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帕金森病大鼠模型中的棕色脂肪组织激活

Brown adipose tissue activation in a rat model of Parkinson's disease.

作者信息

Wang Wenjuan, Meng Xiangzhi, Yang Chun, Fang Dongliang, Wang Xuemeng, An Jiaqiang, Zhang Jingyi, Wang Lulu, Lu Tao, Ruan Hai-Bin, Gao Yan

机构信息

Department of Human Anatomy, Histology, and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.

Cancer Hospital of HuanXing ChaoYang District Beijing, Beijing, China; and.

出版信息

Am J Physiol Endocrinol Metab. 2017 Dec 1;313(6):E731-E736. doi: 10.1152/ajpendo.00049.2017. Epub 2017 Aug 29.

DOI:10.1152/ajpendo.00049.2017
PMID:28851733
Abstract

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson's disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.

摘要

体重和脂肪量的减少是帕金森病(PD)的非运动症状之一。体重减轻主要是由于能量摄入减少和能量消耗增加。虽然PD患者能量摄入不足主要由食欲减退和胃肠吸收受损引起,但能量消耗增加的潜在机制在很大程度上仍不清楚。棕色脂肪组织(BAT)是人类和其他哺乳动物中的关键产热组织,在体温调节和能量代谢中起重要作用;然而,BAT是否参与PD患者的负能量平衡尚未得到验证。在此,我们使用6-羟基多巴胺(6-OHDA)诱导的PD大鼠模型,发现PD大鼠的交感神经(SN)活性、BAT中Ucp1的表达及产热均增加。BAT交感神经去神经支配可阻断交感神经活性,降低BAT中UCP1的表达,并减轻PD大鼠的体重减轻。有趣的是,BAT交感神经去神经支配与腹膜后和附睾白色脂肪组织中交感神经张力降低和脂肪分解减少有关。我们的数据表明,BAT介导的产热可能导致PD患者体重减轻。

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