Premenopausal women exhibit an inherent protection of endothelial function following a high-fat meal
- PMID: 22383760
- PMCID: PMC3343134
- DOI: 10.1177/1933719111418125
Premenopausal women exhibit an inherent protection of endothelial function following a high-fat meal
Abstract
Endogenous estrogens likely increase blood flow and subsequently shear stress but have also been associated with improved endothelial function and cardiovascular protection. In contrast, a high-fat meal is thought to reduce endothelial function and increase cardiovascular risk. Therefore, we tested the hypotheses that fluctuating hormones across the menstrual cycle (1) facilitate an increase in shear rate and explain phase-specific differences in flow-mediated dilation (FMD) and (2) provide vascular protection against the insult of a high-fat meal. Flow-mediated dilation was determined at baseline and 4 hours following a high-fat meal in young women during the menses (M), follicular (F), and luteal (L) phases of the menstrual cycle. Male control participants were studied once. 17β-Estradiol was elevated (P < .05) during the F (5.3 ± 0.7 pg/mL) and L (5.2 ± 0.6 pg/mL) phases when compared to the M (3.9 ± 0.5 pg/mL) phase, and this was accompanied by an elevated FMD in the F and L phases (12.4 ± 1.4% and 11.2 ± 0.9%, respectively) compared to M (8.0 ± 0.9) with no change in shear rate. Female postprandial FMD was similar throughout the menstrual cycle, while men exhibited a 50% reduction (6.4 ± 1 to 3.3 ± 1%; P < .05). Interestingly, the postprandial FMD response was not associated with concentrations of either 17β-estradiol or progesterone. Despite acutely changing ovarian hormones across the menstrual cycle, shear stress is invariant and therefore does not account for the changes in FMD. Additionally, young women appear to have an inherent vascular protection from the insult of a high-fat meal, perhaps helping to explain sex-specific differences in cardiovascular risk.
Conflict of interest statement
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
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