Evidence for an association between the Leu162Val polymorphism of the PPARalpha gene and decreased fasting serum triglyceride levels in glucose tolerant subjects

Pharmacogenetics. 2003 Jul;13(7):417-23. doi: 10.1097/01.fpc.0000054105.48725.5c.

Abstract

The aim of the study was to investigate whether genetic variation in the peroxisome proliferator-activated receptor-alpha (PPARalpha) is associated with type 2 diabetes and altered lipid or carbohydrate metabolism in glucose tolerant subjects. Mutation analyses of PPARalpha were performed in 56 type 2 diabetic patients. Six variants were identified: IVS3 + 76T>C, IVS3-19C>T, IVS4 + 35C>T, Leu162Val, Arg178Gly and Ala268Val. In a case-control study comprising 738 type 2 diabetic patients and 524 glucose tolerant subjects, the three exon variants did not show any significant differences in allele frequencies between type 2 diabetic patients and control subjects. The functional Leu162Val polymorphism was further investigated in genotype-phenotype studies involving 340 young, healthy subjects and 502 middle-aged glucose tolerant subjects. The young, healthy subjects who were heterozygous for the Leu162Val variant had, on average, a 20% decrease in fasting serum triglyceride levels (P=0.014). This finding was replicated in middle-aged subjects (P=0.023). The Leu162Val polymorphism was not related to alterations in insulin sensitivity, insulin release or level of glycaemia. In conclusion, the Leu162Val polymorphism of PPARalpha is associated with a decreased level of fasting serum triglyceride in glucose tolerant white subjects.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Alleles
  • Blood Glucose / metabolism
  • Body Constitution
  • Case-Control Studies
  • DNA Mutational Analysis
  • Denmark
  • Diabetes Mellitus, Type 2 / genetics*
  • Fasting*
  • Female
  • Gene Frequency
  • Genetic Variation
  • Glucose Tolerance Test
  • Heterozygote
  • Humans
  • Insulin / blood
  • Male
  • Middle Aged
  • Point Mutation
  • Polymorphism, Genetic*
  • Receptors, Cytoplasmic and Nuclear / genetics*
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism
  • Triglycerides / blood*
  • Valine / genetics
  • Valine / metabolism
  • White People / genetics

Substances

  • Blood Glucose
  • Insulin
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Triglycerides
  • Valine