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

• DOI: 10.1152/ajpregu.00279.2014
• Publication Date: 2014-11-27T05:23:05Z
• Authors: Abdelhak Mansouri; Gustavo Pacheco-L...; Deepti Ramachandran; Myrtha Arnold; Claudia Leitner; Carina Prip-Buus; Wolfgang Langhans; Núria Morral
• Keywords: Carnitine O-palmitoyltransferase; Steatosis

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