Glucagon (1-29), bovine, human, porcine
(Synonyms: 胰高血糖素; Porcine glucagon) 目录号 : GP21258胰高血糖素是一种由 29 个氨基酸组成的肽，由胰腺 α 细胞分泌，以响应低血糖水平。
Cas No.:16941-32-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: 99.81%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Neutrophils |
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Preparation Method |
Neutrophils obtained treated with PDE-4 inhibitor rolipram (5 µM), glucagon (0.3-3 µM), or vehicle (DMSO 0.1% or medium, respectively) for 3h in vitro at 37 °C in a 5% CO2 atmosphere. |
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Reaction Conditions |
Glucagon (0.3-3 µM)) for 3h at 37 °C |
|
Applications |
Glucagon, at concentrations of 0.3 and 3 uM, inhibited the chemotactic response of neutrophils towards all chemoattractants tested. |
| Animal experiment [2]: | |
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Animal models |
Male A/J mice (18-20 g) |
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Preparation Method |
Aerosolized PBS and increasing methacholine concentrations were nebulized through an inlet of the individual chambers for 2.5 min, and Penh readings were recorded for 5 min following each nebulization. Penh averages were obtained at 1, 3 and 6 h after intranasal treatment with glucagon (1 µg/kg) or 0.9% NaCl sterile solution. |
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Dosage form |
Glucagon (1 µg/kg) for 1, 3 and 6 h |
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Applications |
While using the non-invasive barometric plethysmography,glucagon (1 µg/kg, i.n.) significantly inhibited methacholine-induced bronchospasm in mice. |
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References: [1]. Insuela DBR, Ferrero MR, et,al. Glucagon Reduces Neutrophil Migration and Increases Susceptibility to Sepsis in Diabetic Mice. Front Immunol. 2021 Jul 6;12:633540. doi: 10.3389/fimmu.2021.633540. PMID: 34295325; PMCID: PMC8290340. |
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Glucagon is a 29 amino acid peptide that is secreted from pancreatic α-cells in response to low levels of blood glucose[2]. The best-described effect of glucagon is its action on the liver, where it increases blood glucose through stimulation of gluconeogenesis and glycogenolysis [1]. The non-glycemic effects of glucagon include the regulation of food intake and satiety, lipid homeostasis, insulin secretion and energy expenditure[3].
Glucagon, at concentrations of 0.3 and 3 uM, inhibited the chemotactic response of neutrophils towards all chemoattractants tested[4]. Glucagon may promote insulin secretion in MIN6 cells by reducing the production of cGMP in MIN6 cells and increasing the proliferative activity of MIN6 islet β cell line[8]. Thyroxine and glucagon can significantly reduce the mRNA transcription and protein expression levels of HSPs under high temperature conditions[9].
While using the non-invasive barometric plethysmography,glucagon (1 µg/kg, i.n.) significantly inhibited methacholine-induced bronchospasm in mice[5]. The effects of intraperitoneal glucagon injections on intake of a palatable milk diet were tested in rats maintained with ad lib access to pelleted diet. Injections of 25--800 micrograms/kg glucagon administered at meal onset inhibited meal size by 17--36%, but did not affect the normal postprandial behavioral satiety sequence or elicit any behavioral signs of toxicity[6]. Hepatic portal infusion of 13.6 micrograms glucagon/meal reduced the size of spontaneous meals both early and late in the dark in neurally intact rats, but not in hepatic-vagotomized rats[7].
References:
[1]. Jiang G, Zhang BB. Glucagon and regulation of glucose metabolism. Am J Physiol Endocrinol Metab. 2003 Apr;284(4):E671-8. doi: 10.1152/ajpendo.00492.2002. PMID: 12626323.
[2]. Campbell JE, Drucker DJ. Islet α cells and glucagon--critical regulators of energy homeostasis. Nat Rev Endocrinol. 2015 Jun;11(6):329-38. doi: 10.1038/nrendo.2015.51. Epub 2015 Apr 7. PMID: 25850661.
