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首页> 外文期刊>American Journal of Physiology >IUGR decreases cardiomyocyte endowment and alters cardiac metabolism in a sex- and cause-of-IUGR-specific manner
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IUGR decreases cardiomyocyte endowment and alters cardiac metabolism in a sex- and cause-of-IUGR-specific manner

机译：IUGR减少心肌细胞禀赋，并在性别和原因的情况下改变心脏代谢

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摘要

Intrauterine growth restriction (IUGR) increases the risk of ischemic heart disease in adulthood. Studies in rats suggest cardiac vulnerability is more pronounced in males and in offspring that were exposed to hypoxia in utero. Therefore, we aimed to test the hypotheses that 1) IUGR adolescent males, but not females, have fewer cardiomyocytes and altered expression of cardiometabolic genes compared with controls; and 2) IUGR due to hypoxia has a greater effect on these parameters compared with IUGR due to nutrient restriction. IUGR was induced in guinea pigs by maternal hypoxia (MH; 10% O2, n = 9) or maternal nutrient restriction (MNR; ~30% reduction in food intake, n = 9) in the second half of pregnancy and compared with control (n = 11). At 120 days of age, postmortem was performed and the left ventricle perfusion fixed for stereological determination of cardiomyocyte number or snap frozen to determine the abundance of cardiometabolic genes and proteins by quantitative RT-PCR and Western blotting, respectively. MH reduced the number of cardiomyocytes in female (P < 0.05), but not male or MNR, adolescent offspring. Furthermore, IUGR males had decreased expression of genes responsible for fatty acid activation in the sarcoplasm (FACS) and transport into the mitochondria (AMPK-a2 and ACC; P < 0.05) and females exposed to MH had increased activation/phosphorylation of AMP-activated protein kinase-α (P < 0.05). We postulate that the changes in cardiomyocyte endowment and cardiac gene expression observed in the present study are a direct result of in utero programming, as offspring at this age did not suffer from obesity, hypertension, or left ventricular hypertrophy.
机译：宫内生长限制（IUGR）增加了成年期缺血性心脏病的风险。大鼠的研究表明心脏脆弱性在男性中更加明显，在子宫内暴露于缺氧的后代。因此，我们旨在测试1）IUGR青少年雄性，但不是女性，与对照相比，具有较少的心肌细胞和改变心细素基因的表达; 2）由于营养限制，由于缺氧对这些参数产生了更大的影响。 IUGR被母体缺氧（MH; 10％O 2，N = 9）或母体营养限制（MNR;食物摄入量减少30％，N = 9）在怀孕的后的豚鼠中诱导，与对照相比（ n = 11）。在120天时，进行后期术后和固定的左心室灌注，用于立体学测定心肌细胞数或快速冷冻，以通过定量的RT-PCR和Western印迹测定心肌酶基因和蛋白质的丰富。 MH减少了女性的心肌细胞数量（P <0.05），但不是男性或MNR，青少年后代。此外，IUGR雄性的表达减少了对嗜酸盐（FACS）（FACS）中的脂肪酸活化的基因表达，并运输到线粒体（AMPK-A2和ACC; P <0.05）中，暴露于MH的女性增加了AMP活化的活化/磷酸化蛋白质激酶-α（P <0.05）。我们假设在本研究中观察到的心肌细胞禀赋和心脏基因表达的变化是子宫编程的直接结果，因为该年龄的后代没有肥胖，高血压或左心室肥厚。

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