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首页> 外文期刊>Nutrients >Platycodon grandiflorus Root Extract Attenuates Body Fat Mass, Hepatic Steatosis and Insulin Resistance through the Interplay between the Liver and Adipose Tissue
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Platycodon grandiflorus Root Extract Attenuates Body Fat Mass, Hepatic Steatosis and Insulin Resistance through the Interplay between the Liver and Adipose Tissue

机译:桔梗根提取物通过肝脏和脂肪组织之间的相互作用减轻体脂量,肝脂肪变性和胰岛素抵抗

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摘要

The Platycodon grandiflorus root, a Korean medicinal food, is well known to have beneficial effects on obesity and diabetes. In this study, we demonstrated the metabolic effects of P. grandiflorus root ethanol extract (PGE), which is rich in platycodins, on diet-induced obesity. C57BL/6J mice (four-week-old males) were fed a normal diet (16.58% of kilocalories from fat), high-fat diet (HFD, 60% of kilocalories from fat), and HFD supplemented with 5% ( w / w ) PGE. In the HFD-fed mice, PGE markedly suppressed the body weight gain and white fat mass to normal control level, with simultaneous increase in the expression of thermogenic genes (such as SIRT1 , PPAR α, PGC1 α, and UCP1 ), that accompanied changes in fatty acid oxidation (FAO) and energy expenditure. In addition, PGE improved insulin sensitivity through activation of the PPARγ expression, which upregulates adiponectin while decreasing leptin gene expression in adipocytes. Furthermore, PGE improved hepatic steatosis by suppressing hepatic lipogenesis while increasing expression of FAO-associated genes such as PGC1 α. PGE normalized body fat and body weight, which is likely associated with the increased energy expenditure and thermogenic gene expression. PGE can protect from HFD-induced insulin resistance, and hepatic steatosis by controlling lipid and glucose metabolism.
机译:桔梗根(Platycodon grandiflorus)是韩国的一种药用食品,众所周知对肥胖和糖尿病具有有益作用。在这项研究中,我们证明了富含桔梗的P. grandiflorus根乙醇提取物(PGE)对饮食引起的肥胖的代谢作用。给C57BL / 6J小鼠(四周大的雄性)喂食正常饮食(16.58%的卡路里来自脂肪),高脂饮食(HFD,60%的卡路里来自脂肪)和HFD补充5%(w / w)PGE。在HFD喂养的小鼠中,PGE显着抑制了体重增加和白色脂肪质量,使其达到正常对照水平,同时伴随着变化的生热基因(如SIRT1,PPARα,PGC1α和UCP1)的表达同时增加。在脂肪酸氧化(FAO)和能量消耗方面。此外,PGE通过激活PPARγ表达提高了胰岛素敏感性,PPARγ表达上调了脂联素,同时降低了脂肪细胞中瘦素基因的表达。此外,PGE通过抑制肝脏脂肪生成,同时增加粮农组织相关基因(如PGC1α)的表达,改善了肝脂肪变性。 PGE使体重和体重正常化,这可能与能量消耗增加和热基因表达增加有关。 PGE可通过控制脂质和葡萄糖代谢来预防HFD诱导的胰岛素抵抗和肝脂肪变性。

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