Observations that augmentation of muscular fatty acyl-CoA in obese Zucker rats was much higher than that of ACBD1 and that long-chain acyl-CoA esters activated ATP-sensitive potassium channels inhibiting β-cell excitability obviously implicated ACB-containing proteins in the development of obesity and diabetes [31], [32]. The gene discussed is DBI; the disease is obesity due to melanocortin 4 receptor deficiency.