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

Yoshihiko Izumida, Naoya Yahagi, Yoshinori Takeuchi, Makiko Nishi, Akito Shikama, Ayako Takarada, Yukari Masuda, Midori Kubota, Takashi Matsuzaka, Yoshimi Nakagawa, Yoko Iizuka, Keiji Itaka, Kazunori Kataoka, Seiji Shioda, Akira Niijima, Tetsuya Yamada, Hideki Katagiri, Ryozo Nagai, Nobuhiro Yamada, Takashi KadowakiHitoshi Shimano

研究成果: Article査読

60 被引用数 (Scopus)

抄録

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.

本文言語English
論文番号2316
ジャーナルNature communications
4
DOI
出版ステータスPublished - 2013

ASJC Scopus subject areas

  • 化学 (全般)
  • 生化学、遺伝学、分子生物学(全般)
  • 物理学および天文学(全般)

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