OBJECTIVE: The capacity of the liver to serve as a peripheral sensor in the regulation of food intake has been debated for over half a century. The anatomical position and physiological roles of the liver suggest it is a prime candidate to serve as an interoceptive sensor of peripheral tissue and systemic energy state. Importantly, maintenance of liver ATP levels and within-meal food intake inhibition is impaired in human subjects with obesity and obese pre-clinical models. Previously, we have shown decreased hepatic mitochondrial energy metabolism (i.e., oxidative metabolism & ADP-dependent respiration) in male liver-specific, heterozygous PGC1a mice results in increased short-term diet-induced weight gain with increased within meal food intake. Herein, we tested the hypothesis that decreased liver mitochondrial energy metabolism impairs meal termination following nutrient oral pre-loads. METHODS: Liver mitochondrial respiratory response to changes in ΔG RESULTS: We observed male liver-specific, heterozygous PGC1a mice have reduced mitochondrial response to changes in ΔG CONCLUSION: These data support previous work proposing liver-mediated food intake regulation through modulation of peripheral satiation signals.