We have investigated whether changes in hepatic mitochondrial protein
mass and respiration occur in hyperphagic rats. Hyperphagia was induce
d by a palatable diet. Rats fed such a diet showed a significantly gre
ater energy intake (+40%) without a corresponding greater body weight
gain when compared to control rats. They also showed a significantly h
igher resting metabolic rate (+44%) compared to control rats. The latt
er increase was abolished by propranolol administration and, as such,
was considered to be an adaptative response. No difference in liver mi
tochondrial protein mass was found in hyperphagic rats. On the other h
and, state 3 respiration using succinate as substrate increased, with
no difference in ADP/O ratios and, hence, in the degree of coupling. T
his increase is mediated by the sympathetic nervous system, as it was
abolished by propranolol. The above results indicate an increase in AT
P synthetic capacity and suggest one possible mechanism by which metab
olism contributes to the increased expenditure of hyperphagic rats.