Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Cra. Valldemossa km 7.5, E-07122 Palma de Mallorca, Spain.
Steroids. 2011 Sep-Oct;76(10-11):1051-6. doi: 10.1016/j.steroids.2011.04.009. Epub 2011 Apr 22.
Taking into account the sexual dimorphism previously reported regarding mitochondrial function and biogenesis in brown adipose tissue, the aim of the present study was to go further into these differences by investigating the effect of ovariectomy and 17-β estradiol (E2) replacement on brown adipose tissue mitochondrial function. In this study, fourteen-week-old control female and ovariectomized female Wistar rats were used. Rats were ovariectomized at 5 weeks of age and were treated every 2 days with placebo (OVX group) or E2 (10 μg/kg) (OVX+E2 group) for 4 weeks before sacrifice. We studied the levels of oxidative capacity, antioxidant defence and oxidative damage markers in brown adipose tissue. Moreover, the levels of key elements of mitochondrial biogenesis as well as UCP1 protein levels, as an index of mitochondrial thermogenic capacity, were also determined. In response to ovariectomy, mitochondrial proliferation increased, resulting in less functional mitochondria, since oxidative capacity and antioxidant defences decreased. Although E2 supplementation was able to restore the serum levels of E2 shown by control rats, the treatment reverted the effects of the ovariectomy only in part, and oxidative and antioxidant capacities in OVX+E2 rats did not reach the levels shown by control females. Taking these results into account, we suggest that ovarian hormones are responsible, at least in part, for the sexual dimorphism in BAT mitochondrial function. However, other signals produced by ovary, rather than E2, would play an important role in the control of mitochondrial function in BAT.
考虑到先前报道的棕色脂肪组织中线粒体功能和生物发生的性别二态性,本研究旨在通过研究卵巢切除术和 17-β 雌二醇(E2)替代对棕色脂肪组织线粒体功能的影响,进一步探讨这些差异。在这项研究中,使用了 14 周龄的对照雌性和卵巢切除雌性 Wistar 大鼠。大鼠在 5 周龄时进行卵巢切除术,并在处死前 4 周每隔 2 天用安慰剂(OVX 组)或 E2(10 μg/kg)(OVX+E2 组)进行治疗。我们研究了棕色脂肪组织中氧化能力、抗氧化防御和氧化损伤标志物的水平。此外,还测定了线粒体生物发生的关键元素以及 UCP1 蛋白水平,作为线粒体产热能力的指标。
卵巢切除后,线粒体增殖增加,导致功能性线粒体减少,因为氧化能力和抗氧化防御能力下降。尽管 E2 补充能够恢复对照大鼠的血清 E2 水平,但该治疗仅部分逆转了卵巢切除术的影响,并且 OVX+E2 大鼠的氧化和抗氧化能力并未达到对照雌性大鼠的水平。
考虑到这些结果,我们认为卵巢激素至少部分负责 BAT 线粒体功能的性别二态性。然而,卵巢产生的其他信号,而不是 E2,可能在 BAT 中线粒体功能的控制中发挥重要作用。