High levels of MCP-1 in menopause and their relationship with components of the metabolic syndrome.

Authors

Lourdes Basurto, Violeta Castro-Leyva, Sara Vega-García, Laura L Lugo-Salcedo, Leticia Manuel-Apolinar, Jennyfer M Gaspar-Gurza, Paola Sánchez-Ramos, Ivon K Ruiz-López, Rosalinda Sánchez-Arenas, Sandra Jarquín-López, Nilson A Contreras-Carreto

Published in

Gaceta medica de Mexico. Volume 162. Issue 1. Pages 67-72.

Abstract

The menopause stage involves a significant reduction in circulating estrogen levels, resulting in notable changes to the cardiovascular, metabolic, bone, and immune systems. Monocyte chemoattractant protein-1 (MCP-1) is strongly associated with cardiovascular diseases and obesity. However, it is crucial to establish and clarify the relationship between MCP-1 and metabolic parameters in postmenopausal women.
The objective of this study was to assess the relationship between MCP-1 concentrations and various anthropometric and metabolic markers in premenopausal and postmenopausal women.
A case-control study, including 82 women (41 in postmenopausal stage, and 41 in premenopausal stage), was matched by body mass index (BMI). Insulin, estradiol, and C-reactive protein (CRP) levels were quantified by chemiluminescence and MCP-1 by enzyme-linked immunosorbent assays.
Age was 46.3 ± 2.4 years in premenopausal women and 55.6 ± 5.1 years in postmenopausal women. The MCP-1 level was higher in postmenopausal than premenopausal women (28.7 ± 10.4 vs. 21.3 ± 16.3 pg/mL, p = 0.04). The MCP-1 correlated with BMI (r = 0.39, p = 0.0001), waist circumference (r = 0.34, p = 0.002), CRP (r = 0.33, p = 0.03), high-density lipoprotein cholesterol (r = -0.28, p = 0.02), and visceral adipose tissue (VAT) (r = 0.38, p = 0.0001). Multiple stepwise regression analysis showed that VAT influenced the MCP-1 level.
Menopausal status influences MCP-1 concentrations; however, the relationship of MCP-1 with VAT favors the activation of inflammatory mechanisms, outweighing the effects of hormonal status.

PMID:
42880762
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.

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