This EIA kit is used for quantitative determination of rat/mouse/human GLP-1 in plasma samples. The kit is characterized by sensitive quantification and high specificity. In addition, it is not influenced by other constituents in samples. GLP-1 standard of this kit is a highly purified synthetic product.
Supplementary: Competitive
Applicable Sample: Plasma
Other: GLP-1 is a peptide hormone from the intestinal mucosa, which is produced from its precursor, proglucagon by post transnational processing. The mammalian proglucagon 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 feeding. 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 diabete.
All these approaches have shown remarkable efficacy in both experimental and clinicalstudies. The GLP-1-based therapy of type 2 diabetes, therefore, represents a new and attractive alternative.
Applicable Sample: Plasma
Other: GLP-1 is a peptide hormone from the intestinal mucosa, which is produced from its precursor, proglucagon by post transnational processing. The mammalian proglucagon 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 feeding. 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 diabete.
All these approaches have shown remarkable efficacy in both experimental and clinicalstudies. The GLP-1-based therapy of type 2 diabetes, therefore, represents a new and attractive alternative.
| Product Specifications | |
| Reactivity | Mouse, Rat, Human |
| Documents & Links for Glucagon-like Peptide 1 EIA Kit | |
| Datasheet | yii-yk160-ex_glucagonlike-peptide-1-eia-kit_datasheet.pdf |
| Vendor Page | Glucagon-like Peptide 1 EIA Kit at Cosmo Bio LTD |
| Documents & Links for Glucagon-like Peptide 1 EIA Kit | |
| Datasheet | yii-yk160-ex_glucagonlike-peptide-1-eia-kit_datasheet.pdf |
| Vendor Page | Glucagon-like Peptide 1 EIA Kit |
| Citations for Glucagon-like Peptide 1 EIA Kit – 1 Found |
| McDonald, Sarah D; Pesarchuk, Eric; Don-Wauchope, Andrew; El Zimaity, Hala; Holloway, Alison C. Adverse metabolic effects of a hypercaloric, high-fat diet in rodents precede observable changes in body weight. Nutrition Research (New York, N.y.). 2011;31(9):707-14. PubMed |