Glycogen shortage during fasting triggers liver-brain-adipose neurocircuitry to facilitate fat utilization.
Nat Commun
; 4: 2316, 2013.
Article
in En
| MEDLINE
| ID: mdl-23939267
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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Sympathetic Nervous System
/
Triglycerides
/
Adipose Tissue
/
Fasting
/
Liver Glycogen
Limits:
Animals
Language:
En
Journal:
Nat Commun
Journal subject:
BIOLOGIA
/
CIENCIA
Year:
2013
Document type:
Article
Affiliation country:
Japón