Format

Send to:

Choose Destination
See comment in PubMed Commons below
Nat Commun. 2013;4:2316. doi: 10.1038/ncomms3316.

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

Author information

  • 1Nutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan.

Erratum in

  • Nat Commun. 2013;4:2930.

Abstract

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 glycogenolysis [corrected] 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.

PMID:
23939267
[PubMed - indexed for MEDLINE]
PMCID:
PMC3753545
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group Icon for PubMed Central
    Loading ...
    Write to the Help Desk