ABSTRACT
The concept that signals arising from the gut have the ability to affect endocrine responses and the disposal of carbohydrates has a long history that has classically centered around the modulation of insulin secretion. The term enteroinsular axis was coined to embrace all those factors that contributed to enhance insulin secretion after a meal, and the putative gut hormones were called incretins. Glucose-dependent insulinotropic polypeptide (GIP) was isolated from porcine intestine in 1969, and, initially characterized for its ability to inhibit gastric-acid secretion, was named gastric-inhibitory polypeptide. The relative importance of GIP and Glucagon-like peptide-1 in stimulating insulin secretion in healthy human subjects is difficult to resolve. The importance of the enteroinsular axis in healthy individuals gave rise to the possibility that an incretin defect might be partially responsible for the metabolic abnormalities observed in type 2 diabetes.
