title: Adipokines, inflammation, and visceral adiposity across the menopausal transition: a prospective study.
abstract: BACKGROUND
  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.
  
  
  METHODS
  This was a prospective cohort study of women through the menopausal transition conducted at the University of Washington.
  
  
  METHODS
  Sixty-nine healthy women were followed up longitudinally from premenopausal (aged 45-55 yr) to postmenopausal status (aged 49-60 yr).
  
  
  RESULTS
  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-alpha. 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.
authors.affiliation: Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle, Washington 98195-4626, USA.
authors.forename: Christine G
authors.initials: CG
authors.lastname: Lee
authors.forename: Molly C
authors.initials: MC
authors.lastname: Carr
authors.forename: Susan J
authors.initials: SJ
authors.lastname: Murdoch
authors.forename: Ellen
authors.initials: E
authors.lastname: Mitchell
authors.forename: Nancy F
authors.initials: NF
authors.lastname: Woods
authors.forename: Mark H
authors.initials: MH
authors.lastname: Wener
authors.forename: Wayne L
authors.initials: WL
authors.lastname: Chandler
authors.forename: Edward J
authors.initials: EJ
authors.lastname: Boyko
authors.forename: John D
authors.initials: JD
authors.lastname: Brunzell
mesh_terms: D000005:Abdomen; D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000033:anatomy & histology*; D000328:Adult; D001823:Body Composition / Q000502:physiology*; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D020738:Leptin / Q000097:blood; D008593:Menopause / Q000502:physiology*; D008875:Middle Aged; D017698:Postmenopause / Q000502:physiology; D017697:Premenopause / Q000502:physiology; D011446:Prospective Studies; D014781:Viscera
chemical_list: D054392:Adipokines; D052242:Adiponectin; D020738:Leptin; D002097:C-Reactive Protein