Potentiation of Ecstasy-induced hyperthermia and FAT/CD36 expression in chronically exercised animals

S. Hrometz, Jeremy A. Ebert, K. E. Grice, Sara M. Nowinski, E. Mills, B. Myers, J. E. Sprague
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引用次数: 4

Abstract

ABSTRACT Fatal hyperthermia as a result of 3,4-methylenedioxymethamphetamine (MDMA) use involves non-esterified free fatty acids (NEFA) and the activation of mitochondrial uncoupling proteins (UCP). NEFA gain access into skeletal muscle via specific transport proteins, including fatty acid translocase (FAT/CD36). FAT/CD36 expression is known to increase following chronic exercise. Previous studies have demonstrated the essential role of NEFA and UCP3 in MDMA-induced hyperthermia. The aims of the present study were to use a chronic exercise model (swimming for two consecutive hours per day, five days per wk for six wk) to increase FAT/CD36 expression in order to: 1) determine the contribution of FAT/CD36 in MDMA (20 mg/kg, s.c.)-mediated hyperthermia; and 2) examine the effects of the FAT/CD36 inhibitor, SSO (sulfo-N-succinimidyl oleate), on MDMA-induced hyperthermia in chronic exercise and sedentary control rats. MDMA administration resulted in hyperthermia in both sedentary and chronic exercise animals. However, MDMA-induced hyperthermia was significantly potentiated in the chronic exercise animals compared to sedentary animals. Additionally, chronic exercise significantly reduced body weight, increased FAT/CD36 protein expression levels and reduced plasma NEFA levels. The FAT/CD36 inhibitor, SSO (40 mg/kg, ip), significantly attenuated the hyperthermia mediated by MDMA in chronic exercised but not sedentary animals. Plasma NEFA levels were elevated in sedentary and exercised animals treated with SSO prior to MDMA suggesting attenuation of NEFA uptake into skeletal muscle. Chronic exercise did not alter skeletal muscle UCP3 protein expression levels. In conclusion, chronic exercise potentiates MDMA-mediated hyperthermia in a FAT/CD36 dependent fashion.
摇头丸诱导的慢性运动动物热疗和FAT/CD36表达的增强作用
使用3,4-亚甲基二氧基甲基苯丙胺(MDMA)导致的致命性高热涉及非酯化游离脂肪酸(NEFA)和线粒体解偶联蛋白(UCP)的激活。NEFA通过特定的转运蛋白,包括脂肪酸转位酶(FAT/CD36)进入骨骼肌。已知脂肪/CD36表达在长期运动后增加。先前的研究已经证实了NEFA和UCP3在mdma诱导的热疗中的重要作用。本研究的目的是使用慢性运动模型(每天连续游泳2小时,每周5天,连续6周)增加FAT/CD36表达,以便:1)确定FAT/CD36在MDMA (20 mg/kg, s.c)介导的热疗中的作用;2)研究FAT/CD36抑制剂SSO(磺基- n -琥珀酰油酸酯)对慢性运动和久坐对照大鼠mdma诱导的高温的影响。在久坐和长期运动的动物中,MDMA均导致高热。然而,与久坐不动的动物相比,mdma诱导的热疗在慢性运动动物中显著增强。此外,慢性运动显著降低体重,增加脂肪/CD36蛋白表达水平,降低血浆NEFA水平。FAT/CD36抑制剂SSO (40 mg/kg, ip)可显著降低MDMA介导的慢性运动而非久坐动物的高热。在MDMA之前,久坐和运动的动物接受SSO治疗,血浆NEFA水平升高,表明骨骼肌对NEFA的吸收减弱。慢性运动不改变骨骼肌UCP3蛋白表达水平。总之,慢性运动以FAT/CD36依赖的方式增强mdma介导的热疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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