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

Abstract

The resting metabolic rates [Formula: see text] of rats fed chow (CH) or a "cafeteria" (CAF) diet of highly palatable human foods were measured at thermoneutrality (28 °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 [Formula: see text] 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 [Formula: see text] in either diet group. Two-thirds hepatectomy decreased [Formula: see text] 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 [Formula: see text] 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 [Formula: see text] of CH rats. It reduced the [Formula: see text] of sham-operated CAF rats by 0.94 ± 0.08 mL/min (12%), but had a significantly smaller effect [Formula: see text] in partially hepatectomized CAF rats. This difference suggests that about 70% of the propranolol-inhibitable fraction of the elevated [Formula: see text] 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.