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Allomyrina dichotoma (Arthropoda: Insecta) Larvae Confer Resistance to Obesity in Mice Fed a High-Fat Diet

机译:饲喂高脂饮食的Allomyrina dichotoma(节肢动物:昆虫纲)幼虫赋予小鼠抗肥胖能力

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摘要

To clarify the anti-obesity effect of Allomyrina dichotoma larvae (ADL), we previously reported that ADL block adipocyte differentiation on 3T3-L1 cell lines through downregulation of transcription factors, such as peroxisome proliferator-activated receptor-γ (PPARG) and CCAAT/enhancer binding protein-α (CEBPA). In this study, we tested whether ADL prevent obesity in mice fed a high-fat diet (HFD) and further investigated the mechanism underlying the effects of ADL. All mice were maintained on a normal-fat diet (NFD) for 1 week and then assigned to one of five treatment groups: (1) NFD; (2) HFD; (3) HFD and 100 mg·kg−1·day−1 ADL; (4) HFD and 3000 mg·kg−1·day−1ADL; or (5) HFD and 3000 mg·kg−1·day−1 yerba mate (Ilex paraguariensis, positive control). ADL and yerba mate were administered orally daily. Mice were fed experimental diets and body weight was monitored weekly for 6 weeks. Our results indicated that ADL reduced body weight gain, organ weight and adipose tissue volume in a dose-dependent manner. Body weight gain was approximately 22.4% lower compared to mice fed only HFD, but the difference did not reach the level of statistical significance. Real-time polymerase chain reaction (PCR) analysis revealed that gene expression levels of PPARG, CEBPA and lipoprotein lipase (LPL) in the epididymal fat tissue of HFD-fed mice receiving 3000 mg·kg−1·day−1 ADL were reduced by 12.4-, 25.7-, and 12.3-fold, respectively, compared to mice fed HFD only. Moreover, mice administered ADL had lower serum levels of triglycerides and leptin than HFD-fed mice that did not receive ADL. Taken together our results suggest that ADL and its constituent bioactive compounds hold potential for the treatment and prevention of obesity.
机译:为了阐明小花拟夜蛾幼虫(ADL)的抗肥胖作用,我们先前曾报道ADL通过下调转录因子(例如过氧化物酶体增殖物激活受体-γ(PPARG)和CCAAT /)来阻断3T3-L1细胞系上的脂肪细胞分化。增强子结合蛋白-α(CEBPA)。在这项研究中,我们测试了ADL是否能预防高脂饮食(HFD)喂养的小鼠的肥胖,并进一步研究了ADL作用的潜在机制。将所有小鼠维持正常脂肪饮食(NFD)1周,然后分配给五个治疗组之一:(1)NFD; (2)HFD; (3)HFD和100 mg·kg -1 ·天 -1 ADL; (4)HFD和3000 mg·kg -1 ·天 -1 ADL;或(5)HFD和3000 mg·kg −1 ·天 −1 yerba mate(巴拉圭冬凌草,阳性对照)。每天口服ADL和yerba mate。给小鼠喂食实验饮食并每周监测体重,持续6周。我们的结果表明,ADL以剂量依赖性方式降低了体重增加,器官重量和脂肪组织体积。与仅喂食HFD的小鼠相比,体重增加约低22.4%,但差异未达到统计学意义。实时聚合酶链反应(PCR)分析显示,接受3000 mg·kg -1 ·的HFD喂养小鼠的附睾脂肪组织中PPARG,CEBPA和脂蛋白脂肪酶(LPL)的基因表达水平与仅喂食HFD的小鼠相比,day -1 的ADL分别降低了12.4、25.7-和12.3倍。此外,与未接受ADL的HFD喂养小鼠相比,接受ADL的小鼠血清甘油三酯和瘦素水平较低。综上所述,我们的结果表明ADL及其组成的生物活性化合物具有治疗和预防肥胖症的潜力。

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