title: Estradiol acutely inhibits whole body lipid oxidation and attenuates lipolysis in subcutaneous adipose tissue: a randomized, placebo-controlled study in postmenopausal women.
abstract: BACKGROUND
  Estradiol (E(2)) promotes and maintains the female phenotype characterized by subcutaneous fat accumulation. There is evidence to suggest that this effect is due to increased anti-lipolytic α2A-adrenergic receptors, but whether this requires long-term exposure to E(2) or is an immediate effect is not clear.
  
  
  OBJECTIVE
  To study acute effects of a single dose (4 mg) of 17β-E(2) on regional and systemic lipolysis.
  
  
  METHODS
  Sixteen postmenopausal women (age, 595 years; weight, 6710 kg; and BMI, 24.82.9) were studied in a crossover design: i) placebo and ii) 4 mg E(2). Basal and adrenaline-stimulated regional lipolysis was assessed by microdialysis and substrate oxidation rates by indirect calorimetry. Tissue biopsies were obtained to assess lipoprotein lipase activity and mRNA expression of adrenergic, estrogen, cytokine, and vascular reactivity receptors.
  
  
  RESULTS
  Acute E(2) stimulation significantly attenuated catecholamine-stimulated lipolysis in femoral subcutaneous adipose tissue (interstitial glycerol concentration (micromole/liter) ANOVA time vs treatment interaction, P=0.01) and lipolysis in general in abdominal adipose tissue (ANOVA treatment alone, P<0.05). E(2) also reduced basal lipid oxidation ((mg/kg per min) placebo, 0.58 ± 0.06 vs E(2), 0.45 ± 0.03; P=0.03) and induced a significantly higher expression of anti-lipolytic α2A-adrenergic receptor mRNA (P=0.02) in skeletal muscle tissue as well as an upregulation of eNOS (NOS3) mRNA (P=0.02).
  
  
  CONCLUSIONS
  E(2) acutely attenuates the lipolytic response to catecholamines in subcutaneous adipose tissue, shifts muscular adrenergic receptor mRNA toward anti-lipolytic α2A-receptors, decreases whole body lipid oxidation, and enhances expression of markers of vascular reactivity.
authors.affiliation: Medical Research Laboratories, Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Nørrebrogade, DK-8000 Aarhus C, Denmark. lars.christian.gormsen@ki.au.dk
authors.forename: Lars Christian
authors.initials: LC
authors.lastname: Gormsen
authors.forename: Christian
authors.initials: C
authors.lastname: Høst
authors.forename: Britta Eilersen
authors.initials: BE
authors.lastname: Hjerrild
authors.forename: Steen Bønløkke
authors.initials: SB
authors.lastname: Pedersen
authors.forename: Søren
authors.initials: S
authors.lastname: Nielsen
authors.forename: Jens Sandahl
authors.initials: JS
authors.lastname: Christiansen
authors.forename: Claus Højbjerg
authors.initials: CH
authors.lastname: Gravholt
mesh_terms: D018592:Cross-Over Studies; D015536:Down-Regulation / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects*; D008066:Lipolysis / Q000187:drug effects*; D008875:Middle Aged; D010084:Oxidation-Reduction / Q000187:drug effects; D010919:Placebos; D017698:Postmenopause / Q000187:drug effects* / Q000378:metabolism; D016037:Single-Blind Method; D050151:Subcutaneous Fat / Q000187:drug effects* / Q000378:metabolism; D013997:Time Factors
chemical_list: D010919:Placebos; D004958:Estradiol