Circulating inflammatory markers linked to dysregulated postprandial metabolism in postmenopausal women.

Menopause induces physiological alterations predisposing women to the development of chronic diseases. The evaluation of postprandial responses allows for a comprehensive assessment of metabolism and biomarkers that may predispose to chronic disease risk. By applying a dietary challenge consisting of the ingestion of a liquid, energy-dense mixed meal, followed by blood sampling over a 6-hour period, we conducted a cross-sectional study to investigate the postprandial metabolism in postmenopausal women (PM) aged 50-70 years and women of reproductive age (RA) aged 20 and 40 years. PM body weight was only 10% higher than RA, but the first displayed twice as much (more than 20%) intrabdominal adipose tissue. PM also displayed elevated fasting and postprandial glycemia (∼20%) and lipidemia compared to RA. Differences were also observed in the postprandial levels of lactate. Both groups displayed a similar increase in white blood cell count during the challenge, despite large differences in peripheral blood mononuclear cells (PBMC) gene expression in both fasting and postprandial states, suggesting a pro-inflammatory state and HIF-α and glycolytic pathway activation in PM. Plasma levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) were increased in PM (37 and 52%, respectively). Postprandial plasma levels of incretins presented different kinetics to each group. Our findings reveal that PM display a proinflammatory signature and markers of metabolic deterioration after a 12-h fasting and in the postprandial period when compared to RA.