Another noteworthy mechanism delaying the developmental programming of obesity and insulin metabolism impairment in the offspring of obese mothers is the inhibition of dipeptidyl peptidase IV (DPPIV), a ubiquitous enzyme that acts on incretin hormones, mainly GLP-1 and gastric inhibitory peptide, which maintain glucose homeostasis by increasing insulin secretion and decreasing glucagon secretion [72]. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.