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首页> 外文期刊>American Journal of Physiology >A mechanism underlying mature-onset obesity: evidence from the hyperphagic phenotype of brain-derived neurotrophic factor mutants.
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A mechanism underlying mature-onset obesity: evidence from the hyperphagic phenotype of brain-derived neurotrophic factor mutants.

机译：成熟发病肥胖的潜在机制：来自脑源性神经营养因子突变体的高相表型的证据。

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摘要

Mice deficient in brain-derived neurotrophic factor (BDNF) develop mature-onset obesity, primarily due to overeating. To gain insight into the mechanism of this hyperphagia, we characterized food intake, body weight, meal pattern, and meal microstructure in young and mature mice fed balanced or high-fat diets. Hyperphagia and obesity occurred in mature but not young BDNF mutants fed a balanced diet. This hyperphagia was mediated by increased meal number, which was associated with normal meal size, meal duration, and satiety ratio. In contrast, the high-fat diet induced premature development of hyperphagia and obesity in young BDNF mutants and a similar magnitude hyperphagia in mature mutants. This hyperphagia was supported by increased meal size and was accompanied by a reduced satiety ratio. Thus the mechanism underlying hyperphagia was present before significant weight gain, but whether it occurred, and whether meal frequency or meal size was altered to support it, was modulated by a process associated with aging and by diet properties. Meal pattern changes associated with the balanced diet suggested meal initiation, and the oropharyngeal positive feedback that drives feeding, were enhanced and might have contributed to overeating in BDNF mutants, whereas negative feedback was normal. Consistent with this hypothesis, meal microstructure revealed that all hyperphagic mutant groups exhibited increased intake rates at meal onset. Therefore, the central nervous system targets of BDNF actions may include orosensory brain stem neurons that process and transmit positive feedback or forebrain neurons that modulate its strength.
机译：缺乏脑源性神经营养因子（BDNF）的小鼠会发育成肥胖，主要是由于暴饮暴食。为了深入了解这种食欲亢进的机制，我们对喂养均衡或高脂饮食的年轻和成熟小鼠的食物摄入量，体重，进食模式和进餐微观结构进行了表征。进食均衡饮食的成熟但未出现年轻的BDNF突变体发生吞噬和肥胖。进食过多是由进餐次数增加引起的，进食次数与正常进餐量，进餐时间和饱腹感有关。相反，高脂饮食在年轻的BDNF突变体中引起食欲亢进和肥胖的过早发展，而在成熟的突变体中则引起相似程度的食欲亢进。进食量增加可增加这种食欲，并伴有饱腹感降低。因此，食欲亢进的潜在机制在体重显着增加之前就已经存在，但是它的发生，以及进餐频率或进食量是否改变以支持它，是由与衰老相关的过程和饮食特性所调节的。与均衡饮食相关的膳食模式改变提示开始进食，并且促进进食的口咽正反馈得到增强，并可能导致BDNF突变体暴饮暴食，而负反馈是正常的。与该假设一致，膳食微观结构显示，所有高吞噬突变体组在膳食开始时均显示摄入率增加。因此，BDNF行为的中枢神经系统靶标可能包括处理并传递正反馈的口感脑干神经元或调节其强度的前脑神经元。

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