Department of Obstetrics and Gynecology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-Cho, Tokushima 770-8503, Japan.
Department of Obstetrics and Gynecology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-Cho, Tokushima 770-8503, Japan.
Horm Behav. 2021 Jul;133:105005. doi: 10.1016/j.yhbeh.2021.105005. Epub 2021 Jun 8.
Oxytocin (OT) and its receptor (OTR) play various roles in the central and peripheral regulation of appetite and body weight. Previously, we have shown that the administration of OT markedly decreased appetite and body weight gain in ovariectomized (OVX) obese rats. In addition, recent studies have shown that the endogenous OT system is also affected by endogenous or exogenous estrogen. In this study, we showed that ovariectomy decreased rats' hypothalamic OT/OTR mRNA and serum OT levels, but did not affect their visceral fat OTR mRNA levels. The chronic administration of estradiol (E2) abrogated these ovariectomy-induced changes; i.e., it increased the rats' hypothalamic OT/OTR mRNA and serum OT levels, and may be associated with reductions in food intake and body weight gain. In addition, acute E2 administration increased the rats' hypothalamic OTR mRNA and serum OT levels, but did not affect their hypothalamic OT mRNA levels. Taken together, these results suggest that endogenous OT and/or OTR expression might be positively regulated by E2 and that the suppressive effects of E2 on appetite and body weight gain might be mediated, at least in part, by the OT system. Thus, we consider that OT might be a target hormone to pursue subsequent interventions of menopause for menopause-induced metabolic disorders.
催产素（OT）及其受体（OTR）在食欲和体重的中枢和外周调节中发挥多种作用。以前，我们已经表明，OT 的给药显著降低了去卵巢肥胖大鼠的食欲和体重增加。此外，最近的研究表明，内源性 OT 系统也受内源性或外源性雌激素的影响。在这项研究中，我们表明去卵巢减少了大鼠下丘脑 OT/OTR mRNA 和血清 OT 水平，但不影响其内脏脂肪 OTR mRNA 水平。雌二醇（E2）的慢性给药消除了这些去卵巢引起的变化；即，它增加了大鼠下丘脑 OT/OTR mRNA 和血清 OT 水平，并且可能与食物摄入减少和体重增加有关。此外，急性 E2 给药增加了大鼠下丘脑 OTR mRNA 和血清 OT 水平，但不影响其下丘脑 OT mRNA 水平。总之，这些结果表明内源性 OT 和/或 OTR 表达可能受到 E2 的正向调节，并且 E2 对食欲和体重增加的抑制作用可能至少部分通过 OT 系统介导。因此，我们认为 OT 可能是一种目标激素，可以用于后续干预绝经引起的代谢紊乱。
