Fatty acid starvation of islet tissue triggered deficiency of glucose-stimulated insulin secretion, a progression quickly reversible by addition of exogenous free fatty acids (Stein et al., 1996). In contrast, elevated free fatty acid supply increased glucose-stimulated insulin secretion (Roduit et al., 2004); although if constantly in excess, mainly in involvement with elevated glucose, saturated free fatty acids can lessen insulin synthesis and secretion and stimulate beta cell apoptosis (Lee, 1994). Chronic exposure to elevated free fatty acid and glucose levels can result in glucolipotoxicity with basal hypersecretion of insulin and inhibition of glucose-stimulated insulin secretion at higher concentrations of glucose (Erion et al.,
Fatty acid starvation of islet tissue triggered deficiency of glucose-stimulated insulin secretion, a progression quickly reversible by addition of exogenous free fatty acids (Stein et al., 1996). In contrast, elevated free fatty acid supply increased glucose-stimulated insulin secretion (Roduit et al., 2004); although if constantly in excess, mainly in involvement with elevated glucose, saturated free fatty acids can lessen insulin synthesis and secretion and stimulate beta cell apoptosis (Lee, 1994). Chronic exposure to elevated free fatty acid and glucose levels can result in glucolipotoxicity with basal hypersecretion of insulin and inhibition of glucose-stimulated insulin secretion at higher concentrations of glucose (Erion et al.,