Overfeeding, Autonomic Regulation and Metabolic Consequences

The autonomic nervous system plays an important role in the regulation of body processes in health and disease. Overfeeding and obesity (a disproportional increase of the fat mass of the body) are often accompanied by alterations in both sympathetic and parasympathetic autonomic functions. The overfeeding-induced changes in autonomic outflow occur with typical symptoms such as adiposity and hyperinsulinemia. There might be a causal relationship between autonomic disturbances and the consequences of overfeeding and obesity. Therefore studies were designed to investigate autonomic functioning in experimentally and genetically hyperphagic rats. Special emphasis was given to the processes that are involved in the regulation of peripheral energy substrate homeostasis. The data revealed that overfeeding is accompanied by increased parasympathetic outflow. Typical indices of vagal activity (such as the cephalic insulin release during food ingestion) were increased in all our rat models for hyperphagia. Overfeeding was also accompanied by increased sympathetic tone, reflected by enhanced baseline plasma norepinephrine (NE) levels in both VMH-lesioned animals and rats rendered obese by hyperalimentation. Plasma levels of NE during exercise were, however, reduced in these two groups of animals. This diminished increase in the exercise-induced NE outflow could be normalized by prior food deprivation. It was concluded from these experiments that overfeeding is associated with increased parasympathetic and sympathetic tone. In models for hyperphagia that display a continuously elevated nutrient intake such as the VMH-lesioned and the overfed rat, this increased sympathetic tone was accompanied by a diminished NE response to exercise. This attenuated outflow of NE was directly related to the size of the fat reserves, indicating that the feedback mechanism from the periphery to the central nervous system is altered in the overfed state.

Effect of Skeleton Photoperiod and Food Availability on the Circadian Pattern of Feeding and Drinking in Rats

Feeding and drinking behavior were measured in rats maintained under a 12:12 light-dark (LD) cycle or skeleton photoperiod (SPP). Feeding and drinking were closely associated during the normal LD cycle but under SPP conditions an increased feeding activity during the subjective day was not accompanied by an equivalent increment of water intake. This indicates a stronger coupling of drinking to the subjective night. A restriction of food availability to the subjective light phase did not cause an accompanying complete shift in drinking behavior. These results suggest that drinking is largely dependent on the influence of a circadian oscillator and this association is not disrupted by changes in feeding schedule. A change in food access to the subjective light phase caused partial but not permanent desynchronization between feeding and drinking behavior. Synchrony was reestablished within one day once food was available ad lib. Complete return to the original feeding and drinking patterning took 3 days. It is suggested that separate slave oscillators controlling feeding and drinking are governed by a hypothesized "master" circadian oscillator which remains definitely entrained to the original rhythm by the light pulses of the SPP condition.

Interaction Between Circadian and Caloric Control of Feeding Behavior in the Rat

Feeding at the beginning of the night is probably dependent on the rat's immediate energy requirements while feeding at the end may have an anticipatory function. This latter feeding peak may be mainly controlled by a circadian pacemaker. The aim of this study was to investigate the relative contribution of satiety signals and circadian pacemakers in the control of feeding behavior. Food intake was monitored after infusion of liquid food into the stomach during several parts of the day-night cycle to prevent a possible influence of oral sensations. It is demonstrated that intragastric infusion is more effective in suppressing intake during daytime and the first half of the dark phase than during the second half of the dark phase. Suppressions of food intake are mainly due to delaying the first occurrence of food ingestion, whereas the size of that meal is less affected. During the last period of the night no significant delay could be brought about. These experiments suggest that in the rat a circadian pacemaker dominates feeding motivation during the end of the night thereby strongly interacting with caloric control of feeding behavior.

Daily Rhythms of Feeding in the Genetically Obese and Lean Zucker Rats

Feeding patterns were examined in obese (fa/fa) and lean (Fa/-) adult Zucker rats over the light-dark cycle during 14 days. Obese rats eat more than lean rats especially during the dark phase. Light and dark feeding expressed as percentage of 24 hr intake showed no significant differences between the lean and obese groups. The higher food intake in obese rats is mainly caused by larger meals since obese rats ate fewer meals than lean rats. Only for the obese group differences were observed between mean meal size in light and dark phase. There is some indication that the circadian controlled temporal distribution of meals is different in obese rats compared to lean rats since obese rats eat fewer but larger meals during the first half of the dark phase. During this phase meal size increases gradually in the obese rats, suggesting that the circadian influence on feeding motivation is increased.