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J Gibbs

Publications and source records attributed to J Gibbs.

At least 181 records · Page 10Linked to original sources
PubMed1977

Cholecystokinin and satiety in rats and rhesus monkeys.

When ingested food does not accumulate in the stomach or enter the small intestine, rats do not stop eating. Small amounts of food placed in the small intestine or intraperitoneal injections of the intestinal hormone cholecystokinin (CCK) elicit the full behavioral display of satiety in these sham-feeding rats. In rhesus monkeys, intravenous infusions of CCK produce large, dose-related reductions in meal size. In addition, gastric preloads of calorically trivial amounts of l-phenylalanine, but not d-phenylalanine, produce large reductions in meal size, suggesting that: 1) endogenous CCK acts as a "satiety signal," and 2) certain foods may be very efficient releasers of such a satiety signal. Whether the satiety effect of CCK is physiological in rats and monkeys or operates in humans has not been determined.

Animals↗
PubMed1976

Cholecystokinin-decreased food intake in rhesus monkeys.

Five rhesus monkeys were infused intravenously with partially purified cholecystokinin (CCK) Just prior to a test meal of solid food after overnight food deprivation; CCK produced large, rapid, dose related suppressions of feeding. The lowest dose tested (5 Ivy U/kg body wt) produced a significant inhibition of food intake (26% suppression, P less than 0.05). Equivalent infusions of partially purified CCK or the synthetic COOH-terminal octapeptide of CCK (a pure fragment with all the biological activity of the full molecule) produced equivalent suppressions. In a second experiment, gastric preloads of a potent releaser of endogenous CCK, L-phenylalanine (L-Phe), and a weak releaser, D-phenylalanine (D-Phe) were compared for their relative abilities to suppress food intake at a test meal in nine rhesus monkeys after overnight deprivation. L-Phenylalanine produced large, rapid, dose-related suppressions of feeding, but D-Phe did not. The threshold dose of L-Phe was 0.5 g/kg (32% suppression, P less than 0.01). Neither CCK nor L-Phe caused signs of illness in these experiments. The results demonstrate that intravenous exogenous CCK suppresses feeding in rhesus monkeys and suggest that endogenous CCK has the same effect; they are consistent with the hypothesis that CCK is a satiety signal.

Animals↗
PubMed1975

Cholecystokinin elicits the complete behavioral sequence of satiety in rats.

The behavior of intact rats and rats with chronic gastric fistulas was observed and scored during a 60-min test period when they were offered liquid diet after 17 hr of food deprivation. Intact rats and rats with closed fistulas displayed a specific behavioral sequence at the end of each meal: They stopped eating, engaged in grooming and exploration for a short time, and then rested or slept. Thus, a fixed behavioral sequence characterizes satiety in the rat. Although the behavioral sequence of satiety was fixed, the cessation of feeding was not a sufficient condition for the appearance of the rest of the sequence: Quinine adulteration of the liquid diet stopped sham feeding but did not elicit the complete sequence. Intraperitoneal injection of the intestinal hormone cholecystokinin during sham feeding, however, elicited the complete sequence of satiety. The observation that cholecystokinin not only stops feeding but elicits the complete sequence of satiety supports our hypothesis that endogenous cholecystokinin is a satiety signal for the rat.

Animals↗
PubMed1975

Intestinal satiety in rats.

Infusion of liquid food into the duodenum inhibited sham feeding. The inhibition of sham feeding reflected satiety because the duodenal infusion elicited the complete behavioral sequence characteristic of satiety. The chemical and/or colligative load that the infusion imposed on the intestine appeared to be the adequate stimulus for satiety. Duodenal infusions that inhibit sham feeding and elicit satiety are not aversive because they will not function as the unconditioned stimulus for the formation of a conditioned taste aversion for saccharin. We call the satiety elicited by the infusion of food into the duodenum "intestinal satiety." This emphasizes our belief that satiety is a reflex that can be elicited by the activation of receptors in the wall of the intestine. It is known that the activation of some intestinal receptors releases the hormone cholecystokinin (CCK). Since CCK mimics a duodenal infusion by inhibiting sham feeding and eliciting the complete behavioral sequence of satiety, we suggest, but do not prove, that CCK mediates intestinal satiety in the rat.

Animals↗
PubMed1975

Inhibitions of feeding examined in rhesus monkeys with hypothalamic disconnexions.

In rhesus monkeys with knife cuts which disconnected the ventromedial hypothalamus and produced hypothalamic hyperphagia, we have studied a variety of stimuli known to reduce food intake: weight gain, emotionally arousing stimuli, bitter-tasting food, amphetamine, and pre-prandial intragastric infusion of nutrient. We demonstrate that these animals are similar to animals with ventromedial lesions in passing through a "dynamic" phase of overeating and weight gain and then stabilizing their body weight at a new level by reducing their feeding in a "static" phase. These animals are also more sensitive to the inhibitory effects of noise and bad taste in food. They, however, are less sensitive to the anorexic action of amphetamine. These results suggest that the ventromedial region is not crucial for the inhibitions produced by emotional arousal under our experimental conditions, but plays some role in amphetamine anorexia. Amphetamine is likely to have some specific anorexic action beyond its potential for arousal, since the same animals which are sensitive to the inhibitory effects of arousal are also resistant to amphetamine. Finally these hyperphagic animals do not differ from intact controls in the reduction of food intake produced by preloading with intragastric nutrient. This result is not consistent with the concepts that hypothalamic hyperphagia is caused by a disruption of satiety and that the ventromedial hypothalmic region is a crucial "satiety" centre.

Amphetamine↗
PubMed1975

Cholecystokinin: a putative satiety signal.

The intestinal hormone cholecystokinin (CCK) elicits satiety in rats and inhibits food intake in rhesus monkeys. This behavioral effect is specifically related to the C-terminal octapeptide structure of CCK and is a new biological effect of the hormone. Endogenous CCK released by food entering the duodenum may inhibit feeding and elicit satiety under physiological conditions, but no experimental evidence is availabe on this point. Until such evidence becomes available, we believe that CCK should be considered a putative satiety signal. The satiety effect of CCK suggests a therapeutic role of CCK for human hyperphagia and obesity. An interesting therapeutic alternative to administration of exogenous CCK is the release of endogenous CCK by nutrients such as amino acids. These nutrients can be ingested as preloads which are calorically trivial, but which release significant amounts of CCK. Such preloads inhibit food intake in rhesus monkeys. Their efficacy in man has not been determined.

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