic discovery has resulted in the identification of more than 80 loci with proven roles in development of monogenic and multifactorial forms of nonautoimmune diabetes and obesity. Type 2 diabetes, though poorly understood, is known to be a disease characterized by an inadequate beta-cell response to the progressive insulin resistance that typically accompanies advancing age, inactivity, and weight gain. 1 The disease accounts for substantial morbidity and mortality from adverse effects on cardiovascular risk and disease-specific complications such as blindness and renal failure. 2 The increasing global prevalence of type 2 diabetes is tied to rising rates of obesity 2 — in part a consequence of social trends toward higher energy intake and reduced energy expenditure. However, the mechanisms that underlie individual differences in the predisposition to obesity remain obscure. . . .