Insulin(cattle) (Insulin from bovine pancreas)
(Synonyms: 牛胰岛素; Insulin from bovine pancreas) 目录号 : GC31303
胰岛素是一种由21个和30个氨基酸组成的激素蛋白质。
Cas No.:11070-73-8
Sample solution is provided at 25 µL, 10mM.
| Cell experiment [1]: | |
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Cell lines |
Myotubes cells (C2C12) |
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Preparation Method |
Serum-starved C2C12 cells were treated with the indicated concentrations of thapsigargin, tunicamycin,or SubAB to induct ER stress, for 12–24 h before stimulation with Bovine insulin for 15 min. Cell lysates were analyzed by Western blotting. |
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Reaction Conditions |
100 nM Insulin for 15min. |
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Applications |
24 hours after induction of ER stress, insulin-stimulated S473 phosphorylation of AKT was decreased in C2C12 cells exposed to all ER stress-inducing conditions. |
| Animal experiment [2]: | |
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Animal models |
Mice lacking insulin receptors in tanycytes (IR∆Tan mice) |
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Preparation Method |
IR∆Tan mice were fasted overnight for 16 h and anesthetized with ketamine/xylazine. Insulin was injected in the vena cava and animals were perfused at 5, 10, 20 at 30 min post injection as described below. |
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Dosage form |
0.5 IU/kg Insulin, intravenous(i.v.) injection |
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Applications |
Insulin treatment robustly induced AKT phosphorylation in tanycytes of control mice, and that this activation was largely diminished in tanycytes of IR∆Tan mice. |
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References: [1]. Brown M, Dainty S, et al. Endoplasmic reticulum stress causes insulin resistance by inhibiting delivery of newly synthesized insulin receptors to the cell surface. Mol Biol Cell. 2020 Nov 1;31(23):2597-2629. [2]. Porniece Kumar M, et al. Insulin signalling in tanycytes gates hypothalamic insulin uptake and regulation of AgRP neuron activity. Nat Metab. 2021 Dec;3(12):1662-1679. |
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Insulin is a hormonal protein consisting of two chains of 21 and 30 amino acids. Insulin acts on neurons and glial cells to regulate systemic glucose metabolism and feeding. Insulins(cattle) is a type of native insulins. Insulins(cattle) was used to treat patients presenting with diabetes mellitus[1].
Insulin signaling is initiated by binding of insulin to the insulin receptor, activation of the protein tyrosine kinase domain and tyrosine autophosphorylation of the insulin receptor, and extensive tyrosine phosphorylation of insulin receptor substrate (IRS) proteins, and phosphorylation of S473 in AKT[2]
Injected mice with insulin (i.v., 0.5 IU/ kg−1 body weight) and assessed phosphorylated AKT (pAKT) immunoreactivity in tanycytes. These analyses revealed that insulin treatment robustly induced AKT phosphorylation in tanycytes of control mice, and that this activation was largely diminished in tanycytes of IR∆Tan mice(mice lacking insulin receptors in tanycytes)[3]
References:
[1]. Adams GG, Meal A, Morgan PS, Alzahrani QE, Zobel H, Lithgo R, Kok MS, Besong DTM, Jiwani SI, Ballance S, Harding SE, Chayen N, Gillis RB. Characterisation of insulin analogues therapeutically available to patients. PLoS One. 2018 Mar 29;13(3):e0195010.
[2]. Brown M, Dainty S, et al. Endoplasmic reticulum stress causes insulin resistance by inhibiting delivery of newly synthesized insulin receptors to the cell surface. Mol Biol Cell. 2020 Nov 1;31(23):2597-2629.
[3]. Porniece Kumar M, et al. Insulin signalling in tanycytes gates hypothalamic insulin uptake and regulation of AgRP neuron activity. Nat Metab. 2021 Dec;3(12):1662-1679.
