Glucose-dependent insulinotropic polypeptide

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

It is 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.

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

Like GLP-1 it is released in response to the ingestion of nutrients and promotes insulin secretion by receptor binding on pancreatic beta cells.

GIP modulates glucagon by inhibiting its secretion in states of hyperglycemia and increases glucagon release in states of hypoglycemia.

Treatment with a glucose dependent insulinotropic polypeptide and a GLP-1 receptor agonist together will augment glucose lowering while providing defense against hypoglycemia.

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

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

it suppresses glucagon secretion during hyperglycemia, signals glucagon secretion during hypoglycemia, facilitates postprandial lipid clearance, and promotes satiety.

Incretin GIP is known to inhibit apoptosis of the pancreatic beta cells and to promote their proliferation.

It also stimulates glucagon secretion and fat accumulation. 

When added to basal insulin it demonstrates improved glycemic control in body weight loss without increasing the risk of hypoglycemia and reducing insulin requirements.

GIP receptors are expressed in many organs and tissues including the central nervous system enabling GIP to influence hippocampal memory formation and regulation of appetite and satiety.

GIP is a major player in bone remodeling.

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

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