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Zhao, Hong; Tian, Zhanzhuang; Hao, Jun-wei; Chen, Bo-Ying

doi:10.1186/1477-7827-3-6

Cited by 95 publications

(38 citation statements)

References 25 publications

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“…In this sense, it is worth noting that estrogen production has been reported to shift from ovaries to extragonadal sites when ovarian function fails in young females (Simpson 2003). Moreover, results described in previous reports have shown that circulating estrogen concentration increases gradually with time after ovariectomy in rats, which has been attributed to greater aromatase activity in adipose tissue, among other factors (Zhao et al 2005).…”

Section: Discussionmentioning

confidence: 84%

Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle

Capllonch-Amer¹,

Sbert-Roig²,

Galmés-Pascual³

et al. 2014

Journal of Endocrinology

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Sexual dimorphism has been found in mitochondrial features of skeletal muscle, with female rats showing greater mitochondrial mass and function compared with males. Adiponectin is an insulin-sensitizing adipokine whose expression has been related to mitochondrial function and that is also expressed in skeletal muscle, where it exerts local metabolic effects. The aim of this research was to elucidate the role of sex hormones in modulation of mitochondrial function, as well as its relationship with adiponectin production in rat skeletal muscle. An in vivo study with ovariectomized Wistar rats receiving or not receiving 17b-estradiol (E 2 ) (10 mg/kg per 48 h for 4 weeks) was carried out, in parallel with an assay of cultured myotubes (L6E9) treated with E 2 (10 nM), progesterone (Pg; 1 mM), or testosterone (1 mM). E 2 upregulated the markers of mitochondrial biogenesis and dynamics, and also of mitochondrial function in skeletal muscle and L6E9. Although in vivo E 2 supplementation only partially restored the decreased adiponectin expression levels induced by ovariectomy, these were enhanced by E 2 and Pg treatment in cultured myotubes, whereas testosterone showed no effects. Adiponectin receptor 1 expression was increased by E 2 treatment, both in vivo and in vitro, but testosterone decreased it. In conclusion, our results are in agreement with the sexual dimorphism previously reported in skeletal muscle mitochondrial function and indicate E 2 to be its main effector, as it enhances mitochondrial function and diminishes oxidative stress. Moreover, our data support the idea of the existence of a link between mitochondrial function and adiponectin expression in skeletal muscle, which could be modulated by sex hormones.

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Section: Discussionmentioning

confidence: 84%

Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle

Capllonch-Amer¹,

Sbert-Roig²,

Galmés-Pascual³

et al. 2014

Journal of Endocrinology

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“…A rise in plasma E2 was seen following ovariectomy, albeit at 6 months, that may be attributed to extragonadal aromatization, although the source of substrate is not known [67]. E2 levels in OVX rats given SO alone are probably not due to injections per se or contamination by SO.…”

Section: Resultsmentioning

confidence: 99%

“…Levels of E2 following SO treatment alone may arise from extragonadal sources, such as adipose tissue or liver [67]. A rise in plasma E2 was seen following ovariectomy, albeit at 6 months, that may be attributed to extragonadal aromatization, although the source of substrate is not known [67].…”

Section: Resultsmentioning

confidence: 99%

Dose and Time Effects of Estrogen on Expression of Neuron-Specific Protein and Cyclic AMP Response Element-Binding Protein and Brain Region Volume in the Medial Amygdala of Ovariectomized Rats

Liu

Hanbury

Pandey³

et al. 2008

Neuroendocrinology

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Although estrogen has been shown to be neuroprotective, studies concerning its effect on some behaviors are contradictory, reporting both ameliorative and detrimental effects. A factor involved in hormone efficacy is the estrogen regimen. We reported an effect of 10 µg estrogen for 14 days on the cyclic AMP response element-binding protein (CREB) pathway, including brain-derived neurotrophic factor, in rat medial amygdala (MeA). To determine the effects of estrogen on neuronal numbers and brain region volume in MeA and central nucleus of the amygdala (CeA), we used stereology to test the effect of various estrogen regimens on the number of neuron-specific protein (NeuN)-labeled neurons and brain region volume of MeA and CeA. Ovariectomized rats were injected with vehicle for 14 days, 2.5 µg estradiol benzoate (E2) for 4 or 14 days, or 10 µg estrogen for 14 days. Because NeuN-labeled neuronal number may be related to neuronal survival and upregulation of CREB signaling, we tested the effect of these regimens on levels of phosphorylated CREB (pCREB) labeling in the MeA and CeA. The 2.5 µg estrogen for 14 days regimen increased the mean number of NeuN-labeled neurons and pCREB-labeled cells in the MeA compared to vehicle or 2.5 µg for 4 days. There was an increase in volume of the MeA with 2.5 µg estrogen for 14 days compared to vehicle or 2.5 µg for 4 days. No differences in these parameters were seen in CeA. These data indicate a neuroanatomical heterogeneity of a time effect of estrogen on cells expressing NeuN and pCREB in the MeA versus CeA.

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“…A change in lipid uptake might thus be a possible mechanism that contributes to the estrogen-induced change in lipid metabolism [20]. Ovariectomized rodents exhibit a constant increase in circulating estrogen levels over time (although lower than before ovariectomy), which is related to an increase in aromatase activity in s.c. fat and liver [21].…”

Section: Estrogen Production In Fatmentioning

confidence: 99%

Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism

Mattsson¹,

Olsson

2007

CMC

119

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Women have a higher percentage of body fat than men, and there is a gender-specific difference in fat distribution: Females tend to accumulate fat around the hips, buttocks, and thighs while men have a larger intra-abdominal (visceral) fat mass. After menopause, there is a redistribution of fat depots, and post-menopausal women develop increased amounts of visceral fat. The risk of developing obesity-related diseases is significantly lower in pre-menopausal women compared to men, a difference that is abolished after menopause, suggesting that the female sex steroid estrogen influences adipogenesis and adipose metabolism. Experimentally, estrogen increases the size and number of subcutaneous adipocytes and attenuates lipolysis. Post-menopausal women also develop a more atherogenic lipid pattern and decreased levels of the prothrombotic protein plasminogen activator inhibitor-1, which attenuates fibrinolysis. Pathologically increased circulating cortisol concentration is associated with dysmetabolic features e.g., central obesity, elevated blood pressure, insulin resistance, and dyslipidemia. In "simple obesity," glucocorticoid production is elevated. Peak levels of circulating cortisol are however low or normal, possibly because of increased clearance and/or tissue-specific changes in cortisol production. In addition to the adrenal production of cortisol, cortisol is also generated in adipose tissue by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) which converts inactive cortisone to active cortisol. The enzyme activity in subcutaneous fat increases with increasing body weight. Estrogen seems to have a tissue-specific influence on 11betaHSD1 enzyme activity, attenuating it in liver, kidney, and testis but upregulating 11betaHSD1 mRNA expression in preadipocytes from women. In the present review, we summarize and discuss the interaction between glucocorticoids and sex steroids and their influence on adipocyte metabolism.

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Untitled

Cited by 95 publications

References 25 publications

Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle

Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle

Dose and Time Effects of Estrogen on Expression of Neuron-Specific Protein and Cyclic AMP Response Element-Binding Protein and Brain Region Volume in the Medial Amygdala of Ovariectomized Rats

Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism

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