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GLP-1(32-36)amide Sale

目录号 : GC61540

GLP-1(32-36)amide,一种衍生自糖调节激素GLP-1的C末端的五肽。GLP-1(32-36)amide可抑制糖尿病小鼠的体重增加并调节全身葡萄糖代谢。

GLP-1(32-36)amide Chemical Structure

Cas No.:1417302-71-6

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5 mg
¥2,475.00
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10 mg
¥4,185.00
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产品描述

GLP-1(32-36)amide, a pentapeptide, derived from the C terminus of the glucoregulatory hormone GLP-1. GLP-1(32-36)amide could inhibit weight gain and modulate whole body glucose metabolism in diabetic mice[1][2].

GLP-1(32-36)amide (0.1-10 μM; 24 h) retains cell viability and decreases apoptosis against Streptozotocin (STZ; 1 μM) in INS‐1 cells[2]. Cell Viability Assay[2] Cell Line: INS‐1 cells

GLP-1(32-36)amide (1 μmol/kg; i.p. once daily for 21 d) protects islet from damage, inhibits weight gain, and relieves symptoms of polydipsia in diabetic mice[2].GLP-1(32-36)amide (1 μmol/kg; a single i.p.) slightly reduces the mean glucose lever at 30 min after the challenge of glucose in normal mice[2].GLP-1(32-36)amide (50-70 nmol/kg/d; infusion for 12-16 weeks) prevents the development of diet-induced obesity and hepatic steatosis in high fat-fed mice[3]. Animal Model: Male KM mice (6-8 weeks; 18-22 g) injected with STZ[2]

[1]. Elahi D, et, al. GLP-1(32-36)amide, a novel pentapeptide cleavage product of GLP-1, modulates whole body glucose metabolism in dogs. Peptides. 2014 Sep;59:20-4. [2]. Sun L, et, al. Novel Pentapeptide GLP-1 (32-36) Amide Inhibits β-Cell Apoptosis In Vitro and Improves Glucose Disposal in Streptozotocin-Induced Diabetic Mice. Chem Biol Drug Des. 2015 Dec;86(6):1482-90. [3]. Tomas E, et, al. GLP-1(32-36)amide Pentapeptide Increases Basal Energy Expenditure and Inhibits Weight Gain in Obese Mice. Diabetes. 2015 Jul;64(7):2409-19.

Chemical Properties

Cas No. 1417302-71-6 SDF
分子式 C25H50N10O5 分子量 570.73
溶解度 DMSO: 250 mg/mL (438.04 mM) 储存条件 Store at -20°C
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1 mM 1.7521 mL 8.7607 mL 17.5214 mL
5 mM 0.3504 mL 1.7521 mL 3.5043 mL
10 mM 0.1752 mL 0.8761 mL 1.7521 mL
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Research Update

GLP-1(32-36)amide Pentapeptide Increases Basal Energy Expenditure and Inhibits Weight Gain in Obese Mice

Diabetes 2015 Jul;64(7):2409-19.PMID:25858562DOI:10.2337/db14-1708.

The prevalence of obesity-related diabetes is increasing worldwide. Here we report the identification of a pentapeptide, GLP-1(32-36)amide (LVKGRamide), derived from the glucoincretin hormone GLP-1, that increases basal energy expenditure and curtails the development of obesity, insulin resistance, diabetes, and hepatic steatosis in diet-induced obese mice. The pentapeptide inhibited weight gain, reduced fat mass without change in energy intake, and increased basal energy expenditure independent of physical activity. Analyses of tissues from peptide-treated mice reveal increased expression of UCP-1 and UCP-3 in brown adipose tissue and increased UCP-3 and inhibition of acetyl-CoA carboxylase in skeletal muscle, findings consistent with increased fatty acid oxidation and thermogenesis. In palmitate-treated C2C12 skeletal myotubes, GLP-1(32-36)amide activated AMPK and inhibited acetyl-CoA carboxylase, suggesting activation of fat metabolism in response to energy depletion. By mass spectroscopy, the pentapeptide is rapidly formed from GLP-1(9-36)amide, the major form of GLP-1 in the circulation of mice. These findings suggest that the reported insulin-like actions of GLP-1 receptor agonists that occur independently of the GLP-1 receptor might be mediated by the pentapeptide, and the previously reported nonapeptide (FIAWLVKGRamide). We propose that by increasing basal energy expenditure, GLP-1(32-36)amide might be a useful treatment for human obesity and associated metabolic disorders.

