Lee · The Journal of clinical endocrinology and metabolism 2009 · prospective cohort study · n=69

Adipokines, inflammation, and visceral adiposity across the menopausal transition: a prospective study.

Cited 278 times in the scientific literature.

Level 3 - non-randomized controlled study

Prospective longitudinal cohort study without a parallel control group

PubMed 19126626 · doi:10.1210/jc.2008-0701 · record verified 2026-08-27

What was done

A prospective longitudinal cohort study followed 69 healthy women at the University of Washington across the menopausal transition, from premenopausal status (aged 45–55 years) to postmenopausal status (aged 49–60 years). Fasting blood samples collected at both baseline and follow-up visits were analyzed for adiponectin, leptin, serum amyloid A (SAA), C-reactive protein (CRP), monocyte-chemotactic protein-1 (MCP-1), tissue plasminogen activator antigen (tPA), IL-6, and TNF-alpha. Body composition measures were assessed using BMI, whole-body dual-energy X-ray absorptiometry (DXA), and abdominal computed tomography (CT) scans at the L4–L5 level to quantify intraabdominal and subcutaneous abdominal fat.

What was found

Between the premenopausal and postmenopausal visits, women had statistically significant increases in SAA (P = 0.04), tPA (P = 0.02), MCP-1 (P = 0.001), and adiponectin (P < 0.001). Increase in intraabdominal fat correlated positively with change in SAA (r = 0.31, P = 0.02), CRP (r = 0.56, P < 0.001), tPA (r = 0.40, P = 0.002), and leptin (r = 0.41, P = 0.002), and negatively with change in adiponectin (r = -0.37, P = 0.005). After adjustment for change in subcutaneous abdominal fat, correlations of intraabdominal fat change with CRP, tPA, leptin, and adiponectin remained statistically significant. Absolute values and results for IL-6 and TNF-alpha were not reported in the abstract.

Why it matters

This study shows that visceral fat accumulation across the menopausal transition tracks directly with unfavorable inflammatory and adipokine changes independently of subcutaneous fat, providing a mechanistic link between menopause and heightened cardiometabolic risk.

Limits

The sample size was small (n = 69) and restricted to healthy women from a single center. The study lacked an age-matched non-transitioning control group to distinguish chronological aging from reproductive aging, and absolute biomarker concentrations were omitted from the abstract.

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