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

Abstract

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.

Effect of Cafeteria Diet Feeding on Soleus Intramyocellular Lipid of Wistar Rats

“…This role is usually carried out, at least in rodents, mainly by brown adipose tissue [29], which uncoupling mechanism is nowadays widely known [30]. However, brown adipose tissue thermogenesis does not explain a significant part of whole body adaptive thermogenesis, including the possible role of liver [31], overall inefficiency elicited by thyroid hormones [32], and muscle activity [33]. A higher energy wasting by muscle has been attributed to increased expenditure in maintaining muscle tone [34], but no "chemical" mechanisms have been advanced to explain the role of muscle in wasting energy in thermogenic processes.…”

Adaptive thermogenesis and uncoupling proteins: a reappraisal of their roles in fat metabolism and energy balance

“…Several other tissues and organs (e.g., liver, kidneys, heart, pancreas) are activated by the SNS in response to diet (Table 2), but whether they contribute to DIT is unknown. A role for liver as a major site for DIT has been proposed on the basis that the increase in resting oxygen consumption of rats overfed on a cafeteria-like diet was considerably blunted by partial hepatectomy [29]. However, it is difficult, on the basis of these results, to delineate a role for liver as an effector site for DIT from that of a transducer of energy status [30], since partial hepatectomy may have impaired the transmission of signals from the liver to the dtrueT effectors of DIT.…”

Short‐term oscillations of aortic core temperature and thermogenic organ blood flow in the rat

“…The site of regulatory thermogenesis in the mammal has been placed by most authors on the brown adipose tissue (Rothwell & Stock, 1979b;Girardier, 1983), or in liver (Berry, Clark, Grivell & Wallace, 1985;Ma, Nadeau & Foster, 1987), as well as in muscle for shivering thermogenesis (Hemingway, 1963;Jansky & Hart, 1963).…”