The deficiency and the supplementation of vitamin D and liver: Lessons of chronic fructose-rich diet in mice
The deficiency and the supplementation of vitamin D and liver: Lessons of chronic fructose-rich diet in mice
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DOI：
10.1016/j.jsbmb.2019.105399
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发表时间：
2019-09-01
影响因子：
4.1
通讯作者：
Mandarim-De-Lacerda, Carlos A.
中科院分区：
文献类型：
--
作者：
Maia-Ceciliano, Thais C.;Dutra, Rafaela R.;Mandarim-De-Lacerda, Carlos A.
添加到软饮料和加工食品中的果糖，以及体内经常检测到的维生素D缺乏，是两种越来越多地被认为会导致靶器官病变的侮辱。我们研究了慢性高果糖饮食缺乏和补充维生素D后的肝脏。将60只C57 BL/6成年雄性小鼠分为6组（n = 10），每组10只，分别为对照组（C）、维生素D缺乏对照组（CDD）、维生素D补充对照组（CDS）、果糖组（F）、维生素D缺乏果糖组（FDD）和维生素D补充果糖组（FDS）。维生素D受体和CYP 27 B1的基因表达以及血浆25羟维生素D水平的变化是膳食引起维生素D缺乏或补充的保证。CDD、F和FDD的体重没有变化，但血压（BP）升高，而FDS的BP得到控制。在维生素D缺乏组和果糖组中均观察到胰岛素血症、胰岛素耐受性和抵抗，但补充维生素D后有所改善。CDD组、F组和FDD组均出现脂肪变性和纤维化。此外，F和FDD显示星状细胞（HSC）的活化。CDD、F和FDD组的脂肪生成和炎症基因表达增强，但补充维生素D后减少。总之，我们证明了维生素D缺乏对代谢、肝脏脂肪变性以及与果糖摄入相结合的肝星状细胞活化的肝间质纤维化和脂肪生成、β-氧化和肝脏炎症的改变的不良影响。当动物补充维生素D时，所有这些数据都有所改善。
The fructose added to soft drinks and processed food, as well as frequent detection of vitamin D deficiency in the body, are two insults increasingly considered to cause lesions in target organs. We studied the liver after a chronic high-fructose diet deficient and supplemented with vitamin D. Sixty C57BL/6 mature male mice were allocated into six groups (n = 10) for ten weeks: control (C), control deficient in vitamin D (CDD), control supplemented with vitamin D (CDS), fructose (F), fructose deficient in vitamin D (FDD), and fructose supplemented with vitamin D (FDS). The gene expressions of vitamin D receptor and CYP27B1 and 25 hydroxyvitamin D plasma level ensured that the diets caused vitamin D deficiency or supplementation. Body mass did not change, but blood pressure (BP) increased in CDD, F, and FDD, whereas BP was controlled in FDS. Insulinemia, insulin tolerance and resistance were seen in both vitamin D deficiency and fructose groups but improved with vitamin D supplementation. The steatosis and fibrosis were observed in the CDD, F and FDD groups. Also, F and FDD showed activation of stellate cells (HSC). Lipogenesis and inflammation gene expressions were enhanced in the CDD, F and FDD groups, but diminished with vitamin D supplementation. In conclusion, we demonstrated the adverse effects of vitamin D deficiency on metabolism, liver steatosis and, combined with fructose intake, liver interstitial fibrosis with hepatic stellate cell activation, and alteration of the lipogenesis, beta-oxidation, and liver inflammation. All these data improved when vitamin D was supplemented in the animals.