Related Experiment Videos

Mannose-binding lectin gene polymorphism and risk factors for cardiovascular disease in postmenopausal women

Claudio Lera Orsatti1, Eliana Aguiar Petri Nahás1, Jorge Nahas-Neto1

  • 1Department of Gynecology and Obstetrics, Botucatu Medical School, Sao Paulo State University- UNESP, Botucatu, São Paulo, Brazil.

Insights

Genetic variations in Mannose-binding lectin (MBL2) may influence cardiovascular disease (CVD) risk in postmenopausal women. Polymorphism at codon 54 is linked to reduced hypertension and insulin resistance, key CVD risk factors.

Area of Science:

  • Immunogenetics
  • Cardiovascular Disease Epidemiology
  • Menopause Research

Background:

  • Postmenopausal women exhibit altered inflammatory responses, increasing cardiovascular disease (CVD) susceptibility.
  • Genetic factors play a role in CVD risk.
  • Mannose-binding lectin (MBL), part of the innate immune system, activates complement cascade.

Purpose of the Study:

  • To investigate the association between Mannose-binding lectin gene (MBL2) polymorphisms and cardiovascular risk factors in postmenopausal women.
  • To determine if MBL2 genetic variations influence hypertension and insulin resistance.

Main Methods:

  • Cross-sectional study of 311 Brazilian postmenopausal women (age ≥45).
  • Exclusion criteria included current CVD, diabetes, kidney disease, autoimmune diseases, and cancer.
  • MBL2 polymorphisms at codons 54 and 57 analyzed via PCR; cardiovascular risk factors assessed through clinical, anthropometric, and biochemical evaluations.

Main Results:

  • Codon 54 polymorphism present in 25.8% of women; codon 57 in 12.2%.
  • Codon 54 polymorphism significantly associated with lower odds of hypertension (OR 0.55) and insulin resistance (OR 0.46).
  • No significant association found between codon 57 polymorphism and CVD risk factors.

Conclusions:

  • MBL2 codon 54 polymorphism is associated with reduced risk of hypertension and insulin resistance in postmenopausal women.
  • These findings suggest a potential protective role of specific MBL2 variants against key cardiovascular risk factors.
Abstract

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