title: . Association of HindIII and PvuII genetic polymorphisms of lipoprotein lipase with lipid metabolism and macrovascular events in type 2 diabetic patients.
abstract: OBJECTIVE
  Lipoprotein lipase (LPL) is a key enzyme of lipid metabolism, and its genetic polymorphism may be a candidate for modulating lipid parameters in type 2 diabetic subjects (D2).
  
  
  METHODS
  In a group of 404 type 2 diabetic patients, aged 59.5+/-10.8y, BMI=28.9+/-5.3 kg/m2, HbA1c=8.2+/-1.9%, we studied the H and P polymorphisms at the LPL locus detectable with the restriction enzymes HindIII and PvuII. Patients were separated into 229 males (17H1H1, 84H1H2, 128H2H2 and 51P1P1, 110P1P2, 68P2P2) and 175 females (16H1H1, 69H1H2, 90H2H2 and 51P1P1, 85P1P2, 39P2P2), and compared on the basis of their lipid parameters and their macrovascular complications.
  
  
  RESULTS
  Triglyceride (TG) and HDL-cholesterol(c) concentrations differed between patients with and without coronary heart disease (CHD) (3.44+/-2.09 and 1.96+/-1.40 mmol/l for TGs and 1.05+/-0.24 and 1.34+/-0.40 mmol/l for HDL-c, P<0.001). HDL-c concentrations were lower in male H2H2 and P2P2 subjects (P<0.001), and TG levels were higher in male H2H2 and P2P2 subjects (P<0.0001 for Hind III and P<0.05 for PvuII). Allele frequency of the HindIII and PvuII restriction site was similar to those reported in other Caucasian populations and the presence of the H2/P2 variants was significantly higher in CHD patients. The prevalence of CHD in this population was 18% but was 29% in H2H2 and 38% in P2P2 subjects (P<0.02).
  
  
  CONCLUSIONS
  Thus, HindIII and PvuII polymorphisms seem to exert a modulating role on lipid profile particularly in male D2, contributing to increase the risk of macrovascular events.
authors.affiliation: Service d'Endocrinologie, Maladies Métaboliques et de Médecine Interne, Hôpital Robert Debré, Centre Hospitalo-Universitaire, 51092 Reims, France.
authors.forename: E
authors.initials: E
authors.lastname: Socquard
authors.forename: A
authors.initials: A
authors.lastname: Durlach
authors.forename: C
authors.initials: C
authors.lastname: Clavel
authors.forename: P
authors.initials: P
authors.lastname: Nazeyrollas
authors.forename: V
authors.initials: V
authors.lastname: Durlach
mesh_terms: D000368:Aged; D003327:Coronary Disease / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics; D015257:DNA-Cytosine Methylases; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000201:enzymology* / Q000235:genetics*; D003925:Diabetic Angiopathies / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood*; D008071:Lipoprotein Lipase / Q000235:genetics*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011110:Polymorphism, Genetic; D012307:Risk Factors; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific); D014280:Triglycerides / Q000097:blood
chemical_list: D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; C090528:DNA modification methylase HindIII; C047084:DNA modification methylase PvuII; D015257:DNA-Cytosine Methylases; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific); D008071:Lipoprotein Lipase