Jean Hailes Foundation Research, School of Public Health and Preventative Medicine, Monash University, Melbourne, VIC, Australia.
Diabetologia. 2012 May;55(5):1424-34. doi: 10.1007/s00125-011-2442-8. Epub 2012 Jan 13.
AIMS/HYPOTHESIS: Polycystic ovary syndrome (PCOS) is an insulin resistant (IR) state. Increased skeletal muscle lipid content and impaired mitochondrial biogenesis have been implicated in the pathogenesis of IR. We investigated whether differences in these variables explain the IR of women affected by PCOS and whether improvements in IR with exercise are reflected by changes in these variables.
Sixteen PCOS and 13 non-PCOS overweight women were assessed, and eight PCOS and seven non-PCOS women were reassessed after 12 weeks of moderate and vigorous exercise training. Outcomes included insulin sensitivity (glucose infusion rate [GIR]), skeletal muscle gene expression and protein abundance, enzyme activity of selected mitochondrial components, and computed tomography (CT) attenuation-estimated muscle lipid.
GIR was lower in women with PCOS versus those without (p = 0.01) and increased with exercise in both groups. Baseline CT muscle attenuation suggested a trend to less muscle lipid in PCOS, which increased with exercise training, with a difference in the change in muscle lipid (p = 0.01, age-corrected), compared with non-PCOS women. GIR correlated with PGC1A gene expression across the whole group; skeletal muscle expression of mitochondrial biogenesis markers was not different between groups at baseline, or after training. Neither lipid changes nor mitochondrial changes correlated with changes in GIR.
CONCLUSIONS/INTERPRETATION: Differences in IR in women with and without PCOS were not explained by differences in skeletal muscle lipid or mitochondrial parameters. Improvements in IR with exercise were dissociated from mitochondrial parameters. CT muscle attenuation suggested a differential capacity of PCOS muscle to store lipid compared with non-PCOS.
Clinicaltrials.gov ISRCTN84763265.
National Health & Medical Research Council (Grant number 606553), Monash University and The Jean Hailes Foundation.
目的/假设：多囊卵巢综合征（PCOS）是一种胰岛素抵抗（IR）状态。骨骼肌脂质含量增加和线粒体生物发生受损与 IR 的发病机制有关。我们研究了这些变量的差异是否可以解释受 PCOS 影响的女性的 IR，以及运动对 IR 的改善是否反映在这些变量的变化中。
评估了 16 名 PCOS 和 13 名非 PCOS 超重女性，并在 12 周的中等和剧烈运动训练后重新评估了 8 名 PCOS 和 7 名非 PCOS 女性。结果包括胰岛素敏感性（葡萄糖输注率[GIR]）、骨骼肌基因表达和蛋白丰度、选定线粒体成分的酶活性以及计算机断层扫描（CT）衰减估计的肌肉脂质。
与非 PCOS 女性相比，PCOS 女性的 GIR 较低（p=0.01），并且两组女性的 GIR 在运动后均增加。基线 CT 肌肉衰减表明 PCOS 肌肉中的肌肉脂质趋势较少，随着运动训练增加，与非 PCOS 女性相比，肌肉脂质的变化存在差异（p=0.01，年龄校正）。GIR 与整个组的 PGC1A 基因表达相关；基线时，线粒体生物发生标志物的骨骼肌表达在两组之间没有差异，或在训练后。脂质变化和线粒体变化均与 GIR 的变化无关。
结论/解释：有和没有 PCOS 的女性之间的 IR 差异不能用骨骼肌脂质或线粒体参数来解释。运动对 IR 的改善与线粒体参数无关。CT 肌肉衰减表明 PCOS 肌肉与非 PCOS 肌肉相比，储存脂质的能力存在差异。
Clinicaltrials.gov ISRCTN84763265。
澳大利亚国家健康与医学研究委员会（资助号 606553）、莫纳什大学和杰恩海尔斯基金会。
