Cholecystokinin-decreased food intake in rhesus monkeys

1976 ◽  
Vol 230 (1) ◽  
pp. 15-18 ◽  
Author(s):  
J Gibbs ◽  
JD Falasco ◽  
PR McHugh
Keyword(s):  
Biological Activity ◽  
Food Intake ◽  
Food Deprivation ◽  
Test Meal ◽  
Rhesus Monkeys ◽  
Significant Inhibition ◽  
Solid Food ◽  
Threshold Dose

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.

Adrenergic Stimulation of the Rat Diencephalon and its Effect on Food Intake and Hoarding Activity

1970 ◽  
Vol 22 (2) ◽  
pp. 125-132 ◽  
Author(s):  
J. E. Blundell ◽  
L. J. Herberg
Keyword(s):  
Electrical Stimulation ◽  
Food Intake ◽  
Food Deprivation ◽  
Lateral Hypothalamus ◽  
Adrenergic Stimulation ◽  
Feeding Mechanism ◽  
Stimulation Of ◽  
Nutritional Depletion

The diencephalic area most sensitive to microinjections of noradrenaline lay outside the area of the lateral hypothalamus in which feeding can be produced by electrical stimulation. Injection of either area, including injections that caused increased feeding, failed to have any effect on hoarding activity. Since hoarding can be elicited both by food deprivation and by electrical stimulation of the lateral hypothalamus, these findings indicate biochemical, anatomical and motivational differences between the central feeding mechanism sensitive to adrenergic stimulation, and that responding to electrical stimulation or nutritional depletion. The former mechanism may be disinhibitory; the latter, excitatory.

Sucrose Concentration as Reinforcement for Lever Pressing by Monkeys

1956 ◽  
Vol 2 (3) ◽  
pp. 381-384 ◽  
Author(s):  
Donald G. Conrad ◽  
Murray Sidman
Keyword(s):  
Food Deprivation ◽  
Rhesus Monkeys ◽  
Response Rate ◽  
Sucrose Concentration ◽  
Variable Interval ◽  
Variable Interval Schedule ◽  
Interval Schedule ◽  
Satiation Effect ◽  
Low Concentrations ◽  
Lever Pressing

3 rhesus monkeys were given various concentrations of sucrose for lever pressing on a variable interval schedule of reinforcement. 7 sucrose concentrations were studied at 2 levels of food deprivation. The response rates accelerated rapidly with increasing concentrations, and then declined after reaching a maximum, generally between 15 and 30% sucrose concentration. The decline was attributed to a satiation effect. The higher level of food deprivation tended to increase the response rate at all but the extreme high and low concentrations.

Cholecystokinin is a Satiety Hormone in Humans at Physiological Post-Prandial Plasma Concentrations

1995 ◽  
Vol 89 (4) ◽  
pp. 375-381 ◽  
Author(s):  
Anne Ballinger ◽  
Lorraine McLoughlin ◽  
Sami Medbak ◽  
Michael Clark
Keyword(s):  
Food Intake ◽  
Test Meal ◽  
Plasma Concentrations ◽  
Standard Test ◽  
Saline Infusion ◽  
Reduce Food Intake ◽  
Subsequent Test ◽  
Gut Hormone ◽  
Plasma Cholecystokinin ◽  
Satiety Hormone

1. Intravenous infusions of the brain/gut hormone, cholecystokinin, have been shown to reduce food intake in a subsequent test meal. However, in previous studies the doses administered were large and likely to have produced plasma concentrations far in excess of the normal post-prandial range. 2. In this study cholecystokinin-8 was infused intravenously to six healthy subjects in doses that reproduced physiological post-prandial concentrations. Plasma concentrations of cholecystokinin were measured using a novel sensitive and specific radioimmunoassay. The effect of cholecystokinin-8 infusion on subsequent food intake in a standard test meal was compared with the effect of saline infusion in the same subjects. 3. Food intake (mean ± SEM) was significantly less during cholecystokinin (5092 ± 665 kJ) than during saline infusion (6418 ± 723 kJ, P = 0.03). During cholecystokinin infusion, plasma concentrations increased from 0.45 ± 0.06 pmol/l to 7.28 ± 2.43 pmol/l immediately before the meal. With saline infusion there was no premeal increase in plasma cholecystokinin concentration. 4. This paper describes a novel radioimmunoassay for measurement of plasma concentrations of cholecystokinin. Using this assay we have demonstrated that cholecystokinin is important in control of satiety in humans.

