GIPR Products

Description

GIPR, or Gastric Inhibitory Polypeptide Receptor, mediates GIP-induced secretion of insulin by pancreatic islet beta cells after a meal. GIP is a gastrointestinal peptide hormone of 42 aa that is released from duodenal endocrine K cells after absorption of glucose or fat. Stimulation of the GIPR on pancreatic cells activates adenylyl cyclase and mitogen-activated protein kinase, resulting in increased insulin secretion. Mice with a targeted mutation of GIPR have higher blood glucose levels with impaired initial insulin response after oral glucose load. Analysis of GIPR knockout mice suggest that GIPR defects may contribute to the pathogenesis of diabetes and obesity. Ectopic expression of functional GIPR and its coupling to steroidogenesis has been suggested to be the main cause of food-dependent Cushing's syndrome. Two isoforms of GIPR are produced by alternative splicing. GIPR expression has been reported in human bone, fetal adrenal, and pancreas. Little expression has been identified in normal adult adrenal, but overexpression of GIPR has been observed in the adrenal in food-dependent Cushing's syndrome. GIPR expression has been identified in rat brain, heart, pancreas, and small intestine. ESTs have been isolated from colon libraries.

Bioinformatics

Entrez	25024 Rat 2696 Human
Uniprot	NP_000155 Human NP_000155.1 Human P48546 Human
Product By Gene ID	2696
Alternate Names	gastric inhibitory polypeptide receptor GIP-R Glucose-dependent insulinotropic polypeptide receptor MGC126722 PGQTL2

Research Areas for GIPR

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GPCR
Neuroscience

Related GIPR Blog Posts

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Inhibiting incretin GIP hormone activity in mouse and monkey models to combat obesity By Jamshed Arslan, Pharm. D., PhD. We live in a world where 39% of adults are overweight. Our meals trigger the secretion of various gut-derived metabolic hormones called incretins. Fats and carbohydrates in our die...    Read more.

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