GIP and Its Physiological and Pharmacological Effects

gip peptide

GIP is one of the incretins, a group of hormones that stimulate insulin secretion from pancreatic beta cells after a meal and inhibit glucagon release from the pancreatic alpha cells of the islets of Langerhans. Although the principal function of incretins such as GIP and glucagon-like peptide 1 (GLP-1) is insulinotropic, recent discoveries have uncovered a host of other physiological and pharmacological effects.

One example is the inhibition of adipose tissue inflammation by GIP and GLP-1. The peptides induce secretion of the adipokine resistin, which inhibits lipoprotein lipase in adipose tissues and increases the activity of AMP-activated protein kinase (AMPK). This reversal of inflammatory processes by incretins may contribute to their antiobesity effect.

GIP also stimulates bone formation through suppression of osteoclast apoptosis and facilitation of calcium deposition after meals. This role was confirmed in ovariectomy-induced osteoporosis-prone postmenopausal women, who have thinner bone trabeculae. GIP is also a potent regulator of appetite and satiety. Ovariectomy-induced obesity is prevented by the agonist GIP, and ovariectomy-induced hyperphagia is reversed by the agonists GIP and NPY.

GIP has recently been shown to have direct effects on adipose tissues, as indicated by the observation that chronic HFD feeding results in reduced fat accumulation in GIPR-deficient mice. It has been further established that GIP directly enhances fatty acid incorporation into adipocytes by binding to the GIPR receptor, stimulating secretion of the adipokine lipoprotein-associated triglyceride hydrolase LPL and increasing PI3K/AKT/PKB activity in adipocytes. Moreover, GIPR-dependent repression of p38 MAPK and inhibition of apoptosis in adipocytes by secreted resistin further accentuates this metabolic antiobesity effect of GIPR.


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