Are sex-specific effects of dietary phytosterol intake on adiponectin levels an underlying factor explaining variation in TG/HDL ratio associated with APOE polymorphisms: The Kansas Nutrition Study.

MOSHER MJ, DA DEMARCHI, R. RUBICZ, M ZLOJUTRO, P MELTON, MH CRAWFORD

Albuquerque, New Mexico

Congreso; LXXIX Annual Meeting of the American Association of Physical Anthropologists; 2010

American Association of Physical Anthropologists

Dietary manipulation of plasma lipids remains an integral part of treatment for dyslipidemias and their sequelae of coronary artery disease (CAD). However, substantial conflicting evidence reported in the literature suggests that undetermined gene- by- sex- variation affects dietary response. We examined blood samples for APOE polymorphisms and determined nutrient profiles from dietary diaries of 75 male and 83 female Central Kansas Mennonites. Previously we reported sex-specific associations of plasma lipids to plasma adiponectin, and APOE. Adiponectin, a hormone affecting lipid metabolism, is sexually dimorphic, lowered by both testosterone and higher percentages of visceral adipose tissue (VAT). Here we examine effects of phytosterol intake and APOE on adiponectin and the triglyceride/high-density lipoprotein (TG/HDL) ratio, an indicator of atherogenic dyslipidemias and a marker for (CAD). An inverse relationship between plasma adiponectin levels and TG/HDL ratio was significant in males only (P = 0.005 for males, P=0.106 for females). No significant change was noted after adjustments for age, location, or measures of central fat patterning. No sex-specific variation was found in dietary percent of fatty acids from animal sources. However, phytosterol intake was decidedly higher in females (P= 0.007), yet had no statistical affects on adiponectin levels in females. Sex-specific tertiles denoting the percent of dietary phytosterol were compared. Males whose phytosterol intake was highest were the only ones to have adiponectin matching their female counterparts (P= 0.041). Furthermore, 25% of the variation in male TG/HDL ratios can be explained by APOE by adiponectin interaction (P =0.015). Further sex-specific nutrigenetics comparisons are recommended