Population genetic analyses of susceptibility to increased body weight

Obesity is a complex condition with multifactorial origin. Assuming that such a state is genetically controlled, the aim of our study was to evaluate the degree of genetic homozygosity among overweight and obese individuals by the homozygously recessive characteristics (HRC) test.

We analysed the presence, distribution and individual combination of 15 selected genetically controlled recessive phenotype traits in a sample of 140 individuals with increased body mass index (overweight individuals n = 100 and obese individuals n = 40) and a control group of normal weight individuals (n = 300).

OBESE INDIVIDUALS HAVE SIGNIFICANTLY HIGHER MEAN VALUES FOR GENETIC HOMOZYGOSITY THAN THOSE WITH NORMAL WEIGHT (NORMAL WEIGHT: 3.61 ±1.48; obese: 4.13 ±1.47, p < 0.05) and difference in the presence of certain individual combinations of evaluated phenotype traits (Σχ(2) = 76.9; p < 0.01). There was no difference in average homozygosity of such genetic markers between groups of normal weight and overweight individuals (normal weight: 3.61 ±1.48; overweight: 3.93 ±1.51, p > 0.05) and between groups of overweight and obese individuals (overweight: 3.93 ±1.51; obese: 4.13 ±1.47, p > 0.05). There is no difference in the presence of certain individual combinations of evaluated phenotype traits between overweight and obese individuals (Σχ(2) = 20.6; p > 0.05).

There is a populational genetic difference in the degree of genetic homozygosity and variability between the group of normal weight and group of obese individuals, indicating a possible genetic component. Overweight and obese individuals have a genetic predisposition, but different expression of genetic loads could be one of the possible explanations for different susceptibility to increase of fat mass and body mass index.