Their postprandial rise in circulation is blunted in obesity but hyperstimulated postsurgically, so it is reasonable to hypothesize that a RYGB-induced lowering of plasma BCAAs, one of the culprits that impair glucose metabolism and insulin sensitivity, is in part attributable to enhanced GLP-1 and/or PYY signaling. Here, INS is linked to obesity due to melanocortin 4 receptor deficiency.