Human GLP-1 (7-36) ELISA Kit, Fluorescent

Product details

GLP-1 (7-36) in vitro CatchPoint SimpleStep ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for the quantitative measurement of GLP-1 (7-36) protein in human serum, plasma, and cell culture supernatants.

This CatchPoint SimpleStep ELISA kit has been optimized for Molecular Devices Microplate Readers. Click here for a list of recommended Microplate Readers.
If using a Molecular Devices' plate reader supported by SoftMax® Pro software, a preconfigured protocol for these CatchPoint SimpleStep ELISA Kits is available with all the protocol and analysis settings at www.softmaxpro.org.

The CatchPoint SimpleStep ELISA employs an affinity tag labeled capture antibody and a reporter conjugated detector antibody which immunocapture the sample analyte in solution. This entire complex (capture antibody/analyte/detector antibody) is in turn immobilized via immunoaffinity of an anti-tag antibody coating the well. To perform the assay, samples or standards are added to the wells, followed by the antibody mix. After incubation, the wells are washed to remove unbound material. CatchPoint HRP Development Solution containing the Stoplight Red Substrate is added. During incubation, the substrate is catalyzed by HRP generating a fluorescent product. Signal is generated proportionally to the amount of bound analyte and the intensity is measured in a fluorescence plater reader at 530/570/590 nm Excitation/Cutoff/Emission.

GLP-1 (Glucagon like peptide 1) is part of the group of incretin hormones that are secreted by the gastrointestinal tract in response to food intake to assist glucose stimulated insulin secretion and glucagon suppression. GLP-1 is a 30 aminoacid peptide cleaved from proglucagon and released by the L-cells of the distal ileum. The intracellular precursor of GLP-1 (1-37) is cleaved to form the active peptides GLP-1 (7-37) and GLP-1 (7-36)NH₂. The active peptides bind to the GLP-1 receptor (GLP-1r) expressed in the pancreatic beta cell and are quickly metabolized by the enzyme dipeptidyl peptidase IV (DPP-IV) to form the peptide GLP-1 (9-36), which has no insulin stimulating activity. Binding of active GLP-1 to the receptor, increases cAMP levels and potentiates insulin secretion via Protein Kinase A (PKA) and the cAMP-regulated nucleotide exchange factor (Epac2). GLP-1 and its receptor are also suggested to play a role in the central nervous systems as mediators of satiety. Intracerebroventricular GLP-1 has been shown to induce c-FOS activity in the hypothalamus and the central nucleus of the amygdala, both of which are important in the regulation of appetite.

The role of GLP-1 in chronic diseases is controversial. Patients with type-II diabetes as well as morbidly obese subjects have been shown to have lower secretion of post-prandial GLP-1, which improves with treatment or weight loss. Due to the beneficial effects of active GLP-1 as well as GLP-1r agonists in metabolic diseases, GLP-1 has been proposed to be an effective therapeutic approach to lowering glycemic levels and decreasing body fat content. Furthermore, GLP-1 has been found to be cardioprotective during acute myocardial infarction. In contrast with the GLP-1 protective findings, circulating GLP-1 has also been found to positively correlate with serum triclycerides and high levels are significantly associated with coronary plaque burden in patients receiving coronary CT-angiography.