Direct association of a promoter polymorphism in the CD36/FAT fatty acid transporter gene with Type 2 diabetes mellitus and insulin resistance

E. Corpeleijn*, C. J. H. van der Kallen, M. Kruijshoop, M. G. P. Magagnin, T. W. A. de Bruin, E. J. M. Feskens, W. H. M. Saris, E. E. Blaak

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Aims The membrane-bound fatty acid transporter CD36/FAT may play a role in disturbed fatty acid handling as observed in the metabolic syndrome and Type 2 diabetes mellitus (T2DM). Genetic variation in the CD36 gene may contribute to the aetiology of diabetes.

Methods A population-based cohort in the Netherlands [age > 40 years and body mass index (BMI) > 25 kg/m(2)] of 675 subjects was phenotyped with respect to glucose metabolism with an oral glucose tolerance test and was genotyped for a known 478C -> T substitution and a C/T snp in the upstream promoter region (rs1527479) in the CD36 gene.

Results T2DM was more prevalent in the TT genotype than in the CC genotype. This was most pronounced in women and in subjects with a high BMI (BMI > 27 kg/m(2)). In addition, within the group of diabetic patients, the TT genotype was commoner in subjects with increased homeostasis model assessment (HOMA) index for insulin resistance. The 478C -> T substitution, previously found in the Japanese population, was not found in our caucasian population.

Conclusions This is the first study to show a direct association of a CD36 snp with T2DM. Moreover, within the diabetic subjects, this CD36 snp was associated with insulin resistance (HOMA index).

Original languageEnglish
Pages (from-to)907-911
Number of pages5
JournalDiabetic Medicine
Volume23
Issue number8
DOIs
Publication statusPublished - Aug-2006
Externally publishedYes

Keywords

  • gender
  • gene-environment interactions
  • glucose tolerance
  • lipid metabolism
  • obesity
  • HYPERTENSIVE-RATS
  • SKELETAL-MUSCLE
  • METABOLISM
  • GLUCOSE
  • DEFICIENCY
  • IDENTIFICATION
  • POPULATION
  • MUTATIONS
  • GENDER
  • DEFECT

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