Depriving or pair feeding intact controls induces some persisting regulatory deficits similar to those of the recovered lateral rat.

Abstract

To determine the extent to which acute starvation might contribute to the chronic deficits in regulatory feeding, drinking, and body weight maintenance characteristic of rats with lateral hypothalamic brain lesions, neurologically intact rats were pair-fed (including forced feedings) and pair-watered for 2-4 wk with rats rendered transiently aphagic and adipsic by hypothalamic knife cuts. When the pair-fed rats were subsequently allowed to free-feed, their body weights remained suppressed. In addition, the pair-fed rats failed to eat in response to glucoprivation induced by insulin or 2-deoxy-D-glucose. The pair-fed rat drank less than nondeprived controls, but more than rats with knife cuts, when administered osmotic or volemic challenges to thirst. Other aspects of the recovered lateral syndrome were absent. In a second experiment, intact rats that had recovered from varying durations of semistarvation with or without subsequent forced feedings were tested for regulatory impairments. Deficits in chronic body weight maintenance were found in rats that had been starved and subsequently force-fed. Diminished responses to glucoregulatory challenges were seen in rats that had been starved but not forced-fed as well as in those that had been force-fed but not starved. This impaired eating in response to glucoregulatory challenges abated with repeated testing. Thus, both the acute failure of ingestive behaviors and therapeutic forced feedings can contribute to the impired regulatory eating and driniing that follow recovery from certain types of brain damage.