MOA= promotes uptake (by muscle/fat)/storage of glucose and other ingested nutrients,, reduces glucose output from liver (stim enzymes for glycogen synthesis//inhib enzymes in glycogenolysis and gluconeogenesis)... ENHANCES STORAGE/DEC PRODUCTION
MOA= inc secretion of insulin from functioning pancreatic beta cells by binding to sulfonylurea receptor on the beta cell, leading to closure of ATP- dependent potassium channels, depolarization of the cell membrane, and opening of Ca2+ channels; inc intracellular Ca2+leads to increased insulin secretion
MOA= primary- agonists at the peroxisome proliferator-activated receptor- (PPAR-) located in the adipose tissue, skeletal muscle, and liver, results inc glucose uptake in tissues//Lead to inc insulin-sensitivity and dec insulin resistance
MOA= Reduce blood glucose concentrations by decreasing the rate of glucose abs, Delay the digestion of starch and disaccharides thru inhib of enzyme -glucosidase, located in brush border of intestinal tract that converts oligosaccharides/disaccharides to glucose and other monosaccharides
MOA= inhibit the enzyme DPP-4 from breaking down endogenous GLP-1 and GIP, glucose-dependent inc insulin secretion by pancreas, glucose-dependent glucagon secretion, inc uptake of glucose from blood by tissues, suppress appetite
MOA= Synthetic analogues of human GLP-1 → Glucose-dependent inc insulin secretion by the pancreas, Glucose-dependent dec glucagon secretion, dec gastric emptying, inc satiety