Stich V, Marion-Latard F, Hejnova J, Viguerie N, Lefort C, Suljkovicova H, Langin D, Lafontan M, Berlan M
Department of Sport Medicine and Obesity Unit, Charles University, Prague, 10000 Czech Republic.
J Clin Endocrinol Metab. 2002 Mar;87(3):1274-81. doi: 10.1210/jcem.87.3.8349.
Previous investigations have shown that alpha 2-adrenoceptor (alpha 2-AR) stimulation blunts lipid mobilization during physiological activation of the sympathetic nervous system promoted by exercise in sc abdominal adipose tissue (SCAAT) in obese men. To investigate the effect of a low calorie diet (LCD) on the alpha 2-adrenergic responsiveness and on the expression of alpha 2-AR and beta 2-adrenoceptor (beta 2-AR) in SCAAT, 11 obese women (weight: 99.1 +/- 4.6 kg; body mass index: 34.3 +/- 1.1 kg/m(2)) received a 12-wk diet providing 500 kcal/d less than their usual diet. The exercise-induced alpha 2-adrenergic antilipolytic effect was investigated in SCAAT before and at the end of LCD. Changes in extracellular glycerol concentration and local blood flow were measured in SCAAT during a 45-min exercise bout (50% of heart rate reserve) using a control microdialysis probe and a probe supplemented with the alpha2-AR antagonist phentolamine. SCAAT biopsies were performed for determination of mRNA levels using RT-competitive PCR. Plasma catecholamine responses to exercise bout were not different before and at the end of LCD. Before LCD, the exercise-induced increase in extracellular glycerol concentration was potentiated by phentolamine supplementation, while this potentiating effect of the alpha-antagonist was not observed at the end of LCD. No changes were observed for beta 2-AR and hormone-sensitive lipase mRNA levels, while alpha 2-AR mRNA level was significantly decreased in adipose tissue during LCD. These findings show that alpha 2-AR-mediated antilipolytic action is reduced by a moderate hypocaloric diet and that down-regulation of alpha 2-AR mRNA levels may participate in the decrease of the alpha 2-adrenergic effect revealed by microdialysis.
先前的研究表明,在肥胖男性的皮下腹部脂肪组织(SCAAT)中,运动促进交感神经系统生理激活期间,α2 -肾上腺素能受体(α2 -AR)的刺激会抑制脂质动员。为了研究低热量饮食(LCD)对SCAAT中α2 -肾上腺素能反应性以及α2 -AR和β2 -肾上腺素能受体(β2 -AR)表达的影响,11名肥胖女性(体重:99.1±4.6 kg;体重指数:34.3±1.1 kg/m²)接受了为期12周的饮食,其热量比她们平常的饮食少500千卡/天。在LCD之前和结束时,对SCAAT中运动诱导的α2 -肾上腺素能抗脂解作用进行了研究。在45分钟的运动期间(心率储备的50%),使用对照微透析探针和补充了α2 -AR拮抗剂酚妥拉明的探针,测量SCAAT中的细胞外甘油浓度和局部血流变化。进行SCAAT活检,使用RT-竞争性PCR测定mRNA水平。LCD之前和结束时,血浆儿茶酚胺对运动的反应没有差异。在LCD之前,补充酚妥拉明可增强运动诱导的细胞外甘油浓度升高,而在LCD结束时未观察到这种α拮抗剂的增强作用。β2 -AR和激素敏感性脂肪酶mRNA水平没有变化,而在LCD期间脂肪组织中α2 -AR mRNA水平显著降低。这些发现表明,适度的低热量饮食会降低α2 -AR介导的抗脂解作用,并且α2 -AR mRNA水平的下调可能参与了微透析所揭示的α2 -肾上腺素能效应的降低。