Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11β-HSD1 in the Syrian hamster
Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11β-HSD1 in the Syrian hamster
复制标题
DOI：
10.1152/japplphysiol.01236.2005
复制
发表时间：
2006-05-01
影响因子：
3.3
通讯作者：
Riddell, MC
中科院分区：
文献类型：
--
作者：
Coutinho, AE;Campbell, JE;Riddell, MC
最近的研究表明，内脏脂肪组织和骨骼肌中糖皮质激素（GC）水平升高，由11 β-羟基类固醇脱氢酶1型（11 β-HSD 1）和GC受体（GR）的表达控制，导致胰岛素抵抗增加和代谢综合征。自相矛盾的是，有证据表明，有氧运动可以减弱代谢综合征的发展，尽管它会刺激循环GC水平的急剧增加。为了研究训练改变外周GC作用以维持胰岛素敏感性的假设，将年轻雄性仓鼠随机分为久坐组（S）和训练组（T）（每组n = 8）。T组在4周的研究中有24小时的跑步轮。在肌肉中，T仓鼠的11 β-HSD 1蛋白表达较低，（19.2 +/- 1.40对比22.2 +/- 0.96光密度，P < 0.05），相似的11 β-HSD 1酶活性（0.9 +/-0.27%vs.1.1 +/- 0.26）和较低的GR蛋白表达（9.7 +/-1.86vs.15.1 +/- 1.78光密度，P < 0.01）。在肝脏中，与S相比，T中11 β-HSD 1蛋白表达倾向于较低（19.2 +/- 0.56 vs. 21.4 +/- 1.05，P = 0.07），而酶活性和GR蛋白表达相似。相比之下，内脏脂肪组织中的11 β-HSD 1酶活性在T组比S组高2.7倍（12.9 +/- 3.3 vs. 4.8 +/- 1.5%转化率，P < 0.05），但质量显著较小（0.24 +/- 0.02 vs. 0.71 +/- 0.06 g）。因此，GC调节剂对运动的细胞内适应是组织特异性的，导致骨骼肌中GC作用的减少和内脏脂肪中GC作用的增加。这些适应性变化可能对解释有氧运动对胰岛素抵抗和代谢综合征的其他症状的保护作用具有重要意义。
Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) and GC receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups (n = 8 in each). The T group had 24-h access to running wheels over 4 wk of study. In muscle, T hamsters had lower 11 beta-HSD1 protein expression (19.2 +/- 1.40 vs. 22.2 +/- 0.96 optical density, P < 0.05), similar 11 beta-HSD1 enzyme activity (0.9 +/- 0.27% vs. 1.1 +/- 0.26), and lower GR protein expression (9.7 +/- 1.86 vs. 15.1 +/- 1.78 optical density, P < 0.01) than S hamsters. In liver, 11 beta-HSD1 protein expression tended to be lower in T compared with S (19.2 +/- 0.56 vs. 21.4 +/- 1.05, P = 0.07), whereas both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained similar to 2.7-fold higher 11 beta-HSD1 enzyme activity in T compared with S (12.9 +/- 3.3 vs. 4.8 +/- 1.5% conversion, P < 0.05) but was considerably smaller in mass (0.24 +/- 0.02 vs. 0.71 +/- 0.06 g). Thus the intracellular adaptation of GC regulators to exercise is tissue specific, resulting in decreases in GC action in skeletal muscle and increases in GC action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome.