Body composition, visceral fat distribution and fat oxidation in postmenopausal women using oral or transdermal oestrogen

Reis, Caio Luiz Bitencourt; Melo, Nilson Roberto de; Meirelles, Eduardo S.; Vezozzo, Denise P.; Halpern, Alfredo

doi:10.1016/s0378-5122(03)00159-2

Cited by 58 publications

(26 citation statements)

References 33 publications

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“…Rates of lipid oxidation and REE in the fasted state were similar between groups. These findings are congruent with our previous observations in girls with Turner syndrome (26) and in fasting postmenopausal women (1), but differ from results of lower lipid oxidation during oral CEE replacement in postmenopausal women studied postprandially (25).…”

Section: Discussionsupporting

confidence: 90%

“…There were no differential changes in BMI or percent abdominal fat during the study. This differs from previous studies where lean body mass improved only with TD E 2 (25) and total body fat mass increased using oral estrogen (1,25). However, both these studies used CEE in contrast to 17␤-E 2 , making the current study comparisons more robust.…”

Section: Discussionmentioning

confidence: 58%

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Metabolic Effects of Oral Versus Transdermal 17β-Estradiol (E2): A Randomized Clinical Trial in Girls With Turner Syndrome

Torres-Santiago

Mericq

Taboada

et al. 2013

The Journal of Clinical Endocrinology &Amp; Metabolism

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Context:The long-term effects of pure 17␤-estradiol (E 2 ) depending on route of administration have not been well characterized.Objective: Our objective was to assess metabolic effects of oral vs transdermal (TD) 17␤-E 2 replacement using estrogen concentration-based dosing in girls with Turner syndrome (TS).Patients: Forty girls with TS, mean age 16.7 Ϯ 1.7 years, were recruited.Design: Subjects were randomized to 17␤-E 2 orally or TD. Doses were titrated using mean E 2 concentrations of normally menstruating girls as therapeutic target. E 2 , estrone (E 1 ), and E 1 sulfate (E 1 S) were measured by liquid chromatography tandem mass spectrometry and a recombinant cell bioassay; metabolites were measured, and dual-energy x-ray absorptiometry scan and indirect calorimetry were performed.Main Outcome: Changes in body composition and lipid oxidation were evaluated.Results: E 2 concentrations were titrated to normal range in both groups; mean oral dose was 2 mg, and TD dose was 0.1 mg. After 6 and 12 months, fat-free mass and percent fat mass, bone mineral density accrual, lipid oxidation, and resting energy expenditure rates were similar between groups. IGF-1 concentrations were lower on oral 17␤-E 2 , but suppression of gonadotropins was comparable with no significant changes in lipids, glucose, osteocalcin, or highly sensitive C-reactive protein between groups. However, E 1 , E 1 S, SHBG, and bioestrogen concentrations were significantly higher in the oral group.Conclusions: When E 2 concentrations are titrated to the normal range, the route of delivery of 17␤-E 2 does not affect differentially body composition, lipid oxidation, and lipid concentrations in hypogonadal girls with TS. However, total estrogen exposure (E 1 , E 1 S, and total bioestrogen) is significantly higher after oral 17␤-E 2 . TD 17␤-E 2 results in a more physiological estrogen milieu than oral 17␤-E 2 administration in girls with TS. (J Clin Endocrinol Metab 98: 2716 -2724, 2013) E strogen is indispensable for normal physiological function in females including breast development and feminization, the growth and differentiation of primary sex organs, skeletal maturation, consolidation, and growth. Although a variety of types of estrogen can achieve full feminization in hypogonadal females, it re-

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 58%

Metabolic Effects of Oral Versus Transdermal 17β-Estradiol (E2): A Randomized Clinical Trial in Girls With Turner Syndrome

Torres-Santiago

Mericq

Taboada

et al. 2013

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…In line with the findings of most (14,36,37,38,39), but not all (40), previous studies, whole body lipid oxidation was significantly decreased in our volunteers during E 2 treatment. However, whereas previous studies have been designed to study more long-term effects of estrogens with typical treatment periods lasting 1-12 months, this is to our knowledge the first study in humans reporting immediate effects of estrogen on lipid oxidation.…”

Section: Discussionsupporting

confidence: 93%

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

Gormsen

Høst²,

Hjerrild³

et al. 2012

European Journal of Endocrinology

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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.

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“…While we lacked data regarding the route of estrogen administration during the study, visit 4 of ARIC completed in 1998, at which point >75% of estrogen replacement was oral 24. Topical or vaginal estrogen replacement, as is more common currently, was found to improve lean body mass without affecting fat mass 21, 22, 23. We did not note differences in the rate of change in MetS severity by current estrogen use—although we lacked data regarding dose and adherence to estrogen use, which may have further influenced any effect.…”

Section: Discussionmentioning

confidence: 99%

Progression of Metabolic Syndrome Severity During the Menopausal Transition

Gurka

Vishnu

Santen

et al. 2016

JAHA

124

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BackgroundAfter menopause, women exhibit a higher prevalence of the metabolic syndrome (MetS) and higher risk of cardiovascular disease. However, the timing of changes in MetS severity over the menopausal transition and whether these changes differ by racial/ethnic group remain unclear.Methods and ResultsWe assessed data from 1470 women from the Atherosclerosis Risk in Communities cohort who experienced transition in menopausal status over 10 years (visits 1–4). We used linear mixed models to evaluate changes by menopausal status (premenopause, perimenopause, and postmenopause) in a MetS severity Z‐score and in the individual MetS components. While there were gradual increases in MetS severity over time across menopause stages, black women in particular exhibited more rapid progression in MetS severity during the premenopausal and perimenopausal periods than during the postmenopausal period. In the postmenopausal period (compared with prior periods), white women exhibited unfavorable decreases in high‐density lipoprotein, while black women exhibited favorable alterations in the rate of change for waist circumference, triglycerides, high‐density lipoprotein, and glucose, contributing to the slowed progression of MetS severity. These changes were all observed after adjusting for hormone replacement treatment.ConclusionsDuring menopausal transition, women exhibited rapid increases in MetS severity during the premenopausal and perimenopausal periods, with black women having significant reductions in this increase in severity during the postmenopausal period. These data suggest that the higher prevalence of MetS in postmenopausal women may be caused more by changes during the menopausal transition than by postmenopause. These findings may thus have implications regarding the timing of cardiovascular risk relative to menopause.

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Body composition, visceral fat distribution and fat oxidation in postmenopausal women using oral or transdermal oestrogen

Cited by 58 publications

References 33 publications

Metabolic Effects of Oral Versus Transdermal 17β-Estradiol (E2): A Randomized Clinical Trial in Girls With Turner Syndrome

Metabolic Effects of Oral Versus Transdermal 17β-Estradiol (E2): A Randomized Clinical Trial in Girls With Turner Syndrome

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

Progression of Metabolic Syndrome Severity During the Menopausal Transition

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