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首页> 外文期刊>Cell metabolism >Dietary Fat, but Not Protein or Carbohydrate, Regulates Energy Intake and Causes Adiposity in Mice
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Dietary Fat, but Not Protein or Carbohydrate, Regulates Energy Intake and Causes Adiposity in Mice

机译:膳食脂肪,但不是蛋白质或碳水化合物,调节能量摄入并导致小鼠的肥胖

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摘要

The impacts of different macronutrients on body weight regulation remain unresolved, with different studies suggesting increased dietary fat, increased carbohydrates (particularly sugars), or reduced protein may all stimulate overconsumption and drive obesity. We exposed C57BL/6 mice to 29 different diets varying from 8.3% to 80% fat, 10% to 80% carbohydrate, 5% to 30% protein, and 5% to 30% sucrose. Only increased dietary fat content was associated with elevated energy intake and adiposity. This response was associated with increased gene expression in the 5-HT receptors, and the dopamine and opioid signaling pathways in the hypothalamus. We replicated the core findings in four other mouse strains (DBA/2, BALB/c, FVB, and C3H). Mice regulate their food consumption primarily to meet an energy rather than a protein target, but this system can be over-ridden by hedonic factors linked to fat, but not sucrose, consumption.
机译:不同MACRORERERS对体重调节对体重调节的影响仍未解决,不同的研究表明膳食脂肪增加,碳水化合物增加(特别是糖),或降低的蛋白质可能都刺激过度吞吐量和驱动肥胖症。 我们将C57BL / 6小鼠暴露于29种不同的饮食,从8.3%到80%脂肪,10%至80%碳水化合物,5%至30%蛋白质,5%至30%的蔗糖。 只有增加的膳食脂肪含量与升高的能量摄入和肥胖有关。 该响应与5-HT受体中的基因表达增加以及下丘脑中的多巴胺和阿片类信号传导途径有关。 我们在另外四种鼠标菌株(DBA / 2,BALB / C,FVB和C3H)中复制了核心结果。 小鼠主要调节它们的食物消费,主要是满足能量而不是蛋白质目标,但这种系统可以通过与脂肪相关的蜂窝因素过度缠身,但不是蔗糖,消费。

著录项

  • 来源
    《Cell metabolism》 |2018年第3期|共21页
  • 作者单位

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    Guangdong Key Laboratory of Animal Conservation and Resource Utilization Guangdong Public;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    University of Dali;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    Institute of Biological and Environmental Sciences University of Aberdeen;

    Institute of Biological and Environmental Sciences University of Aberdeen;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

    Guangdong Key Laboratory of Animal Conservation and Resource Utilization Guangdong Public;

    Guangdong Key Laboratory of Animal Conservation and Resource Utilization Guangdong Public;

    Institute of Biological and Environmental Sciences University of Aberdeen;

    State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 内分泌腺疾病及代谢病;
  • 关键词

    fat intake; sucrose intake; protein leverage hypothesis; energy regulation; hedonic overdrive; mice; hypothalamic hunger pathway; obesity; FGF signaling; mTOR signaling;

    机译:脂肪摄入;蔗糖摄入;蛋白质杠杆假设;能量调节;蜂窝溢出;小鼠;下丘脑饥饿途径;肥胖;FGF信令;MTOR信号;

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