期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 308, 期 2, 页码 R131-R137出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00279.2014
关键词
energy homeostasis; carnitine palmitoyltransferase 1a; food intake; metabolic control of eating; liver
类别
资金
- National Institute of Diabetes and Digestive and Kidney Diseases [R01DK078595]
- American Diabetes Association [1-08-RA-135]
- Swiss National Science Foundation [31003A_130665]
- Swiss National Science Foundation (SNF) [31003A_130665] Funding Source: Swiss National Science Foundation (SNF)
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 adenovirus-mediated 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.
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