[3]. Kleinert M, Sachs S,et,al. Glucagon Regulation of Energy Expenditure. Int J Mol Sci. 2019 Oct 30;20(21):5407. doi: 10.3390/ijms20215407. PMID: 31671603; PMCID: PMC6862306.
[4]. Insuela DBR, Ferrero MR, et,al. Glucagon Reduces Neutrophil Migration and Increases Susceptibility to Sepsis in Diabetic Mice. Front Immunol. 2021 Jul 6;12:633540. doi: 10.3389/fimmu.2021.633540. PMID: 34295325; PMCID: PMC8290340.
[5]. Insuela DB, Daleprane JB, et,al. Glucagon induces airway smooth muscle relaxation by nitric oxide and prostaglandin E?. J Endocrinol. 2015 Jun;225(3):205-17. doi: 10.1530/JOE-14-0648. PMID: 26021821.
[6]. Geary N, Smith GP. Pancreatic glucagon and postprandial satiety in the rat. Physiol Behav. 1982 Feb;28(2):313-22. doi: 10.1016/0031-9384(82)90081-6. PMID: 7079345.
[7]. Geary N, Le Sauter J, et,al. Glucagon acts in the liver to control spontaneous meal size in rats. Am J Physiol. 1993 Jan;264(1 Pt 2):R116-22. doi: 10.1152/ajpregu.1993.264.1.R116. PMID: 8430871.
[8].Wu Y Y. The effect of glucagon on insulin secretion in MIN6 cells and the effect of cGMP signaling pathway.2014. MA thesis, Shihezi University.
[9]. Cui Ruilian, et al." Effects of thyroxine and glucagon on heat shock protein expression in Bovine mammary epithelial cells cultured at high temperature in vitro." Chinese Journal of Agriculture 25.06(2010):173-177.
胰高血糖素是一种由 29 个氨基酸组成的肽，由胰腺 α-细胞分泌，以响应低血糖水平[2]。胰高血糖素最好的作用是它对肝脏的作用，它通过刺激糖异生和糖原分解来增加血糖[1]。胰高血糖素的非血糖作用包括调节食物摄入和饱腹感、脂质稳态、胰岛素分泌和能量消耗[3]。
胰高血糖素，浓度为 0.3 和 3 uM，抑制中性粒细胞对所有测试的趋化因子的趋化反应[4]。胰高血糖素可能通过减少MIN6细胞中cGMP的产生和增加MIN6胰岛的增殖活性来促进MIN6细胞的胰岛素分泌 β细胞系[8]。甲状腺素和胰高血糖素可显着降低高温条件下HSPs的mRNA转录和蛋白表达水平[9]。
在使用无创气压体积描记法时，胰高血糖素（1 µ ;g/kg, i.n.) 显着抑制乙酰甲胆碱诱导的小鼠支气管痉挛[5]。腹膜内注射胰高血糖素对可口牛奶饮食摄入量的影响在大鼠中进行了测试，大鼠可以随意食用颗粒饮食。在进餐开始时注射 25--800 微克/千克胰高血糖素可抑制进餐量 17--36%，但不影响正常的餐后饱腹行为序列或引起任何毒性行为迹象[6]。肝门静脉输注 13.6 微克胰高血糖素/餐可减少神经完整大鼠在黑暗中早期和晚期自发进食的量，但对肝迷走神经切断大鼠没有影响[7]。
| Cas No. | 16941-32-5 | SDF | |
| 别名 | 胰高血糖素; Porcine glucagon | ||
| 分子式 | C153H225N43O49S | 分子量 | 3482.75 |
| 溶解度 | H2O : 6.67 mg/mL; DMSO : 2.5 mg/mL | 储存条件 | Store at -20°C, protect from light, dry, sealed |
| 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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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.2871 mL | 1.4356 mL | 2.8713 mL |
| 5 mM | 0.0574 mL | 0.2871 mL | 0.5743 mL |
| 10 mM | 0.0287 mL | 0.1436 mL | 0.2871 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % 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，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Glucagon Receptor Signaling and Glucagon Resistance
Hundred years after the discovery of glucagon, its biology remains enigmatic. Accurate measurement of glucagon has been essential for uncovering its pathological hypersecretion that underlies various metabolic diseases including not only diabetes and liver diseases but also cancers (glucagonomas). The suggested key role of glucagon in the development of diabetes has been termed the bihormonal hypothesis. However, studying tissue-specific knockout of the glucagon receptor has revealed that the physiological role of glucagon may extend beyond blood-glucose regulation. Decades ago, animal and human studies reported an important role of glucagon in amino acid metabolism through ureagenesis. Using modern technologies such as metabolomic profiling, knowledge about the effects of glucagon on amino acid metabolism has been expanded and the mechanisms involved further delineated. Glucagon receptor antagonists have indirectly put focus on glucagon's potential role in lipid metabolism, as individuals treated with these antagonists showed dyslipidemia and increased hepatic fat. One emerging field in glucagon biology now seems to include the concept of hepatic glucagon resistance. Here, we discuss the roles of glucagon in glucose homeostasis, amino acid metabolism, and lipid metabolism and present speculations on the molecular pathways causing and associating with postulated hepatic glucagon resistance.
