WordNet

a substance that retards or stops an activity
relating to or involving the stomach; "gastric ulcer" (同)stomachic, stomachal
restrictive of action; "a repressive regime"; "an overly strict and inhibiting discipline" (同)repressive, repressing
a peptide containing 10 to more than 100 amino acids

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抑制する人(物) / 化学反応抑制剤
胃の,胃に発生する

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/08/26 14:16:42」(JST)

wiki en

Gastric inhibitory polypeptide (GIP), also known as the glucose-dependent insulinotropic peptide, is an inhibiting hormone 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.^[3]

Like all endocrine hormones, it is transported by blood.

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

Functions

It has traditionally been named gastrointestinal inhibitory peptide or gastric inhibitory peptide and was found to decrease the secretion of stomach acid^[4] 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.

It is now believed that the function of GIP is to induce insulin secretion, which is stimulated primarily by hyperosmolarity of glucose in the duodenum.^[5] 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.^[6]

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 been demonstrated in humans only at approx 10 days of age. With 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, as a consequence, difficult to demonstrate physiological or clinical effects. In comparison to insulin its effects are very subtle.

GIP recently appeared as a major player in bone remodelling. 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.^[7] 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.^[8]

Pathology

It has been found that Type 2 diabetics are not responsive to GIP and have lower levels of GIP secretion after a meal when compared to non-diabetics.^[9] In research involving knockout mice, it was found that absence of the GIP receptors correlates with resistance to obesity.^[10]

References

^ Meier JJ, Nauck MA (2005). "Glucagon-like peptide 1(GLP-1) in biology and pathology". Diabetes/Metabolism Research and Reviews. 21 (2): 91–117. doi:10.1002/dmrr.538. PMID 15759282.
^ Efendic S, Portwood N (2004). "Overview of incretin hormones". Hormone and Metabolic Research. 36 (11-12): 742–6. doi:10.1055/s-2004-826157. PMID 15655702.
^ Costanzo, Linda (2014). Physiology. Philadelphia, PA: Saunders/Elsevier. p. 337. ISBN 9781455708475.
^ Kim W, Egan JM (Dec 2008). "The role of incretins in glucose homeostasis and diabetes treatment". Pharmacological Reviews. 60 (4): 470–512. doi:10.1124/pr.108.000604. PMC 2696340. PMID 19074620.
^ Thorens B (Dec 1995). "Glucagon-like peptide-1 and control of insulin secretion". Diabète & Métabolisme. 21 (5): 311–8. PMID 8586147.
^ Boron WF, Boulpaep EL (2009). Medical physiology: a cellular and molecular approach (2nd International ed.). Philadelphia, PA: Saunders/Elsevier. ISBN 9781416031154.
^ Gaudin-Audrain C, Irwin N, Mansur S, Flatt PR, Thorens B, Baslé M, Chappard D, Mabilleau G (Mar 2013). "Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice". Bone. 53 (1): 221–30. doi:10.1016/j.bone.2012.11.039. PMID 23220186.
^ Mieczkowska A, Irwin N, Flatt PR, Chappard D, Mabilleau G (Oct 2013). "Glucose-dependent insulinotropic polypeptide (GIP) receptor deletion leads to reduced bone strength and quality". Bone. 56 (2): 337–42. doi:10.1016/j.bone.2013.07.003. PMID 23851294.
^ Skrha J, Hilgertová J, Jarolímková M, Kunešová M, Hill M (2010). "Meal test for glucose-dependent insulinotropic peptide (GIP) in obese and type 2 diabetic patients". Physiological Research. 59 (5): 749–55. PMID 20406045.
^ Yamada Y, Seino Y (2004). "Physiology of GIP--a lesson from GIP receptor knockout mice". Hormone and Metabolic Research. 36 (11-12): 771–4. doi:10.1055/s-2004-826162. PMID 15655707.

