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本文引用的文献

1
Receptor subtypes and signal transduction mechanisms contributing to the estrogenic attenuation of cannabinoid-induced changes in energy homeostasis.参与雌激素对大麻素诱导的能量平衡变化的受体亚型和信号转导机制。
Neuroendocrinology. 2013;97(2):160-75. doi: 10.1159/000338669. Epub 2012 Aug 28.
2
17β-Estradiol modulates the prolactin secretion induced by TRH through membrane estrogen receptors via PI3K/Akt in female rat anterior pituitary cell culture.17β-雌二醇通过膜雌激素受体通过 PI3K/Akt 调节 TRH 诱导的雌性大鼠垂体前叶细胞培养中的催乳素分泌。
Am J Physiol Endocrinol Metab. 2012 May 1;302(10):E1189-97. doi: 10.1152/ajpendo.00408.2011. Epub 2012 Feb 21.
3
Regulation of leptin expression by 17beta-estradiol in human placental cells involves membrane associated estrogen receptor alpha.17β-雌二醇对人胎盘细胞中瘦素表达的调节涉及膜相关雌激素受体α。
Biochim Biophys Acta. 2012 Apr;1823(4):900-10. doi: 10.1016/j.bbamcr.2012.01.015. Epub 2012 Jan 28.
4
Estrogen effects on the brain: actions beyond the hypothalamus via novel mechanisms.雌激素对大脑的影响:通过新机制作用于下丘脑以外的部位。
Behav Neurosci. 2012 Feb;126(1):4-16. doi: 10.1037/a0026708.
5
The role of NPY in hypothalamic mediated food intake.NPY 在下丘脑介导的摄食中的作用。
Front Neuroendocrinol. 2011 Oct;32(4):398-415. doi: 10.1016/j.yfrne.2011.06.001. Epub 2011 Jun 25.
6
Estradiol acts in the medial preoptic area, arcuate nucleus, and dorsal raphe nucleus to reduce food intake in ovariectomized rats.雌激素在大鼠的视前内侧区、弓状核和中缝背核发挥作用,减少去卵巢大鼠的食物摄入。
Horm Behav. 2011 Jun;60(1):86-93. doi: 10.1016/j.yhbeh.2011.03.009. Epub 2011 Apr 1.
7
Time course of behavioral, physiological, and morphological changes after estradiol treatment of ovariectomized rats.去卵巢大鼠雌激素治疗后行为、生理和形态变化的时间过程。
Physiol Behav. 2011 Jun 1;103(3-4):261-7. doi: 10.1016/j.physbeh.2011.02.017. Epub 2011 Feb 12.
8
Genetic rescue of nonclassical ERα signaling normalizes energy balance in obese Erα-null mutant mice.遗传修复非经典 ERα 信号可使肥胖型 ERα 缺失突变体小鼠的能量平衡恢复正常。
J Clin Invest. 2011 Feb;121(2):604-12. doi: 10.1172/JCI41702. Epub 2011 Jan 18.
9
Estrogen stimulates proliferation and differentiation of neural stem/progenitor cells through different signal transduction pathways.雌激素通过不同的信号转导通路刺激神经干细胞/祖细胞的增殖和分化。
Int J Mol Sci. 2010 Oct 22;11(10):4114-23. doi: 10.3390/ijms11104114.
10
Activation of ERα is necessary for estradiol's anorexigenic effect in female rats.雌激素受体α的激活是雌二醇在雌性大鼠中产生厌食作用所必需的。
Horm Behav. 2010 Nov;58(5):872-7. doi: 10.1016/j.yhbeh.2010.08.012. Epub 2010 Aug 31.

膜相关雌激素受体的激活可减少去卵巢大鼠的食物和水摄入。

Activation of membrane-associated estrogen receptors decreases food and water intake in ovariectomized rats.

机构信息

Department of Psychology, University at Buffalo, State Unioversity of New York, Buffalo, NY 14260, USA.

出版信息

Endocrinology. 2013 Jan;154(1):320-9. doi: 10.1210/en.2012-1858. Epub 2012 Nov 26.

DOI:10.1210/en.2012-1858
PMID:23183173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3529383/
Abstract

Estradiol (E2) decreases food and water intake in a variety of species, including rats. Available evidence suggests that this is mediated by genomic mechanisms that are most often attributed to nuclear estrogen receptors. More recent studies indicate that membrane-associated estrogen receptors (mERs) also can influence gene expression through the activation of transcription factors, yet it is unclear whether mERs are involved in mediating the hypophagic and antidipsetic effects of E2. In the present experiments, we injected E2 or a membrane-impermeable form of E2 (E2-BSA) into the lateral cerebral ventricle of ovariectomized female rats and evaluated the effect on 23 h food and water intake. First, we found that higher doses of E2 were necessary to reduce water intake than were sufficient to reduce food intake. Analysis of drinking microstructure revealed that the decrease in water intake after E2 treatment was mediated by both a decrease in burst number and burst size. Next, the activation of mERs with E2-BSA decreased both overnight food and water intake and analysis of drinking microstructure indicated that the decreased water intake resulted from a decrease in burst number. Finally, E2-BSA did not condition a taste aversion, suggesting that the inhibitory effects on food and water intake were not secondary to malaise. Together these findings suggest that activation of mERs is sufficient to decrease food and water intake in female rats.

摘要

雌二醇(E2)可降低包括大鼠在内的多种物种的食物和水摄入量。现有证据表明,这是通过基因组机制介导的,这些机制通常归因于核雌激素受体。最近的研究表明,膜相关雌激素受体(mERs)也可以通过激活转录因子来影响基因表达,但尚不清楚 mERs 是否参与介导 E2 的食欲减退和抗口渴作用。在本实验中,我们将 E2 或 E2 的一种膜不可渗透形式(E2-BSA)注射到去卵巢雌性大鼠的侧脑室中,并评估其对 23 小时食物和水摄入量的影响。首先,我们发现,与减少食物摄入量相比,需要更高剂量的 E2 才能减少水摄入量。对饮水微观结构的分析表明,E2 处理后水摄入量的减少是由爆发次数和爆发大小的减少介导的。接下来,用 E2-BSA 激活 mERs 可减少整夜的食物和水摄入量,并且对饮水微观结构的分析表明,水摄入量的减少是由于爆发次数的减少所致。最后,E2-BSA 不会引起味觉厌恶,这表明对食物和水摄入量的抑制作用不是不适的次要原因。这些发现表明,mERs 的激活足以减少雌性大鼠的食物和水摄入量。