Glucagon Regulation of Energy Expenditure
Glucagon's ability to increase energy expenditure has been known for more than 60 years, yet the mechanisms underlining glucagon's thermogenic effect still remain largely elusive. Over the last years, significant efforts were directed to unravel the physiological and cellular underpinnings of how glucagon regulates energy expenditure. In this review, we summarize the current knowledge on how glucagon regulates systems metabolism with a special emphasis on its acute and chronic thermogenic effects.
Glucagon's Metabolic Action in Health and Disease
Discovered almost simultaneously with insulin, glucagon is a pleiotropic hormone with metabolic action that goes far beyond its classical role to increase blood glucose. Albeit best known for its ability to directly act on the liver to increase de novo glucose production and to inhibit glycogen breakdown, glucagon lowers body weight by decreasing food intake and by increasing metabolic rate. Glucagon further promotes lipolysis and lipid oxidation and has positive chronotropic and inotropic effects in the heart. Interestingly, recent decades have witnessed a remarkable renaissance of glucagon's biology with the acknowledgment that glucagon has pharmacological value beyond its classical use as rescue medication to treat severe hypoglycemia. In this article, we summarize the multifaceted nature of glucagon with a special focus on its hepatic action and discuss the pharmacological potential of either agonizing or antagonizing the glucagon receptor for health and disease. ? 2021 American Physiological Society. Compr Physiol 11:1759-1783, 2021.
THE ROLE OF GLUCAGON IN THE PATHOPHYSIOLOGY AND MANAGEMENT OF DIABETES
Objective: There is general recognition that insulin and glucagon are the main hormones involved in the pathophysiology of diabetes, but the role of glucagon in diabetes is complex and in some circumstances controversial. The increasing appreciation of the role of glucagon in currently used hypoglycemic agents and the ongoing development of glucagon-targeted therapies underscores glucagon's important contribution in optimizing diabetes management. The current review provides a background on glucagon physiology and pathophysiology and an update for investigators, endocrinologists, and other healthcare providers on glucagon-modulating therapies.
Methods: A literature review was conducted utilizing published literature in PubMed and AccessMedicine including the years 1922-2015 using the following key words: glucagon, bihormonal, diabetes mellitus, glucagon antagonists, glucagon-targeted therapies.
Results: Glucagon is a counterregulatory hormone that promotes hepatic glucose production, thus preventing hypoglycemia in normal physiology. In patients with diabetes mellitus, glucagon secretion may be unregulated, which contributes to problems with glucose homeostasis. Several of the most effective therapies for diabetes have been found to suppress glucagon secretion or action, which may contribute to their success. Additionally, glucagon-specific targeted therapies, such as glucagon receptor antagonists, are being studied at a basic and clinical level.
Conclusion: Glucagon plays an important role in contributing to hyperglycemia in patients with diabetes. Utilizing hypoglycemic agents that decrease glucagon secretion or inhibit glucagon action can help improve glycemic control, making these agents a valuable resource in diabetes therapy.
Glucagon
Despite its infrequent usage, glucagon is an important drug in the ED. It has both well established and less well established indications. This article reviews its role for the practising emergency physician.