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Glucagon (19-29), human Sale

(Synonyms: H2N-Ala-Gln-Asp-Phe-Val-Gln-Trp-Leu-Met-Asn-Thr-OH ) 目录号 : GP10122

Glucagon (19-29), human 是一种有效的胰岛素分泌抑制剂。

Glucagon (19-29), human Chemical Structure

Cas No.:64790-15-4

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5mg
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实验参考方法

Animal experiment:

Rats[1]To test the effect of miniglucagon (Glucagon (19-29)) on stimulated insulin secretion, 8.3 mM glucose is perfused during the experiments, including a 45-min equilibration period, followed by miniglucagon (1, 10, 100, and 1,000 pM) perfused with or without 1 nM tGLP-1. To study the glucagon and miniglucagon secretion, the glucose concentration is switched from 11 to 3 mM after a 45-min stabilization period, and the peptides secreted are measured by radioimmunoassay[1].

References:

[1]. Dalle S, et al. Miniglucagon (glucagon 19-29), a potent and efficient inhibitor of secretagogue-induced insulin release through a Ca2+ pathway. J Biol Chem. 1999 Apr 16;274(16):10869-76.
[2]. Dalle S, et al. Miniglucagon (glucagon 19-29): a novel regulator of the pancreatic islet physiology. Diabetes. 2002 Feb;51(2):406-12.
[3]. Pavoine C, et al. Miniglucagon [glucagon-(19-29)] is a component of the positive inotropic effect of glucagon. Am J Physiol. 1991 May;260(5 Pt 1):C993-9.

产品描述

Glucagon(NH2-His-Ser-Gln-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Lys-Tyr-Leu-Asp-Ser-Arg-Arg-Ala-Gln-Asp-Phe-Val-Gln-Trp-Leu-Met-Asn-Thr-COOH) is a peptide  hormone, secreted by the pancreas, that raises blood glucose levels. Glucagon’s effect is opposite that of insulin, which lowers blood glucose levels. Miniglucagon (Glucagon 19–29) is a potent and efficient inhibitor of secretagogue-induced insulin release through a Ca2+ Pathway*. Miniglucagon is a novel local regulator of the pancreatic islet physiology.  Any abnormal inhibitory tone exerted by this peptide on the β-cell results in impaired insulin secretion, as observed in type 2 diabetes. Miniglucagon is a component of the positive inotropic effect of glucagon. Some evidence has shown that glucagon processing into miniglucagon may be essential for the positive inotropic effect of glucagon on heart contraction. 

References:
1. Reece J, Campbell N (2002). Biology. San Francisco: Benjamin Cummings. ISBN 0-8053-6624-5.
2. Stéphane Dalle, Ghislaine Fontés, Anne-Dominique Lajoix2, Laurence LeBrigand, René Gross, Gérard Ribes, Michel Dufour, Léo Barry, Dung LeNguyen and Dominique Bataille, Miniglucagon (Glucagon 19-29) A Novel Regulator of the Pancreatic Islet Physiology, doi:10.2337/diabetes.51.2.406Diabetes February 2002 vol. 51 no. 2406-412
3. Pavoine C, Brechler V, Kervan A, Blache Kervan, Le-Nguyen D, Laurent S, Bataille D, Pecker F (1991) Miniglucagon [glucagon-(19-29)] is a component of the positive inotropic effect of glucagon. Am J Physiol 260:C993–C999.

Chemical Properties

Cas No. 64790-15-4 SDF
别名 H2N-Ala-Gln-Asp-Phe-Val-Gln-Trp-Leu-Met-Asn-Thr-OH
化学名 Glucagon (19-29), human
Canonical SMILES CC(C)CC(C(=O)NC(CCSC)C(=O)NC(CC(=O)N)C(=O)NC(C(C)O)C(=O)O)NC(=O)C(CC1=CNC2=CC=CC=C21)NC(=O)C(CCC(=O)N)NC(=O)C(C(C)C)NC(=O)C(CC3=CC=CC=C3)NC(=O)C(CC(=O)O)NC(=O)C(CCC(=O)N)NC(=O)C(C)N
分子式 C61H89N15O18S 分子量 1352.51
溶解度 ≥ 135.2mg/mL in DMSO 储存条件 Store at -20°C
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溶解性数据

