{"title":"Electroacupuncture treatment of insulin resistance in diabetes mellitus.","authors":"Philip V Peplow","doi":"10.1136/acupmed-2015-010942","DOIUrl":null,"url":null,"abstract":"Insulin resistance is closely associated with obesity, type 2 diabetes mellitus (DM), hypertension and the metabolic syndrome, and is also a risk factor for cardiovascular disease. There is increasing clinical evidence for the effectiveness of acupuncture as a treatment for insulin resistance.1\n\nFrom a mechanistic point of view, the post-receptor responses and signal transduction pathways that are initiated when insulin binds to its receptor in the cell plasma membrane are well described (http://themedicalbiochemistrypage.org/insulin.php). These include the association of insulin receptor substrates (IRSs) with the insulin receptor (IR), which results in the activation of phosphatidylinositol-3-kinase (PI3K) and growth factor receptor binding protein 2 (GRB2). Activated PI3K phosphorylates membrane phospholipids and the main product is phosphatidylinositol-3,4,5-triphosphate (PIP3), which in turn activates PIP3-dependent kinase 1 (PDK1). PDK1 activates another kinase called protein kinase B (PKB, also known as Akt). Insulin-mediated activation of Akt causes inhibition of lipolysis and gluconeogenesis and activation of protein and glycogen synthesis. Insulin signalling also activates the mitogen activated protein kinase (MAPK) pathway either by IR phosphorylation of Src homology 2 domain-containing protein (SHC), which then interacts with GRB2, or via IRS1 activation. Insulin decreases hepatic glucose production (HGP) and increases the rate of glucose uptake, primarily in striated muscle and adipose tissue. In muscle and fat cells, the clearance of circulating glucose depends on the insulin-stimulated translocation of the glucose transporter 4 (GLUT4) isoform to the …","PeriodicalId":378725,"journal":{"name":"Acupuncture in medicine : journal of the British Medical Acupuncture Society","volume":" ","pages":"347-9"},"PeriodicalIF":0.0000,"publicationDate":"2015-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/acupmed-2015-010942","citationCount":"16","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acupuncture in medicine : journal of the British Medical Acupuncture Society","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1136/acupmed-2015-010942","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 16
Abstract
Insulin resistance is closely associated with obesity, type 2 diabetes mellitus (DM), hypertension and the metabolic syndrome, and is also a risk factor for cardiovascular disease. There is increasing clinical evidence for the effectiveness of acupuncture as a treatment for insulin resistance.1
From a mechanistic point of view, the post-receptor responses and signal transduction pathways that are initiated when insulin binds to its receptor in the cell plasma membrane are well described (http://themedicalbiochemistrypage.org/insulin.php). These include the association of insulin receptor substrates (IRSs) with the insulin receptor (IR), which results in the activation of phosphatidylinositol-3-kinase (PI3K) and growth factor receptor binding protein 2 (GRB2). Activated PI3K phosphorylates membrane phospholipids and the main product is phosphatidylinositol-3,4,5-triphosphate (PIP3), which in turn activates PIP3-dependent kinase 1 (PDK1). PDK1 activates another kinase called protein kinase B (PKB, also known as Akt). Insulin-mediated activation of Akt causes inhibition of lipolysis and gluconeogenesis and activation of protein and glycogen synthesis. Insulin signalling also activates the mitogen activated protein kinase (MAPK) pathway either by IR phosphorylation of Src homology 2 domain-containing protein (SHC), which then interacts with GRB2, or via IRS1 activation. Insulin decreases hepatic glucose production (HGP) and increases the rate of glucose uptake, primarily in striated muscle and adipose tissue. In muscle and fat cells, the clearance of circulating glucose depends on the insulin-stimulated translocation of the glucose transporter 4 (GLUT4) isoform to the …