In subject area: Medicine and Dentistry
Gastric inhibitory polypeptide (GIP) is defined as a key regulator of postprandial glucose metabolism. It is also known as glucose-dependent insulinotropic polypeptide.
AI generated definition based on: Best Practice & Research Clinical Endocrinology & Metabolism, 2004
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2010, Endocrinology (Sixth Edition) Shahrad Taheri, ... Stephen R. Bloom
Gastric inhibitory polypeptide (GIP), also called glucose-dependent insulinotropic polypeptide, is a 42-amino-acid peptide secreted by mucosal K cells, predominantly found in the duodenum and jejunum and to a lesser extent in the ileum and colon. GIP is released into the circulation following a mixed meal and also ingestion of glucose, fat, or amino acids. Fat ingestion appears to be a more potent stimulator of GIP secretion than carbohydrate in humans. The peak concentrations are achieved after 30 to 60 minutes, although this is delayed up to 2 hours following fat ingestion. GIP is cleaved by the enzyme dipeptidyl peptidase IV (DPP-IV), which also hydrolyses glucagon-like peptide 1 (GLP-1) and peptide histidine methionine.
There are conflicting results regarding the role of GIP as a physiologic enterogasterone, but an important action of GIP is its glucoincretin role.15 The GIP response is absent and insulin response blunted in patients with the outdated jejunoileal bypass for morbid obesity. GIP has been implicated in the disordered insulin secretion of several diseases, including chronic pancreatitis, cirrhosis, and Turner's syndrome. Secretion of GIP is enhanced in type 2 diabetes mellitus, but unlike GLP-1, there is little response to exogenous GIP. GIP has been reported to act on adipose tissue and may have an important role in lipid metabolism.16 It enhances fatty acid synthesis, lipoprotein lipase activity, and incorporation of free fatty acids into triglycerides. Several case reports of ACTH-independent, but food-dependent, Cushing's syndrome have suggested that GIP may stimulate adrenal corticosteroid secretion through GIP receptors.17,18 GIP may also have a role in body weight regulation.
2004, Best Practice & Research Clinical Endocrinology & Metabolism Juris J. Meier MD, Michael A. Nauck MD, PhD
Expression of the human GIP gene is controlled by a promoter containing a TATA box (TATAAGG) 28 bp upstream of the putative transcriptional start site. In addition, there are an ‘enhancer core element’ (at position −138) and two CAAT boxes (CCAAT at position −156 and CAAAT at position −169). The GIP promotor contains consensus sequences for an AP-1 and cAMP response elements.22 The expression of the GIP gene may be regulated by nutrients. GIP mRNA increases with oral glucose and lipid loads in rats.23
1988, Advances in Metabolic Disorders W. Creutzfeldt, R. Ebert
In 1970, Brown and Pederson postulated the existence of a polypeptide in porcine duodenojejunal extracts that inhibited motor activity as well as acid and pepsin secretion by the canine stomach. Subsequent purification from impure CCK preparations revealed that this factor is a straight-chain polypeptide with 42 amino acids (Jörnvall et al., 1981). The factor was named gastric inhibitory polypeptide (GIP). By comparison with known gastrointestinal peptides