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1 mM 0.7394 mL 3.6968 mL 7.3937 mL
5 mM 0.1479 mL 0.7394 mL 1.4787 mL
10 mM 0.0739 mL 0.3697 mL 0.7394 mL
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Research Update

The forgotten members of the glucagon family

From proglucagon, at least six final biologically active peptides are produced by tissue-specific post-translational processing. While glucagon and GLP-1 are the subject of permanent studies, the four others are usually left in the shadow, in spite of their large biological interest. The present review is devoted to oxyntomodulin and miniglucagon, not forgetting glicentin, although much less is known about it. Oxyntomodulin (OXM) and glicentin are regulators of gastric acid and hydromineral intestinal secretions. OXM is also deeply involved in the control of food intake and energy expenditure, properties that make this peptide a credible treatment of obesity if the question of administration is solved, as for any peptide. Miniglucagon, the C-terminal undecapeptide of glucagon which results from a secondary processing of original nature, displays properties antagonistic to that of the mother-hormone glucagon: (a) it inhibits glucose-, glucagon- and GLP-1-stimulated insulin release at sub-picomolar concentrations, (b) it reduces the in vivo insulin response to glucose with no change in glycemia, (c) it displays insulin-like properties at the cellular level using only a part of the pathway used by insulin, making it a good basis for developing a pharmacological workaround of insulin resistance.

Effects on the hepatocyte [Ca2+]i oscillator of inhibition of the plasma membrane Ca2+ pump by carboxyeosin or glucagon-(19-29)

Single rat hepatocytes, microinjected with the Ca(2+)-sensitive photoprotein aequorin, respond to agonists acting through the phosphoinositide signalling pathway by the generation of oscillations in cytosolic free Ca2+ concentration ([Ca2+]i). The duration of [Ca2+]i transients generated is characteristic of the receptor species activated; the variability results in differences in the rate of fall of [Ca2+]i from its peak. It is conceivable that the plasma membrane Ca(2+)-ATPase (PM Ca2+ pump) may have an important role in the mechanism underlying agonist specificity. It has recently been shown that an esterified form of carboxyeosin, an inhibitor of the red cell PM Ca2+ pump, is suitable for use in whole cell studies. Glucagon-(19-29) (mini-glucagon) inhibits the Ca2+ pump in liver plasma membranes, mediated by Gs. We show here that carboxyeosin and mini-glucagon inhibit Ca2+ efflux from populations of intact rat hepatocytes. We show that carboxyeosin and mini-glucagon enhance the frequency of oscillations induced by Ca(2+)-mobilizing agonists in single hepatocytes, but do not affect the duration of individual transients. Furthermore, we demonstrate that inhibition of the hepatocyte PM Ca2+ pump enables the continued generation of [Ca2+]i oscillations for a prolonged period following the removal of extracellular Ca2+.

Development of pancreatic glucagon-specific radioimmunoassay with use of synthetic human glucagon (19-29) as immunogen

Production of antisera to des Asn28 Thr29 Homoser27-glucagon; the development of radioimmunoassay for total glucagon-like immunoreactivity in human plasma

Antisera having a strong and strictly constant cross-reactivity for gut-GLI were raised in seven rabbits immunized with immunogen, a conjugate of BSA and des-Asn28, Thr29, Homoser27 -glucagon (CNBr-glucagon). All of the anti-CNBr-glucagon sera exhibited titer and affinity for glucagon sufficiently high enough to develop a sensitive radioimmunoassay. The relative crossreactivity of the antisera to gut-GLI was comparable to that of antiserum K-4023 which strongly crossreacted with gut-GLI. One of the anti-CNBr-glucagon sera, OAL-196, did not react with the glucagon 19-29 fragment at all. The intra- and inter-assay coefficients of variation were 3.8-5.0 and 6.0-7.3%, respectively, in the radioimmunoassay system for total GLI in human plasma using OAL-196. The fasting plasma total GLI was 374 +/- 18 pg/ml. The plasma total GLI during 50 g oral glucose load in normal subjects increased significantly, whereas the plasma IRG level measured with the anti-glucagon 19-29 serum, OAL-123, assay system was lowered. In the gastrectomized subjects, plasma total GLI measured with the present assay system elicited a marked increase following an oral glucose load. These results suggest that the radioimmunoassay using anti-CNBr-glucagon sera will be useful in measuring plasma total GLI.

QUESTION 1: Can mini-glucagon be used to manage hypoglycaemia as an outpatient?