胰岛素是一种由21个和30个氨基酸组成的激素蛋白质。它作用于神经元和胶质细胞,调节全身葡萄糖代谢和进食。牛源胰岛素是一种天然的胰岛素类型,曾被用来治疗糖尿病患者[1]。
胰岛素信号传导是由胰岛素与胰岛素受体结合开始的,激活蛋白酪氨酸激酶区域和胰岛素受体的酪氨酸自磷酸化,并广泛磷酸化胰岛素受体底物（IRS）蛋白以及AKT中S473的磷酸化。
将胰岛素注射到小鼠体内（静脉注射,剂量为每千克体重0.5国际单位）,并评估坦氏细胞中磷酸化AKT（pAKT）的免疫反应性。这些分析显示,胰岛素治疗显著诱导了对照小鼠坦氏细胞中的AKT磷酸化,并且在IR∆Tan小鼠（缺乏坦氏细胞中的胰岛素受体）的坦氏细胞中,这种激活大部分减弱了。[3]
| Cas No. | 11070-73-8 | SDF | |
| 别名 | 牛胰岛素; Insulin from bovine pancreas | ||
| Canonical SMILES | Phe-Val-Asn-Gln-His-Leu-Cys-Gly-Ser-His-Leu-Val-Glu-Ala-Leu-Tyr-Leu-Val-Cys-Gly-Glu-Arg-Gly-Phe-Phe-Tyr-Thr-Pro-Lys-Ala. Gly-Ile-Val-Glu-Gln-Cys-Cys-Ala-Ser-Val-Cys-Ser-Leu-Tyr-Gln-Leu-Glu-Asn-Tyr-Cys-Asn (Disulfide bridge: Cys7-Cys7', Cys19-Cys20', Cys6' | ||
| 分子式 | C254H377N65O75S6 | 分子量 | 5733.49 |
| 溶解度 | Water : 12.5 mg/mL (2.18 mM; adjust pH to 2 with HCl and heat to 60°C) | 储存条件 | Store 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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| 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 | 0.1744 mL | 0.8721 mL | 1.7441 mL |
| 5 mM | 0.0349 mL | 0.1744 mL | 0.3488 mL |
| 10 mM | 0.0174 mL | 0.0872 mL | 0.1744 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。
Insulin: pancreatic secretion and adipocyte regulation
Insulin is the primary acute anabolic coordinator of nutrient partitioning. Hyperglycemia is the main stimulant of insulin secretion, but other nutrients such as specific amino acids, fatty acids, and ketoacids can potentiate pancreatic insulin release. Incretins are intestinal hormones with insulinotropic activity and are secreted in response to food ingestion, thus integrating diet chemical composition with the regulation of insulin release. In addition, prolactin is required for proper islet development, and it stimulates β-cell proliferation. Counterintuitively, bacterial components appear to signal insulin secretion. In vivo lipopolysaccharide infusion acutely increases circulating insulin, which is paradoxical as endotoxemia is a potent catabolic condition. Insulin is a potent anabolic orchestrator of nutrient partitioning, and this is particularly true in adipocytes. Insulin dictates lipid accretion in a dose-dependent manner during preadipocyte development in adipose tissue-derived stromal vascular cell culture. However, in vivo studies focused on insulin's role in regulating adipose tissue metabolism from growing, and market weight pigs are sometimes inconsistent, and this variability appears to be animal, age and depot dependent. Additionally, porcine adipose tissue synthesizes and secretes a number of adipokines (leptin, adiponectin, and so forth) that directly or indirectly influence insulin action. Therefore, because insulin has an enormous impact on agriculturally important phenotypes, it is critical to have a better understanding of how insulin homeostasis is governed.
Principles that govern the folding of protein chains
Is it dietary insulin?
In humans the primary trigger of insulin-specific immunity is a modified self-antigen, that is, dietary bovine insulin, which breaks neonatal tolerance to self-insulin. The immune response induced by bovine insulin spreads to react with human insulin. This primary immune response induced in the gut immune system is regulated by the mechanisms of oral tolerance. Genetic factors and environmental factors, such as the gut microflora, breast milk-derived factors, and enteral infections, control the development of oral tolerance. The age of host modifies the immune response to oral antigens because the permeability of the gut decreases with age and mucosal immune response, such as IgA response, develops with age. The factors that control the function of the gut immune system may either be protective from autoimmunity by supporting tolerance, or they may induce autoimmunity by abating tolerance to dietary insulin. There is accumulating evidence that the intestinal immune system is aberrant in children with type 1 diabetes (T1D). Intestinal immune activation and increased gut permeability are associated with T1D. These aberrancies may be responsible for the impaired control of tolerance to dietary insulin. Later in life, factors that activate insulin-specific immune cells derived from the gut may switch the response toward cytotoxic immunity. Viruses, which infect beta cells, may release autoantigens and potentiate their presentation by an infection-associated "danger signal." This kind of secondary immunization may cause functional changes in the dietary insulin primed immune cells, and lead to the infiltration of insulin-reactive T cells to the pancreatic islets.
Ontogeny of immunoreactive insulin in the fetal bovine pancreas
The aim of this study was to characterize the development of immunoreactive insulin (IRI) in the fetal bovine pancreas. Pancreatic IRI was acid extracted, and both pancreatic and serum IRI were quantitated by RIA. The amount of pancreatic IRI per wet tissue wt in first trimester fetuses was similar to that in the adult animal (8.2 +/- 0.7 and 5.9 +/- 1.7 U/g pancreas, respectively). IRI increased progressively during gestation, attaining 39.2 +/- 6.5 U/g pancreas in the third trimester, 7-fold higher than that in the adult. When pancreatic IRI concentrations were standardized for protein content of the extracts, a decrease was noted between the midsecond and third trimesters. This is most likely the result of dilution of the endocrine portion of the pancreas by the rapidly growing exocrine pancreas. IRI was also detectable in fetal sera from all three trimesters. In contrast to the profile for pancreatic concentrations of IRI, serum concentrations remained constant throughout gestation at approximately 20 microU/ml. Poly(A+)RNA was isolated from adult and fetal pancreata, and the relative levels of preproinsulin mRNA were assessed by DNA/RNA filter hybridization. There was a 2- to 3-fold increase in the relative level of preproinsulin mRNA in fetal pancreata between the first and second trimesters which was maintained through the third trimester. In the adult pancreas, preproinsulin mRNA levels were similar to those in the first trimester fetus. This profile for the ontogeny of pancreatic preproinsulin mRNA was similar to that for pancreatic IRI (units per pancreas) during fetal maturation. We conclude that in the bovine fetus: the endocrine pancreas synthesizes IRI during all three trimesters of development; pancreatic (units per g pancreas), but not serum, concentrations of IRI increase progressively as development proceeds; and the ontogeny of preproinsulin mRNA is paralleled by that of pancreatic IRI (units per pancreas).