GLP1R, a Glucagon Receptor, has been suggested to affect the feelings of satiety or hunger, sensation of glucose levels, control of glucagon sensitivity of islets, and non insulin-dependent diabetes mellitus. Glucagon-like peptide 1 is an incretin hormone produced by enteroendocrine L-cells in the intestinal mucosa. The hormone is released in response to food intake and plays an important role in maintaining blood glucose homeostasis. Stimulation of the GLP-1R by endogenous hormone induces multiple complementary mechanisms, which together result in a lowering of circulating blood glucose levels. These mechanisms include receptor-mediated enhancement of glucose-induced insulin secretion from pancreatic -cells, inhibition of gastric emptying with a delay in the gastrointestinal resorption of nutrients, inhibition of glucagon secretion, and inhibition of food intake. Desensitization of GLP1R on pancreatic beta-cells is one of the causes of non insulin-dependent diabetes mellitus (NIDDM). GLP1R knockout mice are viable, develop normally, but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. Recently it has been shown that overexpression of glucagon-like peptide-1 receptor improves learning in rats (During et al. 2003). GLP1R has been reported in pancreas, brain, heart, kidney, lung, and stomach. ESTs have been isolated from kidney and skin libraries.