title: The transition to menopause reinforces adiponectin production and its contribution to improvement of insulin-resistant state.
abstract: OBJECTIVE
  To evaluate the influence of menopausal status on the serum adiponectin concentration and investigate whether the contribution of adiponectin to insulin resistance is modified by menopausal status.
  
  
  METHODS
  We conducted a population-based, cross-sectional study of 207 premenopausal and 206 postmenopausal Japanese women.
  
  
  METHODS
  Data on anthropometric characteristics, fasting serum adiponectin, glucose and insulin concentrations were used. Insulin resistance (homeostasis model assessment of insulin resistance: HOMA-IR) was calculated.
  
  
  RESULTS
  Postmenopausal women had significantly higher HOMA-IRs than premenopausal women [1.50 (1.42, 1.59) vs 1.18 (1.12, 1.24), geometric mean (1 standard error range), P = 0.005]. Paradoxically, adiponectin levels in postmenopausal women were also significantly higher than those in premenopausal women [10.3 (9.95, 10.7) vs 9.04 (8.71, 9.39), P = 0.028]. Multiple regression analysis showed that body mass index (BMI) was the only significantly independent predictor [standardized partial regression coefficients (sbeta) = 0.319, P < 0.001] for HOMA-IR among premenopausal women, whereas both BMI and adiponectin were the significant predictors among postmenopausal (sbeta = 0.334 and -0.141, P < 0.001 and < 0.05, respectively). When the subjects were restricted to those without metabolic disorders including high blood pressure, hypertriglyceridaemia, hypo-HDL cholesterolaemia and high fasting glucose, adiponectin (sbeta = -0.249, P < 0.05) was the only significant predictor for HOMA-IR among postmenopausal women but BMI was not significant (sbeta = 0.223, P = 0.075).
  
  
  CONCLUSIONS
  The transition to menopause increases serum adiponectin concentrations. And the significant and negative association between adiponectin and HOMA-IR was observed only after menopause. Therefore, adiponectin may play a role in the improvement of an incipient insulin-resistant state after, rather than before, menopause.
authors.affiliation: Department of Public Health/Health Information Dynamics, Nagoya University Graduate School of Medicine, Nagoya, Japan. tamako@med.nagoya-u.ac.jp
authors.forename: Koji
authors.initials: K
authors.lastname: Tamakoshi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yatsuya
authors.forename: Keiko
authors.initials: K
authors.lastname: Wada
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Matsushita
authors.forename: Rei
authors.initials: R
authors.lastname: Otsuka
authors.forename: Pei Ou
authors.initials: PO
authors.lastname: Yang
authors.forename: Kaichiro
authors.initials: K
authors.lastname: Sugiura
authors.forename: Yo
authors.initials: Y
authors.lastname: Hotta
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Mitsuhashi
authors.forename: Seiko
authors.initials: S
authors.lastname: Takefuji
authors.forename: Takaaki
authors.initials: T
authors.lastname: Kondo
authors.forename: Hideaki
authors.initials: H
authors.lastname: Toyoshima
mesh_terms: D052242:Adiponectin / Q000096:biosynthesis / Q000097:blood*; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008593:Menopause / Q000097:blood*; D008875:Middle Aged; D017697:Premenopause / Q000097:blood; D012044:Regression Analysis
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin