Impact of Serum Estradiol on Postprandial Lipemia, Oxidative Stress, and Inflammation Across a Single Menstrual Cycle

Background: An abrupt rise in circulating lipids, oxidative stress, and inflammatory biomarkers is a common finding after ingestion of a high-fat meal. Estradiol, typically provided via hormone replacement therapy to postmenopausal women, has been reported to possess lipidemic, antioxidant, and anti-inflammatory properties, all of which may minimize postprandial oxidative stress. Objective: The purpose of this study was to compare the postprandial triglyceride (TG), oxidative stress, and inflammatory responses after a lipid meal in menstruating women during the early follicular (days 1-3) and preovulatory (day 14) phases of the menstrual cycle. Methods: Healthy normolipidemic women (fasting blood TG, <200 mg/dL) with regular menstrual cycles reported to the Cardiorespiratory/Metabolic Laboratory at the University of Memphis, Memphis, Tennessee (October December 2008) and consumed an identical lipid meal (heavy whipping cream and water) on 2 separate days during the menstrual cycle. Blood samples were collected premeal and 1, 2, 4, and 6 hours postmeal, then assayed for TG, malondialdehyde (MDA), hydrogen peroxide, Trolox equivalent antioxidant capacity (TEAC), nitrate/nitrite, and C-reactive protein (CRP). The AUC was calculated for each variable, and a 2 (menstrual cycle phase) x 5 (time) ANOVA with Tukey post hoc testing was also conducted. Estradiol concentration was measured in premeal samples for verification of cycle phase. Results: Ten women (mean [SD] age, 29 [11] years; 8 white, 2 black; body mass index, 22 [3] kg/m(2)) participated in the study. Despite a higher serum estradiol concentration on day 14 (113 [56] pg/mL) compared with the early follicular phase (61 [34] pg/mL), the TG, oxidative stress, and inflammatory AUC responses to feeding were not significantly different. TG (P = 0.03), MDA (P = 0.02), and hydrogen peroxide (P < 0.001) were significantly increased in response to feeding (time effect), whereas nitrate/nitrite was decreased (P = 0.01). TEAC and CRP were not significantly affected. Conclusions: These data indicate that estradiol, at the concentrations noted in the present study, had no significant effect on postprandial TG or biomarkers of oxidative stress or inflammation in a sample of young, healthy women. It is possible that a greater divergence in circulating estradiol may be needed for significant differences to be detected, as may be the case with chronic hormone replacement therapy in postmenopausal women. (Gend Med. 2010;7:166-178) (c) 2010 Excerpta Medica Inc.