With lipid excess and/or impaired oxidation, as observed in obesity and/or inactivity, flux of long-chain acyl CoAs (LC-CoA) may be redirected into cytosolic lipid species such as diacylglycerols (DAG), triacylglycerols (TG) and ceramides (derivatives of sphingosine and fatty acid metabolism) [5] that are correlated with reductions in insulin signaling and insulin resistance [3], [21]–[23],[31]. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.