Adipokines may link adipose tissue to the inflammatory, metabolic, and immune dysregulation. The variation of adipokine levels within individuals, intercorrelations, and relationships to well-established measures of adiposity are incompletely defined. The main goal of the present study was quantitative evaluation of the genetic interrelationships between obesity and adipokines in normal human population. The study sample comprised 272 families of various sizes, including 530 men and 531 women aged 18–80 years, randomly recruited in rural population living in Russia. Various fatness and fat distribution measures (OB), blood pressure (BP), and plasma levels of several adipokines (AC), such as adiponectin, leptin, resistin, and IGFBP-1, have been measured. The likelihood ratio tests clearly revealed that genetic effect for all studied phenotypes was highly significant (P < 0.001) and accounted for 45.9% ± 8.1%, 33.7% ± 7.9%, 35.7% ± 9.8% of variation for AC, OB, and BP, respectively. The pairwise bivariate analyses showed that strong phenotypic correlation between the obesity (OB) and adipocytokines (AC) was caused by both common genetic and environmental factors (rG = 0.597 ± 0.116, rE = 0.671 ± 0.051). The phenotypic correlation between BP and OB is explained by shared genetic factors only (rG = 0.532 ± 0.109), whereas the phenotypic correlation between BP and AC has only common environment basis (rE = −0.212 ± 0.081) and was mostly due to the correlation observed in females. Our results suggest that genetic factors play a significant role in regulation of variation of the examined traits. The variation of OB traits is almost fully due to genes influencing variation of AC, whereas the correlation between BP and AC is only marginally significant and caused only by shared environment. Am. J. Hum. Biol., 2009. © 2008 Wiley-Liss, Inc.