title: Role of candidate genes in the lipid responses to intensified treatment in Type 2 diabetes.
abstract: OBJECTIVE
  To identify genetic factors related to individual differences in lipid responses to intensified treatment in Type 2 diabetes.
  
  
  METHODS
  After evaluation and intensification of their treatment, 107 Type 2 diabetes patients with poor metabolic control were re-evaluated after mean follow-up time of 15.6 (0, 4) (SE) months. The genes coding major lipid regulatory proteins and their relations to plasma lipid and lipoprotein changes were studied.
  
  
  RESULTS
  During the follow-up, levels of glycohemoglobin A1 (GHBA1) decreased (-1.7%), plasma HDL cholesterol (+0.05 mmol/l) and lipoprotein (a) [Lp(a)] (+4.2 mg/dl) increased, while triglyceride (TG) levels decreased (-1.2mmol/l) despite mean weight gain of 2.1 kg (p from <0.01 to <0.001). Of the gene markers studied, the lipoprotein lipase (LPL) Pvull (p=0.005) independently affected changes in HDL-cholesterol and was associated with the frequency of coronary heart disease (CHD). Lp(a) changes were associated with apolipoprotein B (ApoB) Glu4154Lys polymorphism (p=0.004).
  
  
  CONCLUSIONS
  These results suggest that genetic variations at LPL and ApoB loci are among the factors contributing to the variability in response to lipid parameters to therapy in Type 2 diabetes. LPL Pvull rare allele homozygote status seems to be beneficial with more favorable lipid changes and protection against CHD.
authors.affiliation: Department of Internal Medicine and Biocenter Oulu, University of Oulu, Oulu, Finland. olavi.ukkola@oulu.fi
authors.forename: O
authors.initials: O
authors.lastname: Ukkola
authors.forename: J
authors.initials: J
authors.lastname: Salonen
authors.forename: Y Antero
authors.initials: YA
authors.lastname: Kesäniemi
mesh_terms: D000483:Alleles; D001055:Apolipoproteins B / Q000235:genetics* / Q000502:physiology; D001835:Body Weight; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology; D048909:Diabetes Complications / Q000097:blood / Q000209:etiology / Q000235:genetics*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics* / Q000628:therapy*; D003927:Diet, Diabetic; D050171:Dyslipidemias / Q000097:blood / Q000209:etiology* / Q000235:genetics; D005260:Female; D005819:Genetic Markers; D005838:Genotype; D006442:Glycated Hemoglobin / Q000032:analysis; D006720:Homozygote; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D008071:Lipoprotein Lipase / Q000235:genetics* / Q000502:physiology; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005819:Genetic Markers; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D008071:Lipoprotein Lipase; D017270:Lipoprotein(a); D014280:Triglycerides