Influence of the subfornical organ on meal-associated drinking in rats

2001 ◽  
Vol 280 (3) ◽  
pp. R669-R677 ◽  
Author(s):  
Elizabeth M. Starbuck ◽  
Douglas A. Fitts
Keyword(s):  
Food Intake ◽  
Hypertonic Saline ◽  
Food Deprivation ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Subfornical Organ ◽  
Intragastric Administration ◽  
Drinking Patterns ◽  
Ad Libitum ◽  
Ad Libitum Feeding

A lesion of the subfornical organ (SFO) may disrupt drinking after a meal of dry chow as it does drinking after intragastric administration of hypertonic saline. Food and water intakes of SFO-lesioned (SFOX) and sham-lesioned rats were measured during 90-min tests following various lengths of food deprivation. During the tests, all rats began eating before they began drinking. After 20–24 h of food deprivation, latency to begin drinking after eating had started was longer for SFOX than for sham-lesioned rats. Plasma osmolality was elevated by 2–3% in both lesion groups at 12 min, the latency for sham-lesioned rats to drink, but SFOX rats nevertheless continued eating and delayed drinking. Eating after shorter 4-h food deprivations and ad libitum feeding produced more variable drinking latencies and less consistent effects of SFO lesion. During 24 h of water deprivation, SFO lesion had no effect on the suppression of food intake and did not affect food or water intakes during the first 2 h of subsequent rehydration. These findings indicate that the SFO is involved in initiating water intake during eating and in determining drinking patterns and the amount of water ingested during a meal.

Corticotropin-releasing hormone-binding protein in brain and pituitary of food-deprived obese (fa/fa) Zucker rats

1999 ◽  
Vol 277 (6) ◽  
pp. R1749-R1759 ◽  
Author(s):  
Elena Timofeeva ◽  
Yves Deshaies ◽  
Frédéric Picard ◽  
Denis Richard
Keyword(s):  
Food Intake ◽  
Food Deprivation ◽  
Binding Protein ◽  
Mrna Level ◽  
Zucker Rats ◽  
Pituitary Cells ◽  
Dorsal Part ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Ad Libitum

The present study was conducted to verify whether experimental conditions such as obesity and food deprivation, which promote food intake and reduce thermogenesis, could modify the expression of the corticotropin-releasing hormone (CRH)-binding protein (BP) in the rat brain. In situ hybridization, histochemistry, and immunohistochemistry were used to assess the expression of CRH-BP in lean ( Fa/?) and obese ( fa/fa) Zucker rats that were fed ad libitum, food deprived for 24 h, or food deprived for 24 h and refed for 6 h. In both lean and obese rats, food deprivation led to a reduction in body weight that was accompanied by a reversible increase in plasma corticosterone levels. Food deprivation and, to a lesser degree, obesity induced the expression of CRH-BP mRNA in the dorsal part of the medial preoptic area (MPOA). This induction of the CRH-BP gene led to by food deprivation was confirmed by the appearance in the dorsal part of the MPOA of neurons immunoreactive to CRH-BP. Food deprivation (in particular) and obesity also increased the levels of CRH-BP mRNA in the basolateral amygdala (BLA). The enhanced CRH-BP expression in the MPOA and BLA in response to food deprivation was reversed by refeeding. In lean Fa/? rats, the CRH-BP mRNA level in the pituitary cells was significantly decreased after food deprivation and restored after refeeding. When food was provided ad libitum, the number of cells expressing CRH-BP in the anterior pituitary was significantly higher in lean rats than in obese animals. Food deprivation for 24 h decreased dramatically the number of pituitary cells expressing CRH-BP in lean rats. Altogether, the present results demonstrate that food deprivation and, to a lesser extent, obesity can selectively affect the expression of CRH-BP. Given both the inactivating effect of CRH-BP on the CRH system and the potential roles played by the MPOA and BLA in the thermogenic and anorectic effects of CRH, it can be argued that the induction of the CRH-BP gene in obesity and after food deprivation occurs as a mechanism to reduce energy expenditure and to stimulate food intake.

