Table of Contents
Two gut hormones, glucagon like peptide GLP)-1 and glucose-dependent insulin-tropic polypeptide (GIP, gastric inhibitory polypeptide), act as incretins. GLP-1 is released by the direct actions of luminal food contents on the L cells in the distal jejunum and proximal ileum. New evidence suggests an additional mechanism via the gut-brain axis, involving lower- as well as upper-gut signals, which may activate GLP-1 release even before the luminal nutrients have reached the proximities of L cells. Ethnic differences in GLP-1 concentrations may be due to diet quality in terms of monosaccharides, glucose, fructose, polysaccharides, proteins, and fatty acids, among others. These nutrients may alter GLP-1 receptor responses to food intake and fasting. Novel glucose-lowering agents, the dipeptidyl-peptidase-4 (DPP-4) inhibitors, work by preventing the inactivation of incretin hormones GLP-1 and GIP. Increased degradation of GLP-1 via DPP-4 enzymes is hence an additional mechanism for altering GLP-1 concentrations. DPP-4 inhibitors, used to treat diabetes mellitus type 2, inhibit DPP-4 activity in peripheral plasma, which prevents the inactivation of GLP-1 in the peripheral circulation. The presence of GLP-1 receptors in various organs (heart, brain, liver, pancreas, kidney, muscle and bone) makes their activation possible, thereby offering protection to the related organs.
Keywords: Incretins, glyptins, gut hormones, glucose metabolism