Amylin - CAS 122384-88-7
Category: Inhibitor
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CGRP Receptor
Amylin, islet Amyloid Polypeptide (IAPP), is a 37-residue peptide hormone secreted by pancreatic β-cells. It inhibits insulin-stimulated glucose uptake, delays gastric emptying and promotes satiety. It has glucose lowering effects in vivo. It is also used to study the mechanisms of amyloid deposition and its role in molecular misfolding processes expecially in conditions such as diabetes type II.
Diabetes Associated Peptide Amide human; DAP; IAPP; Insulinoma or Islet amyloid polypeptide; L-​Lysyl-​L-​cysteinyl-​L-​asparaginyl-​L-​threonyl-​L-​alanyl-​L-​threonyl-​L-​cysteinyl-​L-​alanyl-​L-​threonyl-​L-​glutaminyl-​L-​arginyl-​L-​leucyl-​L-​alanyl-​L-​asparaginyl-​L-​phenylalanyl-​L-​leucyl-​L-​valyl-​L-​histidyl-​L-​seryl-​L-​seryl-​L-​asparaginyl-​L-​asparaginyl-​L-​phenylalanylglycyl-​L-​alanyl-​L-​isoleucyl-​L-​leucyl-​L-​seryl-​L-​seryl-​L-​threonyl-​L-​asparaginyl-​L-​valylglycyl-​L-​seryl-​L-​asparaginyl-​L-​threonyl-​, cyclic (2→7)​-​disulfideL-​Tyrosinamide; Human islet amyloid polypeptide-NH2
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1.GLP-1(32-36)amide Pentapeptide Increases Basal Energy Expenditure and Inhibits Weight Gain in Obese Mice.
Tomas E1, Stanojevic V1, McManus K1, Khatri A1, Everill P2, Bachovchin WW2, Habener JF3. Diabetes. 2015 Jul;64(7):2409-19. doi: 10.2337/db14-1708. Epub 2015 Apr 9.
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.
2.Ingestion of coffee polyphenols increases postprandial release of the active glucagon-like peptide-1 (GLP-1(7-36)) amide in C57BL/6J mice.
Fujii Y1, Osaki N1, Hase T1, Shimotoyodome A1. J Nutr Sci. 2015 Mar 3;4:e9. doi: 10.1017/jns.2014.71. eCollection 2015.
The widespread prevalence of diabetes, caused by impaired insulin secretion and insulin resistance, is now a worldwide health problem. Glucagon-like peptide 1 (GLP-1) is a major intestinal hormone that stimulates glucose-induced insulin secretion from β cells. Prolonged activation of the GLP-1 signal has been shown to attenuate diabetes in animals and human subjects. Therefore, GLP-1 secretagogues are attractive targets for the treatment of diabetes. Recent epidemiological studies have reported that an increase in daily coffee consumption lowers diabetes risk. The present study examined the hypothesis that the reduction in diabetes risk associated with coffee consumption may be mediated by the stimulation of GLP-1 release by coffee polyphenol extract (CPE). GLP-1 secretion by human enteroendocrine NCI-H716 cells was augmented in a dose-dependent manner by the addition of CPE, and was compatible with the increase in observed active GLP-1(7-36) amide levels in the portal blood after administration with CPE alone in mice.
3.Characterization of Parallel β-Sheets at Interfaces by Chiral Sum Frequency Generation Spectroscopy.
Fu L1, Wang Z1, Psciuk BT1, Xiao D1, Batista VS1, Yan EC1. J Phys Chem Lett. 2015 Apr 16;6(8):1310-5. doi: 10.1021/acs.jpclett.5b00326. Epub 2015 Mar 27.
Characterization of protein secondary structures at interfaces is still challenging due to the limitations of surface-selective optical techniques. Here, we address the challenge of characterizing parallel β-sheets by combining chiral sum frequency generation (SFG) spectroscopy and computational modeling. We focus on human islet amyloid polypeptide aggregates and a de novo designed short polypeptide at lipid/water and air/glass interfaces. We find that parallel β-sheets adopt distinct orientations at various interfaces and exhibit characteristic chiroptical responses in the amide I and N-H stretch regions. Theoretical analysis indicates that the characteristic chiroptical responses provide valuable information on the symmetry, orientation, and vibrational couplings of parallel β-sheet at interfaces.
4.GLP-1(28-36)amide, the Glucagon-like peptide-1 metabolite: friend, foe, or pharmacological folly?
Taing MW1, Rose FJ2, Whitehead JP3. Drug Des Devel Ther. 2014 Jun 3;8:677-88. doi: 10.2147/DDDT.S35723. eCollection 2014.
The glucagon-like peptide-1 (GLP-1) axis has emerged as a major therapeutic target for the treatment of type 2 diabetes. GLP-1 mediates its key insulinotropic effects via a G-protein coupled receptor expressed on β-cells and other pancreatic cell types. The insulinotropic activity of GLP-1 is terminated via enzymatic cleavage by dipeptidyl peptidase-4. Until recently, GLP-1-derived metabolites were generally considered metabolically inactive; however, accumulating evidence indicates some have biological activity that may contribute to the pleiotropic effects of GLP-1 independent of the GLP-1 receptor. Recent reports describing the putative effects of one such metabolite, the GLP-1-derived nonapeptide GLP-1(28-36) amide, are the focus of this review. Administration of the nonapeptide elevates cyclic adenosine monophosphate (cAMP) and activates protein kinase A, β-catenin, and cAMP response-element binding protein in pancreatic β-cells and hepatocytes.
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CAS 122384-88-7 Amylin

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