首页> 美国卫生研究院文献>Antioxidants >Lyophilized Maqui (Aristotelia chilensis) Berry Induces Browning in the Subcutaneous White Adipose Tissue and Ameliorates the Insulin Resistance in High Fat Diet-Induced Obese Mice
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Lyophilized Maqui (Aristotelia chilensis) Berry Induces Browning in the Subcutaneous White Adipose Tissue and Ameliorates the Insulin Resistance in High Fat Diet-Induced Obese Mice

机译:冻干的马奎(Aristotelia chilensis)浆果诱导皮下白色脂肪组织褐变并改善高脂饮食诱导的肥胖小鼠的胰岛素抵抗

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摘要

Maqui (Aristotelia Chilensis) berry features a unique profile of anthocyanidins that includes high amounts of delphinidin-3-O-sambubioside-5-O-glucoside and delphinidin-3-O-sambubioside and has shown positive effects on fasting glucose and insulin levels in humans and murine models of type 2 diabetes and obesity. The molecular mechanisms underlying the impact of maqui on the onset and development of the obese phenotype and insulin resistance was investigated in high fat diet-induced obese mice supplemented with a lyophilized maqui berry. Maqui-dietary supplemented animals showed better insulin response and decreased weight gain but also a differential expression of genes involved in de novo lipogenesis, fatty acid oxidation, multilocular lipid droplet formation and thermogenesis in subcutaneous white adipose tissue (scWAT). These changes correlated with an increased expression of the carbohydrate response element binding protein b (Chrebpb), the sterol regulatory binding protein 1c (Srebp1c) and Cellular repressor of adenovirus early region 1A–stimulated genes 1 (Creg1) and an improvement in the fibroblast growth factor 21 (FGF21) signaling. Our evidence suggests that maqui dietary supplementation activates the induction of fuel storage and thermogenesis characteristic of a brown-like phenotype in scWAT and counteracts the unhealthy metabolic impact of an HFD. This induction constitutes a putative strategy to prevent/treat diet-induced obesity and its associated comorbidities.
机译:Maqui(智利亚里士多德)浆果具有独特的花色苷特征,其中包括大量的delphinidin-3-O-sambubioside-5-O-葡萄糖苷和delphinidin-3-O-sambubioside,并且对空腹血糖和胰岛素水平显示出积极作用人类和2型糖尿病和肥胖的鼠类模型。在补充了冻干的马奎浆果的高脂饮食诱导的肥胖小鼠中,研究了马奎对肥胖表型的发作和发展以及胰岛素抵抗的潜在分子机制。补充动物饮食的动物表现出更好的胰岛素反应和降低的体重增加,但是在皮下白色脂肪组织(scWAT)中涉及从头脂肪形成,脂肪酸氧化,多细胞脂质滴形成和生热的基因差异表达。这些变化与腺病毒早期区域1A刺激的基因1(Creg1)的糖应答元件结合蛋白b(Chrebpb),固醇调节结合蛋白1c(Srebp1c)和细胞阻遏物表达的增加以及成纤维细胞生长的改善有关因子21(FGF21)信号传导。我们的证据表明,大量的饮食补充可以激活燃料储存的诱导和scWAT中褐色样表型的生热特征,并抵消了HFD对健康的不良影响。这种诱导构成了预防/治疗饮食引起的肥胖及其相关合并症的推定策略。

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