Casquero Andrea Camargo, Berti Jairo Augusto, Teixeira Laura Lauand Sampaio, de Oliveira Helena Coutinho Franco
Department of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas, SP, 13083-862, Brazil.
Centro Universitário de Araraquara, Araraquara, SP, 14801-340, Brazil.
Lipids. 2017 Dec;52(12):981-990. doi: 10.1007/s11745-017-4299-1. Epub 2017 Oct 20.
Regular exercise and anabolic androgenic steroids have opposing effects on the plasma lipoprotein profile and risk of cardio-metabolic diseases in humans. Studies in humans and animal models show conflicting results. Here, we used a mice model genetically modified to mimic human lipoprotein profile and metabolism. They under-express the endogenous LDL receptor gene (R1) and express a human transgene encoding the cholesteryl ester transfer protein (CETP), normally absent in mice. The present study was designed to evaluate the independent and interactive effects of testosterone supplementation, exercise training and CETP expression on the plasma lipoprotein profile and CETP activity. CETP/R1 and R1 mice were submitted to a 6-week swimming training and mesterolone (MEST) supplementation in the last 3 weeks. MEST treatment increased markedly LDL levels (40%) in sedentary CETP/R1 mice and reduced HDL levels in exercised R1 mice (18%). A multifactorial ANOVA revealed the independent effects of each factor, as follows. CETP expression reduced HDL (21%) and increased non-HDL (15%) fractions. MEST treatment increased the VLDL concentrations (42%) regardless of other interventions. Exercise training reduced triacylglycerol (25%) and free fatty acids (20%), increased both LDL and HDL (25-33%), and reduced CETP (19%) plasma levels. Significant factor interactions showed that the increase in HDL induced by exercise is explained by reducing CETP activity and that MEST blunted the exercise-induced elevation of HDL-cholesterol. These results reinforce the positive metabolic effects of exercise, resolved a controversy about CETP response to exercise and evidenced MEST potency to counteract specific exercise benefits.
规律运动和合成代谢雄激素类固醇对人类血浆脂蛋白谱及心血管代谢疾病风险具有相反作用。在人类和动物模型中的研究结果相互矛盾。在此,我们使用了一种经过基因改造以模拟人类脂蛋白谱和代谢的小鼠模型。它们内源性低密度脂蛋白受体基因(R1)表达不足,并表达一种编码胆固醇酯转运蛋白(CETP)的人类转基因,而该蛋白在小鼠中通常不存在。本研究旨在评估睾酮补充、运动训练和CETP表达对血浆脂蛋白谱及CETP活性的独立和交互作用。CETP/R1和R1小鼠接受了为期6周的游泳训练,并在最后3周补充了美睾酮(MEST)。MEST治疗使久坐不动的CETP/R1小鼠的低密度脂蛋白水平显著升高(40%),并使运动的R1小鼠的高密度脂蛋白水平降低(18%)。多因素方差分析揭示了各因素的独立作用,具体如下。CETP表达降低了高密度脂蛋白(21%),并增加了非高密度脂蛋白(15%)组分。无论其他干预措施如何,MEST治疗均使极低密度脂蛋白浓度升高(42%)。运动训练降低了三酰甘油(25%)和游离脂肪酸(20%),使低密度脂蛋白和高密度脂蛋白均升高(25 - 33%),并降低了血浆中CETP水平(19%)。显著的因素交互作用表明,运动诱导的高密度脂蛋白增加是通过降低CETP活性来解释的,并且MEST减弱了运动诱导的高密度脂蛋白胆固醇升高。这些结果强化了运动的积极代谢作用,解决了关于CETP对运动反应的争议,并证明了MEST抵消特定运动益处的效力。