Science子刊:饮食改变味觉,嗜糖可能源于表观遗传变化
创作:orchid 审核:周旸 2020年11月25日
  • 在喂食高糖的果蝇中,表观遗传调节分子PRC2.1与甜味神经元染色质的结合被重新分配,抑制甜味刺激引发的细胞转录调控网络,从而降低果蝇对甜味刺激的敏感性;
  • 高糖饮食7天后,超过80%的甜味刺激相关基因被沉默;
  • 上述果蝇在正常饮食20天后,高糖饮食导致的基因转录活性改变有一半仍然存在,PRC2.1相关的味觉变化持续;
  • PRC2.1是调节甜味感知的关键分子,PRC2.1产生突变或被药理抑制后,果蝇在高糖饮食中的甜味味觉减退情况消失。
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周旸
高糖、高盐、高脂饮食会改变味觉和食物偏好。Science Advances近期发表研究,通过果蝇的高糖饮食模型阐释了新的表观遗传机制,发现表观遗传调节分子PRC2.1参与了高糖饮食导致的基因转录改变,高糖饮食持续性降低果蝇对甜味刺激的敏感度。该结果对于阐释嗜甜相关代谢紊乱机制具有参考价值。
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Science Advances [IF:13.116]

Persistent epigenetic reprogramming of sweet taste by diet

饮食对甜味味觉的持续性表观遗传重编程

10.1126/sciadv.abc8492

2020-11-11, Article

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Diets rich in sugar, salt, and fat alter taste perception and food preference, contributing to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here, we show that in response to a high sugar diet, the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of Drosophila melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Half of these transcriptional changes persist despite returning the animals to a control diet, causing a permanent decrease in sweet taste. Our results uncover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and feeding behavior to promote obesity.

First Authors:
Anoumid Vaziri

Correspondence Authors:
Monica Dus

All Authors:
Anoumid Vaziri,Morteza Khabiri,Brendan T Genaw,Christina E May,Peter L Freddolino,Monica Dus

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