Does calcium mediate the slowing of gastric emptying in primates?

1982 ◽  
Vol 243 (3) ◽  
pp. G200-G203
Author(s):  
J. N. Hunt ◽  
P. R. McHugh
Keyword(s):  
Fatty Acids ◽  
Gastric Emptying ◽  
Tight Junctions ◽  
Test Meal ◽  
Binding Sites ◽  
Rhesus Monkeys ◽  
Disodium Edetate ◽  
Set Up ◽  
Duodenal Epithelium

Disodium edetate (EDTA, 1 g/l) in test meals of water slowed gastric emptying strongly in one human and in four rhesus monkeys. When the binding sites of the EDTA were loaded with calcium before it was given in the test meal, there was little effect on gastric emptying. It is suggested that EDTA takes up calcium from the “tight junctions” of the duodenal epithelium. As a result a signal is set up that slows gastric emptying. It is postulated that the anions of fatty acids produced during the digestion of triglycerides in the duodenum also slow gastric emptying by the same mechanism. We explain how fats, carbohydrates, and proteins could all slow gastric emptying by operating on the same receptor.

The effect of ‘flavour imprinting’ on the acceptability of solid food in weanling rats

1999 ◽  
Vol 1999 ◽  
pp. 225-225
Author(s):  
J. E. L. Day ◽  
E. A. J. Randall ◽  
R. M. Sibly
Keyword(s):  
Food Intake ◽  
Nutritional Status ◽  
Maternal Diet ◽  
Diet Selection ◽  
Solid Food ◽  
Wild Animals ◽  
Weanling Rats ◽  
In The Wild ◽  
Normal Trajectory ◽  
Commercial Environment

Weaning is associated with a dramatic change in the nutritional status of young animals, and many neonates experience a lag in their normal trajectory of growth post-weaning because they have little experience of ingesting solid food. In the wild, animals are able to learn which foods are ‘safe’ through the mammary transfer of volatile flavours present in the maternal diet. This mechanism could be harnessed in a commercial environment by the use of flavour imprinting, a technique where a characteristic flavour is included both in the maternal and weanling's diet (for pilot data see Campbell, 1976). The use of this method could be associated with considerable increases in the profitability of animal production, however, the whole area is poorly understood. The objective of this experiment was to enhance our understanding of the effect of flavour imprinting on the acceptability of solid food, and hence our ability to predict the diet selection and food intake of newly weaned animals.

Infusion of CCK-8 into hepatic-portal vein fails to reduce food intake in rats

1987 ◽  
Vol 252 (5) ◽  
pp. R1015-R1018 ◽  
Author(s):  
D. Greenberg ◽  
G. P. Smith ◽  
J. Gibbs
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Test Meal ◽  
Intraperitoneal Administration ◽  
Meal Size ◽  
Reduce Food Intake ◽  
Hormonal Mechanism ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Intraportal Infusion

If the putative satiating effect of endogenous cholecystokinin (CCK) is produced through a circulating hormonal mechanism, then administration of exogenous CCK into the hepatic-portal vein should decrease meal size. To test this, one form of endogenous CCK, the C-terminal octapeptide CCK-8, was infused intraportally in doses of 4 and 8 micrograms/kg just prior to a test meal. Neither dose decreased food intake after intraportal infusion even though intraperitoneal administration of 4 micrograms/kg CCK-8 decreased meal size approximately 50% in the same rats. The results suggest that if endogenous CCK-8 has a satiating effect, it acts primarily through a paracrine mechanism.

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