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Gastric inhibitory polypeptide
Symbol GIP
Entrez 2695
HUGO 4270
OMIM 137240
RefSeq NM_004123
UniProt P09681
Other data
Locus Chr. 17 q21.3-q22

Gastric inhibitory polypeptide (GIP), also known as the glucose-dependent insulinotropic peptide is a member of the secretin family of hormones.[1]

GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins.[2]


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.

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 has traditionally been called gastrointestinal inhibitory peptide or gastric inhibitory peptide and was believed to neutralize stomach acid 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, it was discovered that these effects are only achieved with higher-than-normal physiological level, and that these results naturally occur in the body through a similar hormone, secretin.

It is now believed that the function of GIP is to induce insulin secretion, which is primarily stimulated by hyperosmolarity of glucose in the duodenum.[3] 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.

GIP is also thought to have significant effects on fatty acid metabolism through stimulation of lipoprotein lipase activity in adipocytes. GIP release has been demonstrated in the ruminant animal and may play a role in nutrient partitioning in milk production (lipid metabolism). GIP is secreted in response to the first maternal feed (colostrum) in goat kids - GIP being measured via umbilical vein before its closure. For ethical reasons GIP secretion has only been demonstrated in humans at approx 10 days of age. In respect to the role of GIP in lipid metabolism, supraphysiological levels have shown a lipogenic action, however the action of collagenase in experimental protocols is known to degrade GIP/ GIP receptors. GIP is part of the diffuse endocrine system and consequently difficult to demonstrate physiological or clinical effects. In comparison to insulin its effects are very subtle.


It has been found that Type 2 diabetics are not responsive to GIP. In a research involving knockout mice, it was found that absence of the GIP receptors correlates with resistance to obesity.[4]


  1. ^ Meier JJ, Nauck MA (2005). "Glucagon-like peptide 1(GLP-1) in biology and pathology". Diabetes Metab. Res. Rev. 21 (2): 91–117. doi:10.1002/dmrr.538. PMID 15759282.  
  2. ^ Efendic S, Portwood N (2004). "Overview of incretin hormones". Horm. Metab. Res. 36 (11-12): 742–6. doi:10.1055/s-2004-826157. PMID 15655702.  
  3. ^ Thorens B (1995). "Glucagon-like peptide-1 and control of insulin secretion". Diabète & métabolisme 21 (5): 311–8. PMID 8586147.  
  4. ^ Yamada Y, Seino Y (2004). "Physiology of GIP--a lesson from GIP receptor knockout mice". Horm. Metab. Res. 36 (11-12): 771–4. doi:10.1055/s-2004-826162. PMID 15655707.  

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