Glycogen shortage during fasting triggers liver-brain-adipose neurocircuitry to facilitate fat utilization.

Glycogen shortage during fasting triggers liver-brain-adipose neurocircuitry to facilitate fat utilization.
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禁食期间的糖原短缺会触发肝脏 - 脑 - 辅助神经记录,以促进脂肪利用。

DOI:
10.1038/ncomms3316
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发表时间:
2013
影响因子:
16.6
通讯作者:
Shimano, Hitoshi
Shimano, Hitoshi
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Izumida, Yoshihiko;Yahagi, Naoya;Takeuchi, Yoshinori;Nishi, Makiko;Shikama, Akito;Takarada, Ayako;Masuda, Yukari;Kubota, Midori;Matsuzaka, Takashi;Nakagawa, Yoshimi;Iizuka, Yoko;Itaka, Keiji;Kataoka, Kazunori;Shioda, Seiji;Niijima, Akira;Yamada, Tetsuya;Katagiri, Hideki;Nagai, Ryozo;Yamada, Nobuhiro;Kadowaki, Takashi;Shimano, Hitoshi

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在禁食期间,动物通过将其能量来源从碳水化合物转移到甘油三酯来保持能量平衡。然而,这一转变的触发因素尚未完全阐明。在这里,我们表明,选择性肝迷走神经切断术通过减弱交感神经介导的脂肪组织脂解来减缓脂肪消耗的速度。通过腺病毒过表达糖原合成酶或转录因子TFE 3的肝糖原预载消除了这种肝-脑-脂肪轴激活。此外,通过敲低糖原磷酸化酶基因来阻断糖酵解并导致糖原含量升高,消除了来自肝脏的脂肪分解信号,这表明糖原是触发这种神经回路的关键。这些结果表明,肝糖原缺乏激活肝-脑-脂肪神经轴,其在长时间禁食条件下将燃料源从糖原转换为甘油三酯中具有重要作用。 在禁食期间,动物将其能量来源从碳水化合物转移到甘油三酯。在这里,Izumida等人报告说,肝脏中的糖原缺乏激活了肝-脑-脂肪组织神经回路,该神经回路发出信号,将燃料来源从肝糖原转换为脂肪细胞中的甘油三酯。
During fasting, animals maintain their energy balance by shifting their energy source from carbohydrates to triglycerides. However, the trigger for this switch has not yet been entirely elucidated. Here we show that a selective hepatic vagotomy slows the speed of fat consumption by attenuating sympathetic nerve-mediated lipolysis in adipose tissue. Hepatic glycogen pre-loading by the adenoviral overexpression of glycogen synthase or the transcription factor TFE3 abolished this liver–brain–adipose axis activation. Moreover, the blockade of glycolysis through the knockdown of the glycogen phosphorylase gene and the resulting elevation in the glycogen content abolished the lipolytic signal from the liver, indicating that glycogen is the key to triggering this neurocircuitry. These results demonstrate that liver glycogen shortage activates a liver–brain–adipose neural axis that has an important role in switching the fuel source from glycogen to triglycerides under prolonged fasting conditions. During fasting, animals shift their energy source from carbohydrates to triglycerides. Here, Izumida et al. report that glycogen shortage in the liver activates a liver–brain–adipose-tissue neurocircuit that signals the switch in fuel source from liver glycogen to triglycerides in fat cells.
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