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The estrogenic reduction in water intake stimulated by dehydration involves estrogen receptor alpha and a potential role for GLP-1
Physiology & Behavior ( IF 2.9 ) Pub Date : 2024-02-06 , DOI: 10.1016/j.physbeh.2024.114484
Julia A. Howell , Andrea A. Edwards , Jessica Santollo

It is well documented that estrogens inhibit fluid intake. Most of this research, however, has focused on fluid intake in response to dipsogenic hormone and/or drug treatments in euhydrated rats. Additional research is needed to fully characterize the fluid intake effects of estradiol in response to true hypovolemia. As such, the goals of this series of experiments were to provide a detailed analysis of water intake in response to water deprivation in ovariectomized female rats treated with estradiol. In addition, these experiments also tested if activation of estrogen receptor alpha is sufficient to reduce water intake stimulated by water deprivation and tested for a role of glucagon like peptide-1 in the estrogenic control of water intake. As expected, estradiol reduced water intake in response to 24 and 48 h of water deprivation. The reduction in water intake was associated with a reduction in drinking burst number, with no change in drinking burst size. Pharmacological activation of estrogen receptor alpha reduced intake. Finally, estradiol-treatment caused a leftward shift in the behavioral dose response curve of exendin-4, the glucagon like peptide-1 agonist. While the highest dose of exendin-4 reduced 10 min intake in both oil and estradiol-treated rats, the intermediate dose only reduced intake in rats treated with estradiol. Together, this series of experiments extends previous research by providing a more thorough behavioral analysis of the anti-dipsogenic effect of estradiol in dehydrated rats, in addition to identifying the glucagon like peptide-1 system as a potential bioregulator involved in the underlying mechanisms by which estradiol reduces water intake in the female rat.

中文翻译:

脱水引起的雌激素水摄入量减少涉及雌激素受体 α 和 GLP-1 的潜在作用

有充分证据表明雌激素会抑制液体摄入。然而,这项研究的大部分内容都集中在水合大鼠对促性激素和/或药物治疗的反应中的液体摄入量。需要进行更多的研究来充分表征雌二醇对真正的低血容量的液体摄入影响。因此,这一系列实验的目的是对接受雌二醇治疗的卵巢切除雌性大鼠缺水时的饮水量进行详细分析。此外,这些实验还测试了雌激素受体α的激活是否足以减少因缺水而刺激的水摄入量,并测试了胰高血糖素样肽-1在雌激素控制水摄入量中的作用。正如预期的那样,雌二醇在 24 小时和 48 小时缺水后减少了水的摄入量。饮水量的减少与突发性饮水次数的减少相关,但突发性饮水量没有变化。雌激素受体α的药理激活减少了摄入量。最后,雌二醇治疗导致 Exendin-4(胰高血糖素样肽-1 激动剂)的行为剂量反应曲线向左移动。虽然最高剂量的 exendin-4 减少了油和雌二醇治疗的大鼠 10 分钟的摄入量,但中间剂量仅减少了雌二醇治疗的大鼠的摄入量。总之,这一系列的实验扩展了之前的研究,对脱水大鼠中雌二醇的抗体力作用进行了更彻底的行为分析,此外还确定了胰高血糖素样肽-1系统作为参与潜在机制的潜在生物调节剂。雌二醇减少雌性大鼠的水摄入量。
更新日期:2024-02-06
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