External links

Gastric inhibitory polypeptide at the US National Library of Medicine Medical Subject Headings (MeSH)
http://web.indstate.edu/thcme/mwking/peptide-hormones.html#gastrin

UpToDate Contents

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1. 健常者および疾患を有する患者における消化管ホルモンの概要 overview of gastrointestinal peptides in health and disease
2. 2型糖尿病治療のためのGlucagon-like peptide-1受容体拮抗剤 glucagon like peptide 1 receptor agonists for the treatment of type 2 diabetes mellitus
3. 2型糖尿病の治療のためのジペプチジルペプチダーゼ4（DPP-4）阻害剤 dipeptidyl peptidase 4 dpp 4 inhibitors for the treatment of type 2 diabetes mellitus
4. 原発性両側副腎皮質大結節性過形成によるクッシング症候群 cushings syndrome due to primary bilateral macronodular adrenal hyperplasia
5. 糖尿病の治療のためのアミリン類似体 amylin analogs for the treatment of diabetes mellitus

English Journal

Dual modulation of GIP and glucagon action by the low molecular weight compound 4-hydroxybenzoic acid 2-bromobenzylidene hydrazide.

Franklin ZJ, McDonnell B, Montgomery IA, Flatt PR, Irwin N.SourceSAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences, University of Ulster, Coleraine, UK.
Diabetes, obesity & metabolism.Diabetes Obes Metab.2011 Aug;13(8):742-9. doi: 10.1111/j.1463-1326.2011.01401.x.
AIM: The presence of functional gastric inhibitory polypeptide (GIP) receptors on adipocytes and knowledge that GIP plays a key role in fat deposition suggests a beneficial effect of GIP receptor antagonism in obesity and insulin resistance. GIP receptor antagonists studied to date are peptidic GIP
PMID 21418501

Metabolic characterization of volume overload heart failure due to aorto-caval fistula in rats.

Melenovsky V, Benes J, Skaroupkova P, Sedmera D, Strnad H, Kolar M, Vlcek C, Petrak J, Benes J Jr, Papousek F, Oliyarnyk O, Kazdova L, Cervenka L.SourceDepartment of Cardiology and Center for Cardiovascular Research, Institute for Clinical and Experimental Medicine-IKEM, Videnska 1958/9, Prague 4, 140 21, Czech Republic. vojtech.melenovsky@ikem.cz
Molecular and cellular biochemistry.Mol Cell Biochem.2011 Aug;354(1-2):83-96. Epub 2011 Apr 5.
Metabolic interactions between adipose tissue and the heart may play an active role in progression of heart failure (HF). The aim of the study was to examine changes in myocardial and adipose tissue metabolism and gene expression in a rat HF model induced by chronic volume overload. HF was induced b
PMID 21465236

Japanese Journal

The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice.

Ogawa Eiichi,Hosokawa Masaya,Harada Norio,Yamane Shunsuke,Hamasaki Akihiro,Toyoda Kentaro,Fujimoto Shimpei,Fujita Yoshihito,Fukuda Kazuhito,Tsukiyama Katsushi,Yamada Yuichiro,Seino Yutaka,Inagaki Nobuya
Biochemical and biophysical research communications 404(1), 115-120, 2011-01-07
… Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. … Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. …
NAID 120002737766

症例インクレチン関連薬が奏功した症例

藤田洋平,片岡隆太郎,藤木典隆 [他]
大阪府立急性期・総合医療センター医学雑誌 34(1), 51-53, 2011
NAID 40019212240

「胃抑制ペプチド」

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

　　[★]

英: gastric inhibitory peptide gastric inhibitory polypeptide GIP
同: 糖依存性インスリン放出ペプチド glucose-dependent insulin-releasing peptide
関: 消化管ホルモン、ホルモン

種類

分類

消化管ホルモン

性状

ポリペプチド 43aa

産生組織

十二指腸、空腸の粘膜(K細胞)

標的組織

受容体

作用

消化管内の糖・脂肪酸の存在によりインスリンの放出を刺激

GIP is sometimes called "glucose-dependent insulinotropic" peptide because it stimulates pancreatic insulin secretion in the presence of hyperglucemia.