GLP-1(32-36)amide, a novel pentapeptide cleavage product of GLP-1, modulates whole body glucose metabolism in dogs

Peptides 2014 Sep;59:20-4.PMID:24937653DOI:10.1016/j.peptides.2014.06.004.

We have previously demonstrated in human subjects who under euglycemic clamp conditions GLP-1(9-36)amide infusions inhibit endogenous glucose production without substantial insulinotropic effects. An earlier report indicates that GLP-1(9-36)amide is cleaved to a nonapeptide, GLP-1(28-36)amide and a pentapeptide GLP-1(32-36)amide (LVKGR amide). Here we study the effects of the pentapeptide on whole body glucose disposal during hyperglycemic clamp studies. Five dogs underwent indwelling catheterizations. Following recovery, the dogs underwent a 180 min hyperglycemic clamp (basal glucose +98 mg/dl) in a cross-over design. Saline or pentapeptide (30 pmol kg(-1) min(-1)) was infused during the last 120 min after commencement of the hyperglycemic clamp in a primed continuous manner. During the last 30 min of the pentapeptide infusion, glucose utilization (M) significantly increased to 21.4±2.9 mg kg(-1) min(-1)compared to M of 14.3±1.1 mg kg(-1)min(-1) during the saline infusion (P=0.026, paired t-test; P=0.062, Mann-Whitney U test). During this interval, no significant differences in insulin (26.6±3.2 vs. 23.7±2.5 μU/ml, P=NS) or glucagon secretion (34.0±2.1 vs. 31.7±1.8 pg/ml, P=NS) were observed. These findings demonstrate that under hyperglycemic clamp studies the pentapeptide modulates glucose metabolism by a stimulation of whole-body glucose disposal. Further, the findings suggest that the metabolic benefits previously observed during GLP-1(9-36)amide infusions in humans might be due, at least in part, to the metabolic effects of the pentapeptide that is cleaved from the pro-peptide, GLP-1(9-36)amide in the circulation.

GLP-1 receptor independent pathways: emerging beneficial effects of GLP-1 breakdown products

Eat Weight Disord 2017 Jun;22(2):231-240.PMID:28040864DOI:10.1007/s40519-016-0352-y.

The glucagon-like peptide-1 (GLP-1) axis has emerged as a major therapeutic target for the treatment of type 2 diabetes and, recently, of obesity. The insulinotropic activity of the native incretin hormone GLP-1(7-36)amide, which is mainly exerted through a unique G protein-coupled receptor (GLP-1R), is terminated via enzymatic cleavage by dipeptidyl peptidase-IV that generates a C-terminal GLP-1 metabolite GLP-1(9-36)amide, the major circulating form in plasma. GLP-1(28-36)amide and GLP-1(32-36)amide are further cleavage products derived from GLP-1(7-36)amide and GLP-1(9-36)amide by the action of a neutral endopeptidase known as neprilysin. Until recently, GLP-1-derived metabolites were generally considered metabolically inactive. However, emerging evidence indicates that GLP-1 byproducts have insulinomimetic activities that may contribute to the pleiotropic effects of GLP-1 independently of the canonical GLP-1R. The recent studies reporting the beneficial effects of the administration of these metabolites in vivo and in vitro are the focus of this review. Collectively, these results suggest that GLP-1 metabolites inhibit hepatic glucose production, exert antioxidant cardio- and neuroprotective actions, reduce oxidative stress in vasculature and have both anti-apoptotic and proliferative effects in pancreatic β-cells, putatively by the modulation of mitochondrial functions. These findings have implication in energy homeostasis, obesity and its associated metabolic and cardiovascular complications as well as incretin-based therapies for the treatment of diabetes and obesity.