GLP-1 is a peptide hormone from the intestinal mucosa, which is produced from its precursor, proglucagon by post transnational processing. The mammalian proglucagon 1) is synthesized in the neuroendocrine L-cell of the intestine and the alpha-cells of the pancreas. It contains within its structure the sequences of glucagon and two glucagon-like peptides (GLP-1 and GLP-2) in tandem flanked at their amino and carboxyl termini by dibasic residues. GLP-1 is a 37 amino acids peptide and produced in the small intestine and in the pancreas in the human, in either C-terminal-amidated on glycine-extended form. GLP1 (7–36) amide and its receptor are present in several brain regions and may play a role in the physiological control of feeding4). Several reports have been presented as follows as to the biological activities of GLP-1. GLP-1 (7–37) and (7–36) amide is known as one of the most potent insulin secretagogues. GLP-1 (7–36) amide was supposed to improved glycemic control in patients with type 2 diabetes by increasing insulin secretion, by inhibiting glucagon secretion and by delaying gastric emptying rather than by altering extrapancreatic glucose metabolism. Intravenous GLP-1(7–37) and (7–36)amide could normalize fasting hyperglycaemia in type 2 diabetic patients. Hyperglycaemia during parenteral nutrition could be controlled by exogenous GLP-1, whereas the chronic therapy of type 2 diabetes required GLP-1 derivatives with longer duration of action. Recombinant GLP-1 (7–36) amide was recently shown to cause significant weight loss in type 2 diabetics when administered for 6 weeks as a continuous subcutaneous infusion, 5-day treatment of hereby obese human subjects with GLP-1 at high doses by prandial subcutaneous infusion promptly slowed gastric emptying as a probable mechanism of action of increased satiety, decreased hunger and reduced food intake with an ensuing weight loss. A G-protein-coupled receptor, GPR120, which is abundantly expressed in intestine, functions as a receptor for unsaturated long-chain FFAs (free fatty acids). The stimulation of GPR120 by FFAs promotes the secretion of GLP-1 in vitro (measured by YK160, Yanaihara Institute Inc) and in vivo, and increases circulation insulin, indicate that GPR120-mediated GLP-1 secretion induced by dietary FFAs is important in the treatment of diabetes. All these approaches have shown remarkable efficacy in both experimental and clinical studies. The GLP-1-based therapy of type 2 diabetes, therefore, represents a new and attractive alternative. Yanaihara Institute Inc. developed a quantitative EIA kit with high specificity and sensitivity (detection limit 0.206 ng/mL) for rat/mouse/human GLP-1 as a useful tool for these necessaries.
- References to Glucagon-Like Peptide-1 (GLP-1)