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Effects of gut microbiota on leptin expression and body weight are lessened by high-fat diet in mice

机译:通过小鼠的高脂饮食来减少肠道微生物对瘦蛋白表达和体重的影响

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摘要

Aberration in leptin expression is one of the most frequent features in the onset and progression of obesity, but the underlying mechanisms are still unclear and need to be clarified. This study investigated the effects of the absence of gut microbiota on body weight and the expression and promoter methylation of the leptin. Male C57 BL/6 J germ-free (GF) and conventional (CV) mice (aged 4-5 weeks) were fed either a normal-fat diet (NFD) or a high-fat diet (HFD) for 16 weeks. Six to eight mice from each group, at 15 weeks, were administered exogenous leptin for 7 d. Leptin expression and body weight gain in GF mice were increased by NFD with more CpG sites hypermethylated at the leptin promoter, whereas there was no change with HFD, compared with CV mice. Adipose or hepatic expression of genes associated with fat synthesis (Acc1,FasandSrebp-1c), hydrolysis and oxidation (Atgl,Cpt1a,Cpt1c,Ppar-alpha andPgc-1 alpha) was lower, and hypothalamus expression ofPomcandSocs3was higher in GF mice than levels in CV mice, particularly with NFD feeding. Exogenous leptin reduced body weight in both types of mice, with a greater effect on CV mice with NFD. AdiposeLep-Rexpression was up-regulated, and hepaticFasand hypothalamicSocs3were down-regulated in both types of mice. Expression of fat hydrolysis and oxidative genes (Atgl,Hsl,Cpt1a,Cpt1c,Ppar-alpha andPgc-1 alpha) was up-regulated in CV mice. Therefore, the effects of gut microbiota on the leptin expression and body weight were affected by dietary fat intake.
机译:瘦素表达的像差是发病和肥胖进展中最常见的特征之一,但潜在的机制仍然不清楚,并且需要澄清。本研究研究了肠道微生物缺乏对体重的影响和瘦素的表达和启动子甲基化。雄性C57 BL / 6 J B组(GF)和常规(CV)小鼠(4-5周龄)喂养常规脂肪饮食(NFD)或高脂饮食(HFD)16周。每组六至八只小鼠在15周内施用外源性瘦素7天。通过NFD通过NFD在瘦蛋白启动子上具有更多的CpG位点,瘦素表达和体重增加增加了GF小鼠的体重增加,而与CV小鼠相比,HFD没有变化。与脂肪合成(ACC1,Fasandsreb-1c),水解和氧化(ATGL,CPT1A,CPT1C,PPAR-α和PPGC-1α)的脂肪糖或肝脏表达较低,Homcandsocs3剩下的丘脑表达高于GF小鼠比水平更高CV小鼠,特别是NFD喂养。外源性瘦素在两种类型的小鼠中减少体重,对具有NFD的CV小鼠具有更大的影响。脂肪素重新表达是上调的,肝卓越的下丘脑癌在两种小鼠中下调。脂肪水解和氧化基因的表达(ATGL,HSL,CPT1A,CPT1C,PPAR-Alpha和PGC-1α)在CV小鼠中调节。因此,通过膳食脂肪摄入量对肠道微生物对瘦素表达和体重的影响受到影响。

著录项

  • 来源
    《The British Journal of Nutrition》 |2020年第4期|共11页
  • 作者单位

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

    Capital Med Univ Natl Ctr Childrens Hlth Dept Child Hlth Care Ctr Beijing Childrens Hosp Beijing 100045 Peoples R China;

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

    Capital Med Univ Beijing Childrens Hosp Natl Ctr Childrens Hlth Lab Nutr &

    Dev Beijing Pediat Res Inst Beijing 100045 Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 营养卫生、食品卫生;
  • 关键词

    Leptin expression; Leptin resistance; Gut microbiota; Diet-induced obesity; SCFA;

    机译:瘦素表达;瘦素抵抗;肠微生物肿;饮食诱导的肥胖;SCFA;

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