GIP (human)
(Synonyms: 抑胃肽; Gastric Inhibitory Peptide (GIP), human) 目录号 : GC17838
胃抑制多肽，也称为葡萄糖依赖性促胰岛素多肽 (GIP)，是一种由 42 个氨基酸组成的肽，在维持葡萄糖和脂质稳态方面发挥着重要作用。
Cas No.:100040-31-1
Sample solution is provided at 25 µL, 10mM.
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Gastric inhibitory polypeptide, also known as glucose-dependent insulinotropic polypeptide (GIP), is a 42-amino acid peptide that plays an important role in maintaining glucose and lipid homeostasis. Although originally discovered as an inhibitor of gastric acid secretion, its principal physiological property is its role as an incretin peptide, in which it mediates the enteroinsular axis. GIP is synthesized by enteroendocrine K-cells of the duodenum/proximal jejunum, and its secretion is stimulated postprandially. GIP signaling stimulates glucose absorption in enterocytes, potentiates endogenous glucose-dependent insulin release from islet beta-cells, increases glucose uptake while inhibiting lipolysis in adipocytes, increases nutrient uptake into bone, and inhibits bone resorption [1].
The competition binding experiments were carried out in transiently transfected COS-7 cells using 125I GIP as radioligand. For the homologous competition binding, an IC50 value of 5.2 nM was observed [2]. GIP receptor messenger RNA was detected by RT-PCR and RNase protection assay. Receptors were detected in binding studies (IC50 26.7 +/- 0.7 nM). GIP stimulated glycerol release with an EC50 of 3.28 +/- 0.63 nM [3].
Perfusion of the pancreas with 1 nM GIP increased insulin secretion significantly (P[2]. The effects of GIP on fat metabolism in vivo may depend upon the circulating insulin level, and that meal-released GIP may elevate circulating fatty acids, thus optimizing pancreatic β-cell responsiveness to stimulation by glucose and GIP [3].
References:
[1].Zhang CY, Boylan MO, Arakawa H, Wolfe MM. Effects of gastric inhibitory polypeptide (GIP) immunoneutralization on mouse motor coordination and memory. Peptides. 2020 Mar;125:170227.
[2].Deacon CF, Plamboeck A, Rosenkilde MM, de Heer J, Holst JJ. GIP-(3-42) does not antagonize insulinotropic effects of GIP at physiological concentrations. Am J Physiol Endocrinol Metab. 2006 Sep;291(3):E468-75.
[3].McIntosh CH, Bremsak I, Lynn FC, Gill R, Hinke SA, Gelling R, Nian C, McKnight G, Jaspers S, Pederson RA. Glucose-dependent insulinotropic polypeptide stimulation of lipolysis in differentiated 3T3-L1 cells: wortmannin-sensitive inhibition by insulin. Endocrinology. 1999 Jan;140(1):398-404.
胃抑制多肽,也称为葡萄糖依赖性促胰岛素多肽 (GIP),是一种由 42 个氨基酸组成的肽,在维持葡萄糖和脂质稳态方面发挥着重要作用。虽然最初被发现是胃酸分泌的抑制剂,但其主要生理特性是其作为肠促胰岛素肽的作用,在该肽中它介导肠岛叶轴。 GIP 由十二指肠/近端空肠的肠内分泌 K 细胞合成,其分泌在餐后受到刺激。 GIP 信号刺激肠细胞对葡萄糖的吸收,增强胰岛 β 细胞释放内源性葡萄糖依赖性胰岛素,增加葡萄糖摄取,同时抑制脂肪细胞的脂肪分解,增加骨骼对营养的摄取,并抑制骨吸收[1] .