胃酸抑制作用？(エンテロガストロン enterogastrone)　←　否定的

外分泌

↓：胃：胃酸分泌　←　上に書いてあることと違う・・・
↓：腸：腸液分泌抑制(QB CBT vol2 p.295)

内分泌

↑：膵：インスリン放出

分泌の調整

↑

脂肪酸、アミノ酸、経口グルコース投与

分子機構

臨床関連

生合成

「エンテロガストロン」

　　[★]

英: enterogastrone
関: 胃抑制ペプチド, gastric inhibitory polypeptide, GIP、胃酸分泌抑制ホルモン

小腸粘膜由来の消化管ホルモン;胃酸分泌抑制作用は疑問視

「GIP」

　　[★]

胃抑制ペプチド gastric inhibitory polypeptide
巨細胞間質性肺炎 giant cell interstitial pneumonia

「胃酸分泌抑制ホルモン」

　　[★]

英: gastric inhibitory polypeptide, enterogastrone
関: 胃酸分泌、胃酸

「胃抑制ポリペプチド」

　　[★]

英: gastric inhibitory polypeptide、GIP
関: 胃酸分泌抑制ホルモン

「inhibitor」

　　[★]

n.

阻害剤、阻害薬、抑制薬、抑制剤、(内在性物質について)インヒビター、抑制物質

関: blocker、depressant、suppressant

「inhibitory」

　　[★]

抑制性の、抑制的な、阻害性の

関: inhibiting、suppressive

「gastric」

　　[★]

adj.

胃の

関: gastro、stomach、ventriculi、ventriculus

「polypeptide」

　　[★]

n.

(化合物)ポリペプチド

関: peptide

[pmid15759282-1] Meier JJ, Nauck MA (2005). "Glucagon-like peptide 1(GLP-1) in biology and pathology". Diabetes/Metabolism Research and Reviews. 21 (2): 91–117. doi:10.1002/dmrr.538. PMID 15759282.

[pmid15655702-2] Efendic S, Portwood N (2004). "Overview of incretin hormones". Hormone and Metabolic Research. 36 (11-12): 742–6. doi:10.1055/s-2004-826157. PMID 15655702.

[3] Costanzo, Linda (2014). Physiology. Philadelphia, PA: Saunders/Elsevier. p. 337. ISBN 9781455708475.

[pmid19074620-4] Kim W, Egan JM (Dec 2008). "The role of incretins in glucose homeostasis and diabetes treatment". Pharmacological Reviews. 60 (4): 470–512. doi:10.1124/pr.108.000604. PMC 2696340. PMID 19074620.

[pmid8586147-5] Thorens B (Dec 1995). "Glucagon-like peptide-1 and control of insulin secretion". Diabète & Métabolisme. 21 (5): 311–8. PMID 8586147.

[6] Boron WF, Boulpaep EL (2009). Medical physiology: a cellular and molecular approach (2nd International ed.). Philadelphia, PA: Saunders/Elsevier. ISBN 9781416031154.

[pmid23220186-7] Gaudin-Audrain C, Irwin N, Mansur S, Flatt PR, Thorens B, Baslé M, Chappard D, Mabilleau G (Mar 2013). "Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice". Bone. 53 (1): 221–30. doi:10.1016/j.bone.2012.11.039. PMID 23220186.

[pmid23851294-8] Mieczkowska A, Irwin N, Flatt PR, Chappard D, Mabilleau G (Oct 2013). "Glucose-dependent insulinotropic polypeptide (GIP) receptor deletion leads to reduced bone strength and quality". Bone. 56 (2): 337–42. doi:10.1016/j.bone.2013.07.003. PMID 23851294.

[pmid20406045-9] Skrha J, Hilgertová J, Jarolímková M, Kunešová M, Hill M (2010). "Meal test for glucose-dependent insulinotropic peptide (GIP) in obese and type 2 diabetic patients". Physiological Research. 59 (5): 749–55. PMID 20406045.

[pmid15655707-10] Yamada Y, Seino Y (2004). "Physiology of GIP--a lesson from GIP receptor knockout mice". Hormone and Metabolic Research. 36 (11-12): 771–4. doi:10.1055/s-2004-826162. PMID 15655707.

リンク元	「胃抑制ペプチド」「エンテロガストロン」「GIP」「胃酸分泌抑制ホルモン」「胃抑制ポリペプチド」
関連記事	「inhibitor」「inhibitory」「gastric」「polypeptide」

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案内

gastric inhibitory polypeptide