首页> 外文期刊>Nutrients >Seabuckthorn Leaves Extract and Flavonoid Glycosides Extract from Seabuckthorn Leaves Ameliorates Adiposity, Hepatic Steatosis, Insulin Resistance, and Inflammation in Diet-Induced Obesity
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Seabuckthorn Leaves Extract and Flavonoid Glycosides Extract from Seabuckthorn Leaves Ameliorates Adiposity, Hepatic Steatosis, Insulin Resistance, and Inflammation in Diet-Induced Obesity

机译:沙棘叶中的沙棘叶提取物和类黄酮糖苷提取物可改善饮食诱发的肥胖症,肝脂肪变性,胰岛素抵抗和炎症。

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The aim of the current study was to elucidate the effect of seabuckthorn leaves (SL) extract and flavonoid glycosides extract from seabuckthorn leaves (SLG) on diet-induced obesity and related metabolic disturbances, and additionally, to identify whether flavonoid glycosides and other components in SL can exert a possible interaction for the prevention of metabolic diseases by comparing the effect of SL and SLG. C57BL/6J mice were fed a normal diet (ND, AIN-93G purified diet), high-fat diet (HFD, 60 kcal% fat), HFD + 1.8% ( w / w) SL (SL), and HFD + 0.04% ( w / w ) SLG (SLG) for 12 weeks. In high fat-fed mice, SL and SLG decreased the adiposity by suppressing lipogenesis in adipose tissue, while increasing the energy expenditure. SL and SLG also improved hepatic steatosis by suppressing hepatic lipogenesis and lipid absorption, whilst also enhancing hepatic fatty acid oxidation, which may be linked to the improvement in dyslipidemia. Moreover, SL and SLG improved insulin sensitivity by suppressing the levels of plasma GIP that were modulated by secreted resistin and pro-inflammatory cytokine, and hepatic glucogenic enzyme activities. SL, especially its flavonoid glycosides (SLG), can protect against the deleterious effects of diet-induced obesity (DIO) and its metabolic complications such as adiposity, dyslipidemia, inflammation, hepatic steatosis, and insulin resistance.
机译:本研究的目的是阐明沙棘叶(SLG)的沙棘叶(SL)提取物和黄酮苷提取物对饮食诱导的肥胖症和相关代谢紊乱的影响,此外,该方法还可以确定沙棘叶中的黄酮苷和其他成分是否通过比较SL和SLG的作用,SL可以发挥可能的相互作用来预防代谢性疾病。 C57BL / 6J小鼠的饮食为正常饮食(ND,AIN-93G纯化饮食),高脂饮食(HFD,60 kcal%脂肪),HFD + 1.8%(w / w)SL(SL)和HFD + 0.04 %(w / w)SLG(SLG),持续12周。在高脂饮食小鼠中,SL和SLG通过抑制脂肪组织中的脂肪生成而降低了肥胖,同时增加了能量消耗。 SL和SLG还可以通过抑制肝脏脂肪生成和脂质吸收来改善肝脏脂肪变性,同时还可以增强肝脏脂肪酸的氧化,这可能与血脂异常的改善有关。此外,SL和SLG通过抑制血浆GIP的水平来改善胰岛素敏感性,该水平受分泌的抵抗素和促炎性细胞因子以及肝糖原酶活性的调节。 SL,特别是其类黄酮糖苷(SLG),可以预防饮食引起的肥胖(DIO)及其代谢并发症(如肥胖,血脂异常,炎症,肝脂肪变性和胰岛素抵抗)的有害影响。

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