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Adipokines, Inflammation, and Visceral Adiposity across the Menopausal Transition: A Prospective Study

Department of Medicine (C.G.L., M.C.C., S.J.M., J.D.B.), Division of Metabolism, Endocrinology and Nutrition, University of Washington Medical Center, and Departments of Family and Child Nursing (E.M., N.F.W.) and Laboratory Medicine (M.H.W., W.L.C.), University of Washington, Seattle, Washington 98195; and Veterans Affairs Puget Sound Health Care System (E.J.B.), Seattle, Washington 98108

Address all correspondence and requests for reprints to: Christine G. Lee, M.D., Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, 1959 NE Pacific Street, Box 356426, Seattle, Washington 98195-4626.

Context: Postmenopausal women have greater visceral adiposity compared with premenopausal women. Adipokines are associated with increased adiposity, insulin resistance, and atherosclerosis.

Objective: The objective of the study was to assess changes in adipokines and inflammatory markers through the menopausal transition and correlate them with changes in visceral adiposity.

Design and Setting: This was a prospective cohort study of women through the menopausal transition conducted at the University of Washington.

Participants: Sixty-nine healthy women were followed up longitudinally from premenopausal (aged 45–55 yr) to postmenopausal status (aged 49–60 yr).

Outcome: On premenopausal and postmenopausal visits, fasting blood was drawn for adiponectin, leptin, serum amyloid A (SAA), C-reactive protein (CRP), monocyte-chemotactic protein-1, tissue plasminogen activator antigen (tPA), IL-6, and TNF-. Body composition measures were assessed by body mass index, whole-body dual x-ray absorptiometry scan, and computed tomography scan of the abdomen at the lumbar 4–5 level.

Results: Women had a statistically significant increase in SAA, tPA, monocyte-chemotactic protein-1, and adiponectin between the two measurement occasions (P = 0.04, P = 0.02, P = 0.001, and P < 0.001, respectively). The increase in intraabdominal fat was correlated positively with the 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 correlated with the change in adiponectin (r = –0.37, P = 0.005). After adjustment for change in sc abdominal fat, the correlation between change in CRP, tPA, leptin, and adiponectin remained significantly associated with change in intraabdominal fat.

Conclusions: Women going through the menopausal transition have deleterious changes in inflammatory markers and adipokines that correlate with increased visceral adiposity.