Evidence for liver as the major site of the diet-induced thermogenesis of rats fed a "cafeteria" diet.

The resting metabolic rates (VO2) of rats fed chow (CH) or a "cafeteria" (CAF) diet of highly palatable human foods were measured at thermoneutrality (28 degrees C) before and shortly after two-thirds hepatectomy or sham operation, and again after administration of propranolol (5 mg/kg). CAF rats initially had a 17% and 1.2 mL/min higher mean resting VO2 than CH rats, a difference usually considered to represent the diet-induced thermogenesis (DIT) that CAF rats develop during overconsumption of the diet. Sham operation did not significantly affect resting VO2 in either diet group. Two-thirds hepatectomy decreased VO2 by about 1.0 mL/min more (125% more) in CAF rats than in CH rats, from which it may be estimated that the CAF rats initially had a liver VO2 about 1.6 mL/min higher than that of the CH rats, a difference more than sufficient to fully account for their apparent DIT. Propranolol did not significantly affect the VO2 of CH rats. It reduced the VO2 of sham-operated CAF rats by 0.94 +/- 0.08 mL/min (12%), but had a significantly smaller effect (delta VO2 = -0.50 +/- 0.05 mL/min) in partially hepatectomized CAF rats. This difference suggests that about 70% of the propranolol-inhibitable fraction of the elevated VO2 of the CAF rats, presumably a measure of sympathetically mediated DIT, resided in the liver. This study thus points to the liver as the major (70-100%) effector of the DIT of CAF rats.