Enhancing hepatic mitochondrial fatty acid oxidation stimulates eating in food-deprived mice

Abdelhak Mansouri, Gustavo Pacheco-López, Deepti Ramachandran, Myrtha Arnold, Claudia Leitner, Carina Prip-Buus, Wolfgang Langhans, Núria Morral

Research output: Contribution to journalArticle

2 Scopus citations


Hepatic fatty acid oxidation (FAO) has long been implicated in the control of eating. Nevertheless, direct evidence for a causal relationship between changes in hepatic FAO and changes in food intake is still missing. Here we tested whether increasing hepatic FAO via adenovirusmediated expression of a mutated form of the key regulatory enzyme of mitochondrial FAO carnitine palmitoyltransferase 1A (CPT1mt), which is active but insensitive to inhibition by malonyl-CoA, affects eating and metabolism in mice. CPT1mt expression increased hepatocellular CPT1 protein levels. This resulted in an increase in circulating ketone body levels in fasted CPT1mt-expressing mice, suggesting an increase in hepatic FAO. These mice did not show any significant changes in cumulative food intake, energy expenditure, or respiratory quotient after 4-h food deprivation. After 24-h food deprivation, however, the CPT1mt-expressing mice displayed increased food intake. Thus expression of CPT1mt in the liver increases hepatic FAO capacity, but does not inhibit eating. Rather, it may even stimulate eating after prolonged food deprivation. These data do not support the hypothesis that an increase in hepatic FAO decreases food intake.

Original languageEnglish (US)
Pages (from-to)R131-R137
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number2
StatePublished - Jan 15 2015


  • Carnitine palmitoyltransferase 1a
  • Energy homeostasis
  • Food intake
  • Liver
  • Metabolic control of eating

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

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