No abstract

After 3-hr food deprivation, rats with gastric fistulas ate liquid food with the fistula closed (normal feeding) or open (sham feeding). Meal size (MS) was larger, latency to rest (LR) after a meal was longer, and intermeal interval (IMI) was shorter during sham feeding than during normal feeding. The putative satiety signal cholecystokinin (CCK, 20% pure) decreased MS and LR and increased IMI during sham feeding. After CCK (30 U/kg) the MS, LR, and IMI were the same during sham feeding as during normal feeding. The synthetic octapeptide (OCT) of CCK, which has the known biological actions of the complete hormone, reproduced the effects of CCK (30 U/kg) on MS and LR but not on IMI. Ingestive behavior was not nonspecifically suppressed by CCK or OCT because water drinking was not inhibited by CCK or OCT. The CCK and OCT were also tested for their ability to serve as unconditioned stimuli (UCS) for the formation of a conditioned taste aversion (CTA) in the 3-hr food-deprived sham-feeding rat. The OCT (30 U/kg) did not serve as a UCS for a CTA in the same sham-feeding conditions in which OCT produced normal MS and LR. Impure CCK (30 U/kg), however, did serve as a UCS for a CTA under these conditions. The differential effectiveness of CCK and OCT for IMI and CTA may be due to non-CCK factors in the impure extract of CCK. These experiments demonstrate that the preabsorptive food-contingent stimuli of sham feeding plus exogenous CCK are sufficient for normal short-term satiety under certain conditions, and they provide further evidence consistent with the hypothesis that cholecystokinin produces satiety in rats.Cholecystokinin (CCK), a gut hormone nous CCK is a satiety signal terminating a released into the blood upon preabsorptive normal meal during spontaneous feeding, food-contingent stimulation of the intestinal Indeed, the satiety effect of CCK has not mucosa, has been identified as a putative been studied under experimental conditions signal for short-term satiety (Smith & Gibbs, that resemble those of normal feeding. 1975). Although exogenous CCK decreasesBecause normal satiety (or normal feedfeeding in adult rats (Gibbs, Young, & ing) is marked by distinct meals and inter-Smith, 1973a) and monkeys (Gibbs, Falasco, meal intervals, a signal important for & McHugh, 1976) and suppresses sham short-term satiety should affect meal size feeding in rats (Antin, Gibbs, Holt, Young, and/or intermeal interval. The effect of & Smith, 1975; Gibbs, Young, & Smith, CCK on these parameters is not known. 1973b), it remains unclear whether endoge-The experiments reported here determine the effect of CCK on three behavioral mea-This research was supported by National Institutes sur es of satiety (meal size, latency to rest, of Health Fellowship MH05135 (to F. S. Kraly), Career and intermeal interval) in rats sham feeding Development Award NS38601 (to G. P. Smith), Re-a liquid diet after 3-hr food deprivation, search Grants AM17240 and MH15455; and the Line-Since this period of food deprivation is Xu^SprintsshouldbesenttoF.ScottKr...

No abstract

Much of normal drinking occurs around mealtime. Little is known about the physiological mechanisms that control normal drinking, despite the identification of neurological substrates and physiological mechanisms for drinking in response to homeostatic deficit. This review follows the course of ingested food along the gastrointestinal tract where food elicits a neuroendocrine cascade of events with the potential for mobilizing drinking. This perspective helps to identify histamine, and perhaps insulin and serotonin, as serving vagally mediated mechanisms that can elicit drinking around mealtime to preclude homeostatic imbalance.

Drinking after intragastric hypertonic solutions was examined to determine whether increased plasma osmolality always accompanied initiation of drinking. A 2-ml infusion through a gastric catheter was the beginning of tests in Sprague-Dawley male rats. Latency to drink was shorter and 1-h water intake was greater for increasing concentrations of NaCl (600, 1,200, and 1,800 mosmol/kg) compared with baseline (290 mosmol/kg). Although 600, 900, or 1,200 mosmol/kg NaCl elicited drinking, such infusions failed to change systemic plasma osmolality, and 900 mosmol/kg also failed to change plasma sodium, protein, renin activity, or packed cell volume at the initiation of drinking. Intragastric 900 mosmol/kg sodium bicarbonate, sodium isethionate, potassium chloride, lithium chloride, and mannitol differentially increased water intake. Total subdiaphragmatic vagotomy abolished drinking elicited by intragastric NaCl; selective gastric or hepatic vagotomy attenuated intake under some conditions. These results support the hypothesis of a vagally mediated, gastrointestinal and/or hepatic-portal, osmosensitive mechanism for initiation of drinking in advance of postprandial increases in systemic osmolality.