{"title":"PPARs and their role in diabetic dyslipidaemia","authors":"Manish Khanolkar","doi":"10.4172/2153-0637.C1.003","DOIUrl":null,"url":null,"abstract":"T 2 diabetes (T2D) is often associated with metabolic syndrome that is characterised by a peculiar dyslipidaemia comprising of elevated serum triglyceride levels in association with low HDL-Cholesterol levels (HDL-C). This disordered metabolic state leads to a build up of fatty acids in the liver and skeletal muscles, making these tissues resistant to the effects of insulin. The initial response of the body to insulin resistance is to increase insulin production that is effected by the beta cells of pancreas. Eventually, the beta cells are overwhelmed and can no longer produce enough insulin to maintain normoglycaemia, leading to the development of T2D.","PeriodicalId":89585,"journal":{"name":"Journal of glycomics & lipidomics","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2015-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of glycomics & lipidomics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2153-0637.C1.003","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
T 2 diabetes (T2D) is often associated with metabolic syndrome that is characterised by a peculiar dyslipidaemia comprising of elevated serum triglyceride levels in association with low HDL-Cholesterol levels (HDL-C). This disordered metabolic state leads to a build up of fatty acids in the liver and skeletal muscles, making these tissues resistant to the effects of insulin. The initial response of the body to insulin resistance is to increase insulin production that is effected by the beta cells of pancreas. Eventually, the beta cells are overwhelmed and can no longer produce enough insulin to maintain normoglycaemia, leading to the development of T2D.