竞争结合实验是在瞬时转染的 COS-7 细胞中进行的,使用 125I GIP 作为放射配体。对于同源竞争结合,观察到 IC50 值为 5.2 nM [2]。通过RT-PCR和RNase保护试验检测GIP受体信使RNA。在结合研究中检测到受体 (IC50 26.7 +/- 0.7 nM)。 GIP 刺激甘油释放,EC50 为 3.28 +/- 0.63 nM [3]。
用 1 nM GIP 灌注胰腺可显着增加胰岛素分泌（P[2]。GIP 对体内脂肪代谢的影响可能取决于循环中的胰岛素水平,而膳食释放的GIP 可能会增加循环脂肪酸,从而优化胰腺 β 细胞对葡萄糖和 GIP 刺激的反应性[3]。
| Kinase experiment [1]: | |
|
Preparation Method |
The cells were grown and transfected as described in GIP Receptor Signaling.125I labeled GIP was used as radioligand, and the competition binding analysis was performed on intact cells, seeded at a concentration of 50,000 cells/well, on the second day after transfection, the cells were incubated for 16 h at 4°C in 0.25 ml of buffer consisting of 25 mM Tris HCl, pH 7.4, and 5 mM MgCl2, using 15 pM 125I-GIP as radioligand. Increasing concentrations of unlabeled GIP, ranging from 10-11 to 10-6 M, were used as competitors. The competition binding was terminated by washing the cells once with 1 ml of binding buffer, and subsequently, the cells were lysed by the addition of 1 ml of lysis buffer (8 M carbamide, 3 M acetic acid, 2% Nonidet-P 40). The binding data were analyzed and IC50 values determined using nonlinear regression analysis. |
|
Reaction Conditions |
16 h at 4°C |
|
Applications |
For the homologous competition binding, IC50 value of GIP was observed to be 5.2 nM. |
| Cell experiment [2]: | |
|
Cell lines |
3T3-L1 cells |
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Preparation Method |
Following incubation of 3T3-L1 cells, for the time periods indicated in figure legends, GIP in the incubation medium were precipitated with 1/10 vol. of 7% (wt/vol) ZnSO4, incubated on ice for 10 min, and 1/5 vol. 0.1 m NaOH added at room temp. The mixture was centrifuged and the supernatant assayed for glycerol with an enzymatic assay. |
|
Reaction Conditions |
10 min |
|
Applications |
GIP stimulated glycerol release with an EC50 of 3.28 +/- 0.63 Nm. |
| Animal experiment [1]: | |
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Animal models |
Male Wistar rats (390–440 g, 12 wk old) |
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Preparation Method |
GIP was dissolved in 0.9% NaCl containing 1% HSA and infused into the arterial line with the use of a syringe pump to give final perfusate concentrations of 1 nM GIP. After a basal period, peptides were infused alone for 10-min periods separated by 15-min rest periods, during which time endocrine secretion returned to basal levels. |
|
Dosage form |
1 nM GIP |
|
Applications |
Perfusion of the pancreas with 1 nM GIP increased insulin secretion significantly (P<0.001) relative to basal secretion during perfusion with 10 mM glucose alone. |
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References: [1]. Deacon CF, Plamboeck A, Rosenkilde MM, de Heer J, Holst JJ. GIP-(3-42) does not antagonize insulinotropic effects of GIP at physiological concentrations. Am J Physiol Endocrinol Metab. 2006 Sep;291(3):E468-75. [2]. McIntosh CH, Bremsak I, Lynn FC, Gill R, Hinke SA, Gelling R, Nian C, McKnight G, Jaspers S, Pederson RA. Glucose-dependent insulinotropic polypeptide stimulation of lipolysis in differentiated 3T3-L1 cells: wortmannin-sensitive inhibition by insulin. Endocrinology. 1999 Jan;140(1):398-404. |
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| Cas No. | 100040-31-1 | SDF | |
| 别名 | 抑胃肽; Gastric Inhibitory Peptide (GIP), human | ||
| Canonical SMILES | CC[C@]([C@@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/C/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](N)([H])CC1=CC=C(O)C=C1)([H])C)([H])CCC(O)=O)([H])[C@@](O)([H])C)([H])CC2=CC=CC=C2)([H])[C@@](CC)([H])C) | ||
| 分子式 | C226H338N60O66S | 分子量 | 4983.58 |
| 溶解度 | Soluble to 1 mg/ml in water | 储存条件 | Desiccate at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.2007 mL | 1.0033 mL | 2.0066 mL |
| 5 mM | 0.0401 mL | 0.2007 mL | 0.4013 mL |
| 10 mM | 0.0201 mL | 0.1003 mL | 0.2007 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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