{"title":"一种新型肽COX52-69通过调节BK通道活性抑制高糖诱导的胰岛素分泌。","authors":"Qian Lin, Jingtao Liu, Hengling Chen, Wenwu Hu, Weiqiong Lei, Meijie Wang, Xianguang Lin, Yongning Zhang, Huiting Ai, Su Chen, Chenhong Li","doi":"10.2174/0113892037249620231010063637","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Excessive insulin is the leading cause of metabolic syndromes besides hyperinsulinemia. Insulin-lowering therapeutic peptides have been poorly studied and warrant urgent attention.</p><p><strong>Objectives: </strong>The main purpose of this study, was to introduce a novel peptide COX<sub>52-69</sub> that was initially isolated from the porcine small intestine and possessed the ability to inhibit insulin secretion under high-glucose conditions by modulating large conductance Ca<sup>2+</sup>-activated K<sup>+</sup> channels (BK channels) activity.</p><p><strong>Methods and results: </strong>Enzyme-linked immunosorbent assay results indicate that COX<sub>52-69</sub> supressed insulin release induced by high glucose levels in pancreatic islets and animal models. Furthermore, electrophysiological data demonstrated that COX<sub>52-69</sub> can increase BK channel currents and hyperpolarize cell membranes. Thus, cell excitability decreased, corresponding to a reduction in insulin secretion.</p><p><strong>Conclusion: </strong>Our study provides a novel approach to modulate high glucose-stimulated insulin secretion in patients with hyperinsulinemia.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A Novel Peptide COX<sub>52-69</sub> Inhibits High Glucose-induced Insulin Secretion by Modulating BK Channel Activity.\",\"authors\":\"Qian Lin, Jingtao Liu, Hengling Chen, Wenwu Hu, Weiqiong Lei, Meijie Wang, Xianguang Lin, Yongning Zhang, Huiting Ai, Su Chen, Chenhong Li\",\"doi\":\"10.2174/0113892037249620231010063637\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Excessive insulin is the leading cause of metabolic syndromes besides hyperinsulinemia. Insulin-lowering therapeutic peptides have been poorly studied and warrant urgent attention.</p><p><strong>Objectives: </strong>The main purpose of this study, was to introduce a novel peptide COX<sub>52-69</sub> that was initially isolated from the porcine small intestine and possessed the ability to inhibit insulin secretion under high-glucose conditions by modulating large conductance Ca<sup>2+</sup>-activated K<sup>+</sup> channels (BK channels) activity.</p><p><strong>Methods and results: </strong>Enzyme-linked immunosorbent assay results indicate that COX<sub>52-69</sub> supressed insulin release induced by high glucose levels in pancreatic islets and animal models. Furthermore, electrophysiological data demonstrated that COX<sub>52-69</sub> can increase BK channel currents and hyperpolarize cell membranes. Thus, cell excitability decreased, corresponding to a reduction in insulin secretion.</p><p><strong>Conclusion: </strong>Our study provides a novel approach to modulate high glucose-stimulated insulin secretion in patients with hyperinsulinemia.</p>\",\"PeriodicalId\":10859,\"journal\":{\"name\":\"Current protein & peptide science\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current protein & peptide science\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.2174/0113892037249620231010063637\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current protein & peptide science","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.2174/0113892037249620231010063637","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
A Novel Peptide COX52-69 Inhibits High Glucose-induced Insulin Secretion by Modulating BK Channel Activity.
Background: Excessive insulin is the leading cause of metabolic syndromes besides hyperinsulinemia. Insulin-lowering therapeutic peptides have been poorly studied and warrant urgent attention.
Objectives: The main purpose of this study, was to introduce a novel peptide COX52-69 that was initially isolated from the porcine small intestine and possessed the ability to inhibit insulin secretion under high-glucose conditions by modulating large conductance Ca2+-activated K+ channels (BK channels) activity.
Methods and results: Enzyme-linked immunosorbent assay results indicate that COX52-69 supressed insulin release induced by high glucose levels in pancreatic islets and animal models. Furthermore, electrophysiological data demonstrated that COX52-69 can increase BK channel currents and hyperpolarize cell membranes. Thus, cell excitability decreased, corresponding to a reduction in insulin secretion.
Conclusion: Our study provides a novel approach to modulate high glucose-stimulated insulin secretion in patients with hyperinsulinemia.
期刊介绍：
Current Protein & Peptide Science publishes full-length/mini review articles on specific aspects involving proteins, peptides, and interactions between the enzymes, the binding interactions of hormones and their receptors; the properties of transcription factors and other molecules that regulate gene expression; the reactions leading to the immune response; the process of signal transduction; the structure and function of proteins involved in the cytoskeleton and molecular motors; the properties of membrane channels and transporters; and the generation and storage of metabolic energy. In addition, reviews of experimental studies of protein folding and design are given special emphasis. Manuscripts submitted to Current Protein and Peptide Science should cover a field by discussing research from the leading laboratories in a field and should pose questions for future studies. Original papers, research articles and letter articles/short communications are not considered for publication in Current Protein & Peptide Science.
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