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首页> 外文期刊>The Journal of Nutritional Biochemistry >Ellagic acid modulates lipid accumulation in primary human adipocytes and human hepatoma Huh7 cells via discrete mechanisms
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Ellagic acid modulates lipid accumulation in primary human adipocytes and human hepatoma Huh7 cells via discrete mechanisms

机译：鞣花酸通过离散机制调节人原代脂肪细胞和人肝癌Huh7细胞中脂质的积累

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Previously, we have reported that consumption of a muscadine grape phytochemical powder (MGP) decreased lipid accumulation in high-fat fed mice. The aim of this study was to identify the responsible polyphenolic constituents and elucidate the underlying mechanisms. In mice, MGP supplementation significantly reduced visceral fat mass as well as adipocyte size. To determine whether MGP affects adipogenesis or hypertrophic lipid accumulation, we used a human adipogenic stem cell (hASCs) model. Among the MGP, ellagic acid (EA) was identified as a potent negative regulator of adipogenesis of hASCs. In addition, EA substantially decreased the conversion of [H-3]-acetyl CoA into fatty acids (FAs), suggesting that EA inhibits de novo synthesis of FA in mature adipocytes. Similarly, MGP supplementation significantly decreased hepatic triglyceride (TG) levels. The TG-lowering effects of EA were confirmed in human hepatoma Huh7 cells. EA reduced [H-3]-oleic acid esterification into [H-3]-TG as well as the de novo synthesis of FA from [H-3]-acetyl CoA in Huh7 cells. Intriguingly, EA also increased oxygen consumption rate and beta-oxidation-related gene expression. Taken together, EA attenuated new fat cell formation and FA biosynthesis in adipose tissue, while it reduced the synthesis of TG and FA and increased FA oxidation in the liver. These results suggest that EA exerts unique lipid-lowering effects both in adipose tissue and liver via discrete mechanisms. (C) 2015 Elsevier Inc. All rights reserved.
机译：以前，我们已经报道食用麝香葡萄葡萄植物化学粉末（MGP）会降低高脂喂养小鼠的脂质蓄积。这项研究的目的是确定负责任的多酚成分并阐明其潜在机理。在小鼠中，MGP补充剂可显着减少内脏脂肪量以及脂肪细胞大小。为了确定MGP是否会影响脂肪形成或肥大性脂质积累，我们使用了人类脂肪形成干细胞（hASCs）模型。在MGP中，鞣花酸（EA）被确定为hASCs脂肪形成的有效负调节剂。此外，EA大大降低了[H-3]-乙酰基CoA向脂肪酸（FAs）的转化，表明EA抑制了成熟脂肪细胞中FA的从头合成。同样，补充MGP可以显着降低肝甘油三酯（TG）水平。在人肝癌Huh7细胞中证实了EA的TG降低作用。 EA减少了Huh7细胞中[H-3]-油酸酯化为[H-3] -TG以及从[H-3]-乙酰基CoA从头开始合成FA。有趣的是，EA还增加了耗氧率和与β氧化有关的基因表达。综上所述，EA减弱了脂肪组织中新的脂肪细胞形成和FA生物合成，同时减少了TG和FA的合成并增加了肝脏中FA的氧化。这些结果表明，EA通过离散机制在脂肪组织和肝脏中均具有独特的降脂作用。 （C）2015 Elsevier Inc.保留所有权利。

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