Department of Food Science and Human Nutrition, University of Florida, Gainesville, FL, USA; Department of Nutrition and Health Sciences, University of Nebraska, Lincoln, NE, USA.
Department of Food Science and Human Nutrition, University of Florida, Gainesville, FL, USA.
J Nutr Biochem. 2015 Jan;26(1):82-90. doi: 10.1016/j.jnutbio.2014.09.010. Epub 2014 Oct 20.
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 [(3)H]-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 [(3)H]-oleic acid esterification into [(3)H]-TG as well as the de novo synthesis of FA from [(3)H]-acetyl CoA in Huh7 cells. Intriguingly, EA also increased oxygen consumption rate and β-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.
先前，我们已经报道过，鼠李葡聚糖多酚粉（MGP）的摄入可以减少高脂肪饮食喂养的小鼠体内脂肪的堆积。本研究旨在确定起作用的多酚成分，并阐明其潜在的机制。在小鼠体内，MGP 的补充显著减少了内脏脂肪质量和脂肪细胞的大小。为了确定 MGP 是否影响脂肪生成或肥大性脂质积累，我们使用了人脂肪生成干细胞（hASCs）模型。在 MGP 中，鞣花酸（EA）被鉴定为 hASCs 脂肪生成的有效负调节剂。此外，EA 显著降低了 [(3)H]-乙酰辅酶 A 转化为脂肪酸（FAs），表明 EA 抑制成熟脂肪细胞中 FA 的从头合成。同样，MGP 的补充显著降低了肝甘油三酯（TG）水平。EA 在人肝癌 Huh7 细胞中证实了降低 TG 的作用。EA 减少了 [(3)H]-油酸酯化为 [(3)H]-TG，以及 [(3)H]-乙酰辅酶 A 从头合成 FA。有趣的是，EA 还增加了耗氧量和 β-氧化相关基因的表达。综上所述，EA 可减弱脂肪组织中新脂肪细胞的形成和 FA 生物合成，同时减少肝脏中 TG 和 FA 的合成，并增加 FA 的氧化。这些结果表明，EA 通过不同的机制在脂肪组织和肝脏中发挥独特的降脂作用。
