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首页> 外文期刊>Journal of Cellular Physiology >Involvement of nutrients and nutritional mediators in mitochondrial 3‐hydroxy‐3‐methylglutaryl‐CoA synthase gene expression
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Involvement of nutrients and nutritional mediators in mitochondrial 3‐hydroxy‐3‐methylglutaryl‐CoA synthase gene expression

机译：参与的营养和营养介质进入线粒体3羟基量3 methylglutaryl应承担的弱点合酶基因表达

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摘要

Mitochondrial 3‐hydroxy‐3‐methylglutaryl‐CoA (HMG‐CoA) synthase (HMGCS2) catalyses the first step of ketogenesis and is critical in various metabolic conditions. Several nutrient molecules were able to differentially modulate HMGCS2 expression levels. Docosahexaenoic acid (DHA, C22:6, n‐3), eicosapentaenoic acid (EPA, C20:5, n‐3), arachidonic acid (AA, C20:4, n‐6), and glucose increased HMGCS2 mRNA and protein levels in HepG2 hepatoma cells, while fructose decreased them. The effect of n‐6 AA resulted significantly higher than that of n‐3 PUFA, but when combined all these molecules were far less efficient. Insulin reduced HMGCS2 mRNA and protein levels in HepG2 cells, even when treated with PUFA and monosaccharides. Several nuclear receptors and transcription factors are involved in HMGCS2 expression regulation. While peroxysome proliferator activated receptor α (PPAR‐α) agonist WY14643 increased HMGCS2 expression, this treatment was unable to affect PUFA‐mediated regulation of HMGCS2 expression. Forkhead box O1 (FoxO1) inhibitor AS1842856 reduced HMGCS2 expression and suppressed induction promoted by fatty acids. Cells treatment with liver X receptor alpha (LXRα) agonist T0901317 reduced HMGCS2 mRNA, indicating a role for this transcription factor as suppressor of HMGCS2 gene. Previous observations already indicated HMGCS2 expression as possible nutrition status reference: our results show that several nutrients as well as specific nutritional related hormonal conditions are able to affect significantly HMGCS2 gene expression, indicating a relevant role for PUFA, which are mostly derived from nutritional intake. These insights into mechanisms of its regulation, specifically through nutrients commonly associated with disease risk, indicate HMGCS2 expression as possible reference marker of metabolic and nutritional status.
机译：Mitochondrial 3‐hydroxy‐3‐methylglutaryl‐CoA(HMG - CoA应承担)合成酶(HMGCS2)催化作用酮生成步骤和各是至关重要的代谢的条件。可以调节不同HMGCS2吗表达水平。C22:6 n量3)、二十碳五烯酸(EPA、C20:5n量3),花生四烯酸(AA, C20:4, n量6)葡萄糖增加HMGCS2 mRNA和蛋白水平在HepG2肝癌细胞,而果糖下降他们。高于3 PUFA n量,但是当总和所有这些分子都更有效。胰岛素HMGCS2信使rna和蛋白质水平降低HepG2细胞,即使接受PUFA和单糖。转录因子参与HMGCS2表达调控。地理扩散者激活受体α(PPARα)受体激动剂WY14643 HMGCS2表达增加,这一点治疗无法影响PUFA的介导监管HMGCS2表达式。(FoxO1)抑制剂AS1842856 HMGCS2减少表达和抑制感应得到脂肪酸。受体α(LXRα)受体激动剂T0901317减少HMGCS2 mRNA,表明一个角色转录因子作为HMGCS2的抑制基因。HMGCS2表达尽可能的营养状态参考:我们的结果表明,几个营养以及相关的特定营养能够影响荷尔蒙的条件明显HMGCS2基因表达,表示大多的PUFA的相关作用来自营养摄入。其监管机制,明确通过营养普遍联系在一起疾病风险,表明HMGCS2表达式可能的代谢和参考标记营养状况。

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