{"title":"急性心肌梗死患者血清促肾上腺素水平降低","authors":"Hou-you Yu , Peng Zhao , Ming-chun Wu , Jian Liu , Wen Yin","doi":"10.1016/j.regpep.2014.04.001","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><p><span>Adropin is a recently identified bioactive protein that is important for energy homeostasis and maintaining </span>insulin sensitivity<span>. We sought to detect serum adropin levels in acute myocardial infarction (AMI) patients.</span></p></div><div><h3>Methods</h3><p>We enrolled 138 AMI patients, 114 stable angina pectoris (SAP) patients and 75 controls. Adropin levels were measured by enzyme-linked immunosorbent assay (ELISA).</p></div><div><h3>Results</h3><p>Serum adropin levels were significantly lower in patients with AMI compared with SAP patients or controls (<em>P</em> <!--><<!--> <!-->0.01). Multivariate logistic regression demonstrated that lower adropin was the independent predictor for the presence of AMI in coronary artery disease (CAD) patients (<em>P</em> <!--><<!--> <span>0.01). Serum adropin levels were negatively associated with body mass index (BMI) (</span><em>P</em> <!--><<!--> <span>0.01) and triglyceride levels (</span><em>P</em> <!--><<!--> <!-->0.05) in AMI patients.</p></div><div><h3>Conclusion</h3><p>Decreased serum adropin levels are associated with the presence of AMI in CAD patients. These results revealed that adropin might represent as a novel biomarker for predicting AMI onset in CAD patients.</p></div>","PeriodicalId":20853,"journal":{"name":"Regulatory Peptides","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.regpep.2014.04.001","citationCount":"90","resultStr":"{\"title\":\"Serum adropin levels are decreased in patients with acute myocardial infarction\",\"authors\":\"Hou-you Yu , Peng Zhao , Ming-chun Wu , Jian Liu , Wen Yin\",\"doi\":\"10.1016/j.regpep.2014.04.001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><p><span>Adropin is a recently identified bioactive protein that is important for energy homeostasis and maintaining </span>insulin sensitivity<span>. We sought to detect serum adropin levels in acute myocardial infarction (AMI) patients.</span></p></div><div><h3>Methods</h3><p>We enrolled 138 AMI patients, 114 stable angina pectoris (SAP) patients and 75 controls. Adropin levels were measured by enzyme-linked immunosorbent assay (ELISA).</p></div><div><h3>Results</h3><p>Serum adropin levels were significantly lower in patients with AMI compared with SAP patients or controls (<em>P</em> <!--><<!--> <!-->0.01). Multivariate logistic regression demonstrated that lower adropin was the independent predictor for the presence of AMI in coronary artery disease (CAD) patients (<em>P</em> <!--><<!--> <span>0.01). Serum adropin levels were negatively associated with body mass index (BMI) (</span><em>P</em> <!--><<!--> <span>0.01) and triglyceride levels (</span><em>P</em> <!--><<!--> <!-->0.05) in AMI patients.</p></div><div><h3>Conclusion</h3><p>Decreased serum adropin levels are associated with the presence of AMI in CAD patients. These results revealed that adropin might represent as a novel biomarker for predicting AMI onset in CAD patients.</p></div>\",\"PeriodicalId\":20853,\"journal\":{\"name\":\"Regulatory Peptides\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.regpep.2014.04.001\",\"citationCount\":\"90\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Regulatory Peptides\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0167011514000275\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Regulatory Peptides","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0167011514000275","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Serum adropin levels are decreased in patients with acute myocardial infarction
Objective
Adropin is a recently identified bioactive protein that is important for energy homeostasis and maintaining insulin sensitivity. We sought to detect serum adropin levels in acute myocardial infarction (AMI) patients.
Methods
We enrolled 138 AMI patients, 114 stable angina pectoris (SAP) patients and 75 controls. Adropin levels were measured by enzyme-linked immunosorbent assay (ELISA).
Results
Serum adropin levels were significantly lower in patients with AMI compared with SAP patients or controls (P < 0.01). Multivariate logistic regression demonstrated that lower adropin was the independent predictor for the presence of AMI in coronary artery disease (CAD) patients (P < 0.01). Serum adropin levels were negatively associated with body mass index (BMI) (P < 0.01) and triglyceride levels (P < 0.05) in AMI patients.
Conclusion
Decreased serum adropin levels are associated with the presence of AMI in CAD patients. These results revealed that adropin might represent as a novel biomarker for predicting AMI onset in CAD patients.
期刊介绍：
Regulatory Peptides provides a medium for the rapid publication of interdisciplinary studies on the physiology and pathology of peptides of the gut, endocrine and nervous systems which regulate cell or tissue function. Articles emphasizing these objectives may be based on either fundamental or clinical observations obtained through the disciplines of morphology, cytochemistry, biochemistry, physiology, pathology, pharmacology or psychology.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
