TY - JOUR
T1 - Adipokines, inflammation, and visceral adiposity across the menopausal transition
T2 - A prospective study
AU - Lee, Christine G.
AU - Carr, Molly C.
AU - Murdoch, Susan J.
AU - Mitchell, Ellen
AU - Woods, Nancy F.
AU - Wener, Mark H.
AU - Chandler, Wayne L.
AU - Boyko, Edward J.
AU - Brunzell, John D.
N1 - Funding Information:
This work was supported by National Institutes of Health Grants HL30086, HL64322, and NR04141, and K23 Grant RR16067 (to M.C.C.) and a grant from the Bristol Myers Squibb Foundation. These studies were performed with the support of the University of Washington Clinical Nutrition Research Unit (DK35816), the University of Washington General Clinical Research Center (M01-RR-00037), and the University of Washington Diabetes Endocrinology Research Center, which is funded by the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases Grant P30 DK-17047.
PY - 2009/4
Y1 - 2009/4
N2 - 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-α. 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.
AB - 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-α. 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.
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U2 - 10.1210/jc.2008-0701
DO - 10.1210/jc.2008-0701
M3 - Article
C2 - 19126626
AN - SCOPUS:65249119817
VL - 94
SP - 1104
EP - 1110
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 4
ER -