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首页> 外文期刊>Laboratory investigation >Cardiac hypertrophy in mice with long-chain acyl-CoA dehydrogenase or very long-chain acyl-CoA dehydrogenase deficiency
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Cardiac hypertrophy in mice with long-chain acyl-CoA dehydrogenase or very long-chain acyl-CoA dehydrogenase deficiency

机译：具有长链酰基辅酶A脱氢酶或极长链酰基辅酶A脱氢酶缺乏症的小鼠心脏肥大

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Cardiac hypertrophy is a common finding in human patients with inborn errors of long-chain fatty acid oxidation. Mice with either very long-chain acyl-coenzyme A dehydrogenase deficiency (VLCAD–/–) or long-chain acyl-coenzyme A dehydrogenase deficiency (LCAD–/–) develop cardiac hypertrophy. Cardiac hypertrophy, initially measured using heart/body weight ratios, was manifested most severely in LCAD–/– male mice. VLCAD–/– mice, as a group, showed a mild increase in normalized cardiac mass (8.8% hypertrophy compared with all wild-type (WT) mice). In contrast, LCAD–/– mice as a group showed more severe cardiac hypertrophy (32.2% increase compared with all WT mice). On the basis of a clear male predilection, we analyzed the role of dietary plant estrogenic compounds commonly found in mouse diets because of soy or alfalfa components providing natural phytoestrogens or isoflavones in cardioprotection of LCAD–/– mice. Male LCAD–/– mice fed an isoflavone-free test diet had more severe cardiac hypertrophy (58.1% hypertrophy compared with WT mice fed the same diet). There were no significant differences in the female groups fed any of the diets. Echocardiography measurement performed on male LCAD-deficient mice fed a standard diet at the age of ~3 months confirmed the substantial cardiac hypertrophy in these mice compared with WT controls. Left ventricular (LV) wall thickness of the interventricular septum and posterior wall was remarkably increased in LCAD–/– mice compared with that of WT controls. Accordingly, the calculated LV mass after normalization to body weight was increased by about 40% in the LCAD–/– mice compared with WT mice. In summary, we found that metabolic cardiomyopathy, expressed as hypertrophy, developed in mice because of either VLCAD deficiency or LCAD deficiency; however, LCAD deficiency was the most profound and seemed to be attenuated either by endogenous estrogen (in females) or by phytoestrogens present in the diet as isoflavones (in males).
机译：在患有先天性长链脂肪酸氧化错误的人类患者中，心脏肥大是常见的发现。患有长链酰基辅酶A脱氢酶缺乏症（VLCAD – / –）或长链酰基辅酶A脱氢酶缺乏症（LCAD – / –）的小鼠会出现心脏肥大。最初使用心脏/体重比测量的心脏肥大在LCAD – / –雄性小鼠中最为严重。 VLCAD – / –小鼠作为一个整体，表现出正常心脏质量的轻度增加（与所有野生型（WT）小鼠相比，肥大率为8.8％）。相反，作为一组的LCAD – / –小鼠表现出更严重的心脏肥大（与所有WT小鼠相比，增加了32.2％）。在明确的男性偏爱基础上，我们分析了在小鼠饮食中常见的膳食植物雌激素化合物的作用，因为大豆或苜蓿成分可提供天然植物雌激素或异黄酮在LCAD – / –小鼠的心脏保护中。饲喂无异黄酮测试饮食的雄性LCAD – / –小鼠具有更严重的心脏肥大（与饲喂相同饮食的WT小鼠相比，肥大为58.1％）。喂养任何饮食的女性组没有显着差异。对在3个月大时进食标准饮食的雄性LCAD缺陷型小鼠进行的超声心动图测量证实，与野生型对照组相比，这些小鼠的心脏肥大。与野生型对照组相比，LCAD – / –小鼠左室间隔和后壁的左心室（LV）壁厚度显着增加。因此，与野生型小鼠相比，归一化至体重后的LCAD – / –小鼠计算的LV质量增加了约40％。总之，我们发现由于VLCAD缺乏症或LCAD缺乏症，小鼠出现了代谢性心肌病，表现为肥大。然而，LCAD缺乏症是最严重的，并且似乎被内源性雌激素（女性）或饮食中以异黄酮形式存在的植物雌激素（男性）减轻了。

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