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首页> 外文期刊>Cellular Physiology and Biochemistry >Hyperthyroidism Evokes Myocardial Ceramide Accumulation
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Hyperthyroidism Evokes Myocardial Ceramide Accumulation

机译：甲状腺功能亢进引起心肌神经酰胺蓄积

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Background: Thyroid hormones (THs) are key regulators of cardiac physiology as well as modulators of different cellular signals including the sphingomyelin/ceramide pathway. The objective of this study was to examine the effect of hyperthyroidism on the metabolism of sphingolipids in the muscle heart. Methods: Male Wistar rats were treated for 10 days with triiodothyronine (T3) at a dose of 50μg/100g of body weight. Animals were then anaesthetized and samples of the left ventricle were excised. Results: We have demonstrated that prolonged, in vivo, T3 treatment increased the content of sphinganine (SFA), sphingosine (SFO), ceramide (CER) and sphingomyelin (SM), but decreased the level of sphingosine-1-phosphate (S1P) in cardiac muscle. Accordingly, the changes in sphingolipids content were accompanied by a lesser activity of neutral sphingomyelinase and without significant changes in ceramidases activity. Hyperthyroidism also induced activation of AMP-activated protein kinase (AMPK) with subsequently increased expression of mitochondrial proteins: cytochrome c oxidase IV (COX IV), β-hydroxyacyl-CoA dehydrogenase (β-HAD), carnityne palmitoyltransferase I (CPT I) and nuclear peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α). Conclusions: We conclude that prolonged T3 treatment increases sphingolipids metabolism which is reflected by higher concentration of SFA and CER in heart muscle. Furthermore, hyperthyroidism-induced increase in heart sphingomyelin (SM) concentration might be one of the mechanisms underlying maintenance of CER at relatively low level by its conversion to SM together with decreased S1P content.
机译：背景：甲状腺激素（THs）是心脏生理的关键调节剂，也是包括鞘磷脂/神经酰胺途径在内的不同细胞信号的调节剂。这项研究的目的是检查甲状腺功能亢进症对肌肉心脏鞘脂代谢的影响。方法：雄性Wistar大鼠用三碘甲状腺素（T 3 ）治疗50天，剂量为50μg/ 100g体重。然后麻醉动物，并切除左心室样品。结果：我们证明了延长的T 3 体内治疗会增加鞘氨醇（SFA），鞘氨醇（SFO），神经酰胺（CER）和鞘磷脂（SM）的含量，但降低了心肌中的1磷酸鞘氨醇（S1P）。因此，鞘脂含量的变化伴随着中性鞘磷脂酶活性降低，而陶瓷酶活性没有明显变化。甲状腺功能亢进症还诱导AMP激活的蛋白激酶（AMPK）的激活，随后增加了线粒体蛋白的表达：细胞色素c氧化酶IV（COX IV），β-羟酰基-CoA脱氢酶（β-HAD），肉碱棕榈酸转移酶I（CPT I）和核过氧化物酶体增殖物激活受体-γcoactivator-1α（PGC1α）。结论：我们得出结论，延长T 3 治疗可增加鞘脂的代谢，这可通过心肌中SFA和CER的浓度升高来反映。此外，甲亢导致的心肌鞘磷脂（SM）浓度增加可能是将CER转化为SM并降低S1P含量而将CER维持在较低水平的基础之一。

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