GIP promotes obesity pathogenesis through the following mechanisms: (1) enhancing postprandial energy storage via nutrient partitioning; (2) increasing lipoprotein lipase activity and regulating its release in adipose tissue through receptor binding, stimulating de novo lipogenesis and lipid storage; (3) facilitating free fatty acid re-esterification; and (4) enhancing intestinal nutrient absorption [51,52,53]. The gene discussed is LPL; the disease is obesity due to melanocortin 4 receptor deficiency.