Gastric inhibitory polypeptide (GIP)

Gastric inhibitory polypeptide

Glucose-dependent insulinotropic polypeptide (GIP), also known as Gastric inhibitory polypeptide or gastric inhibitory peptide (also abbreviated as GIP), is an inhibiting hormone of the secretin family of hormones.

Gastric inhibitory peptide (GIP) is produced by the mucosal duodenal cells in response to chyme containing high amounts of carbohydrate, proteins, and fatty acids. 

Main function of GIP is to decrease gastric emptying.

It is is a weak inhibitor of gastric acid secretion.

Its main role is to stimulate insulin secretion.

Gene location Chromosome 17 

GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins.

GIP is derived from a 153-amino acid proprotein encoded by the GIP gene and circulates as a biologically active 42-amino acid peptide. 

It is synthesized by K cells, which are found in the mucosa of the duodenum and the jejunum of the gastrointestinal tract.

Like all endocrine hormones, it is transported by blood.

Gastric inhibitory polypeptide receptors are seven-transmembrane proteins found on beta-cells in the pancreas.

It decreases the secretion of stomach acid to protect the small intestine from acid damage, reduces the rate at which food is transferred through the stomach, and inhibit the GI motility and secretion of acid. 

The function of GIP is to induce insulin secretion, which is stimulated primarily by hyperosmolarity of glucose in the duodenum.

GIP”s new name of glucose-dependent insulinotropic peptide, while retaining the acronym GIP.

The amount of insulin secreted is greater when glucose is administered orally than intravenously.

GIP’s role is as an incretin, and it inhibit apoptosis of the pancreatic beta cells and to promote their proliferation, glucagon secretion and fat accumulation. 

GIP receptors are expressed in many organs and tissues including the central nervous system.

GIP influences hippocampal memory formation and regulation of appetite and satiety.

Type 2 diabetics are not responsive to GIP and have lower levels of GIP secretion after a meal when compared to non-diabetics.

GIP has fewer organ specific actions than GLP-1, but it may positively influence adipose tissue regulation of lipid storage, and it has direct activity in the CNS.

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