The reduced suppression of FFAs during the OGTT in those with greater degrees of obesity indicates that, above a certain adiposity threshold, both lower responsiveness to insulin resulting in non-suppressed lipolysis and greater FFA release as well as reduced FFA clearance (not evaluated in this analysis) result in greater circulating FFA concentrations that create lipotoxic effects and alter glucose metabolism [26, 27]. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.