Estradiol acutely inhibits whole body lipid oxidation and attenuates lipolysis in subcutaneous adipose tissue: a randomized, placebo-controlled study in postmenopausal women

Abstract

Context: 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 a2A-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 17b-E 2 on regional and systemic lipolysis. Methods: Sixteen postmenopausal women (age, 59G5 years; weight, 67G10 kg; and BMI, 24.8G2.9) 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, PZ0.01) 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, 0.58G0.06 vs E 2 , 0.45G0.03; PZ0.03) and induced a significantly higher expression of anti-lipolytic a2A-adrenergic receptor mRNA (PZ0.02) in skeletal muscle tissue as well as an upregulation of eNOS (NOS3) mRNA (PZ0.02). Conclusion: E 2 acutely attenuates the lipolytic response to catecholamines in subcutaneous adipose tissue, shifts muscular adrenergic receptor mRNA toward anti-lipolytic a2A-receptors, decreases whole body lipid oxidation, and enhances expression of markers of vascular reactivity.

Risk Assessment on Anastomotic Leakage after Rectal Cancer Surgery: An Analysis of 753 Patients

“…Obviously more collagen than men accumulated by premenopausal women implied that a young lady has a high level collagen formation capacity while the postmenopausal hasn't. These come outs manifest that the female hormones are related to collagen deposition, and the estrogen is a protected factor of AL presumably and mediately (Markiewicz et al, 2007;Aznal et al, 2012;Gormsen et al, 2012).…”

Estradiol does not directly regulate adipose lipolysis

“…13,28 In humans, a single dose of E2 attenuated catecholamine-stimulated lipolysis in femoral subcutaneous adipose. 7 In our hands, CL was equally effective in increasing whole-body lipolysis in SHAM, OVX and OVX E2 rats. Unlike Darimont et al, 15 who found increased responsiveness of subcutaneous adipose to isoproterenol infusion after 7 d of E2 injection, we did not observe an augmentation of serum FFA or glycerol in OVX E2 rats after 2 weeks of treatment.…”

“…The changes we 32 and others. 7,14 have observed in subcutaneous tissue suggest it may be more affected by the chronic absence of E2.…”

“…4,5 There is some evidence in humans that E2 is antilipolytic through its potentiation of insulin's suppression of lipolysis, 6 and inhibition of catecholamine-stimulated lipolysis in subcutaneous adipose tissue. 7 Our understanding of the mechanisms by which E2 regulates lipolysis in vivo are largely derived from the ovariectomized (OVX) rodent model. Whole-body circulating FFA concentrations are decreased in OVX mice, but increased after treatment with E2 for 60 d. 8 Further evidence points to visceral adipose tissue as a site of impaired lipolyis in the absence of E2.…”

Visceral obesity and cardiometabolic risk: features of hormonal and immune regulation

“…Под влиянием эстрадиола увеличивается экспрес-сия антилиполитических α2A-адренергических рецеп-торов в подкожной жировой клетчатке, в особенности в феморальной области, в то время как в ВЖТ данный эффект отсутствует [34]. Назначение эстрадиола кры-сам с удаленными яичниками приводило к увеличе-нию утилизации глюкозы адипоцитами, снижению артериального давления, концентрации инсулина, увеличению экспрессии рецепторов, активирующих пролиферацию пероксисом-гамма (PPAR-γ) в адипо-цитах, в то время как экспрессия PPAR-α возрастала в печени [35].…”