Refeeding after fasting in the rat: effects of dietary-induced obesity on energy balance regulation.

Obesity was induced in male Sprague-Dawley rats by overfeeding a cafeteria-style diet. The obesity was characterized by both adipocyte hypertrophy and hyperplasia. Body weight was then reduced by starvation to match that of control animals that had been fed ordinary Purina Chow. The previously obese rats were then refed to match the same body weight as controls, or given the same amount of Purina Chow as consumed by the controls. This resulted in a remaining moderate obesity, now due only to adipocyte hyperplasia with normal fat cell size. The previously obese rats needed less energy to keep their body weight equal to controls, and they spontaneously ate less than controls. They were, however, less food efficient because they did not accumulate as much energy in fat and protein depots during the period of refeeding as the controls did, and consequently must have transformed more energy into heat. This is in sharp contrast to nonobese animals subjected to a similar experimental procedure. Lipogenic enzymes and lipoprotein lipase activity in adipose tissue as well as plasma insulin concentrations were elevated in overfed rats but normalized during refeeding of Chow after fasting.

Refeeding after fasting in the rat: energy substrate fluxes and replenishment of energy stores.

Rats were fasted and refed and concentrations of plasma glucose, glycerol, triglyceride, insulin, and glucagon as well as glucose kinetics after injection of labeled glucose and glycerol were determined. In addition, concentrations and synthesis in vivo (from tritiated water) and in vitro of glycogen, triglycerides, and protein were followed in liver, muscle, and adipose tissues. The refeeding state after fasting was characterized by a decrease in glucose and triglyceride concentrations in plasma. Glucose turnover rate was increased. Protein losses were repleted, first in the liver then in muscle tissue. Synthesis of glycogen and lipid increased above control in liver and adipose tissue. These results are compatible with an increased outflux during refeeding of different energy substrates from plasma into the depleted protein and energy stores to an extent causing lower concentration of these substrates. Such phenomena might be of importance for energy intake regulation during the phase.