title: [Lipoprotein lipase and diabetic cardiomyopathy].
abstract: Lipoprotein lipase (LPL) hydrolyzes plasma triglyceride-rich lipoproteins into free fatty acids (FFA) to provide energy for cardiac tissue. During diabetes, cardiac energy supply is insufficient due to defected utilization of glucose. As a compensation of cardiac energy supply, FFAs are released through the hydrolysis of very low density lipoprotein (VLDL) and chylomicrons (CM) due to activation of LPL activity. In diabetic patients, activated LPL activity and elevated FFAs result in the intracellular accumulation of reactive oxygen species and lipids in myocardium and potentially induce the diabetic cardiomyopathy (DCM). The present review summarizes the regulatory mechanisms of myocardial LPL and the pathogenesis of DCM induced by LPL and provides novel therapeutic targets and pathways for DCM.
authors.forename: Xiang-Yu
authors.initials: XY
authors.lastname: Liu
authors.forename: Wei-Dong
authors.initials: WD
authors.lastname: Yin
authors.forename: Chao-Ke
authors.initials: CK
authors.lastname: Tang
mesh_terms: D002914:Chylomicrons; D058065:Diabetic Cardiomyopathies; D005230:Fatty Acids, Nonesterified; D005947:Glucose; D006801:Humans; D008071:Lipoprotein Lipase; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D014280:Triglycerides
chemical_list: D002914:Chylomicrons; D005230:Fatty Acids, Nonesterified; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030087:lipoprotein triglyceride; D008071:Lipoprotein Lipase; D005947:Glucose