Gastric inhibitory polypeptide

Source: Wikipedia, the free encyclopedia.
(Redirected from
Glucose-dependent insulinotropic polypeptide
)
GIP
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_004123

NM_008119

RefSeq (protein)

NP_004114

NP_032145

Location (UCSC)Chr 17: 48.96 – 48.97 MbChr 11: 95.92 – 95.92 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Gastric inhibitory polypeptide (GIP), also known as glucose-dependent insulinotropic polypeptide is an inhibiting hormone of the secretin family of hormones.[5] While it is a weak inhibitor of gastric acid secretion, its main role, being an incretin, is to stimulate insulin secretion.[6]

GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins,[7] which stimulate insulin release on oral food intake.

Synthesis and transport

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.[8]

Like all

hormones
, it is transported by blood.

.

Functions

It has traditionally been named gastrointestinal inhibitory peptide or gastric inhibitory peptide and was found to decrease the secretion of

stomach acid[9] to protect the small intestine from acid damage, reduce the rate at which food is transferred through the stomach, and inhibit the GI motility and secretion of acid. However, this is incorrect, as it was discovered that these effects are achieved only with higher-than-normal physiological level, and that these results naturally occur in the body through a similar hormone, secretin.[10]

It is now believed that the function of GIP is to induce

hyperosmolarity of glucose in the duodenum.[11] After this discovery, some researchers prefer the 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.[12]

In addition to its role as an 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. 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.[13]

GIP recently appeared as a major player in bone remodeling. Researchers at Universities of Angers and Ulster evidenced that genetic ablation of the GIP receptor in mice resulted in profound alterations of bone microarchitecture through modification of the adipokine network.[14] Furthermore, the deficiency in GIP receptors has also been associated in mice with a dramatic decrease in bone quality and a subsequent increase in fracture risk.[15] However, the results obtained by these groups are far from conclusive because their animal models give discordant answers and these works should be analysed very carefully.[citation needed]

Pathology

It has been found that

knockout mice, it was found that absence of the GIP receptors correlates with resistance to obesity.[17]

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000159224Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000014351Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. S2CID 39547553
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  14. S2CID 36280105. Archived from the original
    (PDF) on 2018-07-21. Retrieved 2018-11-20.
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External links