Genetic and environmental determination of tracking in subcutaneous fat distribution during adolescence

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Maarten W Peeters
  • Gaston P Beunen
  • Hermine H Maes
  • Loos, Ruth
  • Albrecht L Claessens
  • Robert Vlietinck
  • Martine A Thomis

BACKGROUND: The distribution of fat and adipose tissue is an important predictor of disease risk. Variation in fat distribution during adolescence is correlated with fat distribution in adulthood.

OBJECTIVE: The objective was to gain insight into the relative contribution of genes and environment to the stability of subcutaneous fat distribution from early adolescence into young adulthood.

DESIGN: Ratio of trunk to extremity skinfold thickness (TER) data from the Leuven Longitudinal Twin Study (n = 105 Belgian twin pairs followed from 10 to 18 y of age) was entered into a longitudinal path analysis.

RESULTS: The best-fitting model included additive genetic sources of variance and nonshared environment. Heritabilities ranged between 84.3% (95% CI: 63.9-92.3%) and 88.6% (95% CI: 76.5-94.1%) in boys and between 78.4% (95% CI: 59.3-88.3%) and 88.3% (95% CI: 77.0-93.8%) in girls. The majority of the phenotypic tracking (boys: 0.40-0.78; girls: 0.38-0.72) could be attributed to the moderate-to-high genetic correlations (rG) (between 0.27-0.84 and 0.38-0.80 for the various age intervals in boys and girls, respectively). This rG could be attributed to both genetic sources of variance, which are the same throughout adolescence, as well as genetic sources of variance that are "switched-on" at a certain age, the effect of which is then transmitted to subsequent observations. Environmental correlations (rE) in boys ranged between 0.51 and 0.70 but contributed relatively little to phenotypic tracking because the amount of variance explained by the environment was low (11.4-15.7%). In girls rE was low to moderate at best (0.09-0.48).

CONCLUSION: Phenotypic tracking in subcutaneous fat distribution during adolescence is predominantly explained by additive genetic sources of variance.

OriginalsprogEngelsk
TidsskriftThe American Journal of Clinical Nutrition
Vol/bind86
Udgave nummer3
Sider (fra-til)652-60
Antal sider9
ISSN0002-9165
DOI
StatusUdgivet - sep. 2007
Eksternt udgivetJa

ID: 258453942