Untangling the effects of hunger, anxiety, and nausea on energy intake during intravenous cholecystokinin octapeptide (CCK-8) infusion (original) (raw)
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Effects of cholecystokinin-octapeptide (CCK-8) on food intake and gastric emptying in man
Physiology & Behavior, 1988
Effects of cholecystokinin-octapeptide (CCK-8) on food intake and gastric emptying in man. PHYSIOL BEHAV 44(4/5) 645-649, 1988.-Food intake and gastric emptying were measured simultaneously after cholecystokinin-octapeptide (CCK-8) and saline infusions in order to test the hypothesis that reduction in gastric emptying mediates the effect of CCK-8 on food intake. Each of twelve nonobese healthy men received intravenous infusions of CCK-8 and saline on separate nonconsecutive days after they had consumed 500 g of tomato soup tagged with technetium-99-DTPA. Intake of a test meal was measured 20 min after consumption of the soup while gastric emptying was simultaneously monitored by gamma emission scintigraphy of the soup. Food intake and gastric emptying of the soup were both significantly reduced by CCK-8 infusions in comparison to saline. There was a significant correlation between the amount of the test meal eaten and the amount of soup emptied during the period the test meal was being eaten, but not before the meal, only on days when CCK-8 was infused. Differences in intakes between days when saline was infused and days when CCK-8 was infused did not correlate with differences in gastric emptying of soup. These results suggest that CCK may amplify signals of satiety in proportion to the fullness of the stomach. Gastric emptying per se may not mediate the effects of CCK-8 on food intake. Cholecystokinin Gastric emptying Human feeding Food intake Preloads Satiety TWO lines of investigation led to this experiment. The first
Abdominal vagal mediation of the satiety effects of CCK in rats
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2004
CCK type 1 (CCK1) receptor antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated in part by CCK action at CCK1 receptors on vagal sensory nerves innervating the small intestine. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of Nα-3-quinolinoyl-d-Glu- N,N-dipentylamide, does not. At dark onset, non-food-deprived control rats and rats with subdiaphragmatic vagotomies received a bolus injection of devazepide (2.5 μmol/kg iv) or a 3-h infusion of A-70104 (3 μmol·kg−1·h−1 iv) either alone or coadministered with a 2-h intragastric infusion of peptone (0.75 or 1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. In control rats both antagonists stimulated food intake and attenuated the anorexic response to intragastric infusion of peptone. In contrast, only devazepide was effective in stimulating food intake in vagotomized rats. Thus endoge...
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2000
Cholecystokinin (CCK) interacts with neural signals to induce satiety in several species, but the mechanisms are unclear. We therefore tested the hypothesis that alimentary CCK (CCK-A) receptors mediate the interaction of CCK with an appetizer on food intake in humans. CCK octapeptide (CCK-8, 0.75 μg infused over 10 min) or saline (placebo) with concomitant infusions of saline (placebo) or loxiglumide, a specific CCK-A antagonist, was infused into 16 healthy men with use of a double-blind, four-period design. All subjects received a standard 400-ml appetizer (amounting to 154 kcal) but were free to eat and drink thereafter as much as they wished. The effect of these infusions on feelings of hunger and satiety and on food intake was quantified. CCK-8 induced a reduction in calorie intake ( P < 0.05) compared with saline. Furthermore, a decrease in hunger feelings ( P < 0.05, saline-CCK-8 vs. all other treatments) and an increase in fullness were observed. These effects were ant...
Cholecystokinin-octapeptide (CCK-8) decreases food intake in man
American Journal of Clinical Nutrition
In comparison with a saline infusion, the infusion of the C-terminal octapeptide of cholecystokinin (4 ng/kg/min) decreased food intake by an average of 122 g in a group of 12 lean men without objective evidence of untoward side effects. Shapes of the cumulative intake curves under the two conditions were similar, but subjects ate less and stopped eating sooner when receiving octapeptide than when receiving saline. These results are consistent with the hypothesis that cholecystokinin is an endogenous signal for postprandial satiety. The results offer promise for the possible use of the octapeptide as an appetite suppressant.
Progress in Neurobiology, 1998
AbstractÐThis review evaluates the various lines of evidence supporting the hypothesis that cholecystokinin (CCK) released from the small intestine during feeding plays a physiological role in mediating satiety. Issues considered include, the eects of systemic injection of CCK on consummatory and operant feeding, the role of the vagus nerve, the eects of CCK A and CCK B receptor antagonists, and the neuroendocrine responses to exogenous CCK.
Peptides, 2016
Context: CCK is understood to play a major role in appetite regulation. Difficulties in measuring CCK have limited the potential to assess its profile in relation to food-induced satiety. Improvements in methodology and progress in theoretical understanding of satiety/satiation make it timely for this to be revisited. Objective: First, examine how physiologically relevant postprandial CCK8/33(s) profiles are influenced by fat (HF) or carbohydrate (HCHO) meals. Second, to examine relationships between postprandial CCK and profiles of satiety (hunger/fullness) and satiation (meal size). Participants and Design: Sixteen overweight/obese adults (11female/5male) participated in a randomised-crossover study (46years,29.8kg/m 2) in a university research centre. Plasma was collected preprandially and for 180min postprandially. Simultaneously, ratings of hunger/fullness were tracked for 180min before an ad libitum lunch was provided. Results: CCK8/33(s) levels increased more rapidly and reached a higher peak following HF compared to HCHO breakfast (F (1,15) =14.737,p<0.01). Profiles of hunger/fullness did not differ between conditions (F (1,15) =0.505,p=0.488;F (1,15) =2.277,p=0.152). There was no difference in energy intake from the ad libitum meal (HF-3958 versus HCHO-3925kJ; t (14) =0.201,p=0.844). CCK8/33(s) profiles were not associated with subjective appetite during early and late phases of satiety; nor was there an association between CCK8/33(s) and meal size. Conclusions: These results demonstrate CCK levels were higher after HF meal compared to HCHO isocaloric meal. There was no association between CCK levels and intensity of satiety, or with meal size. Under these circumstances, CCK does not appear to play a unique independent role in satiety/satiation. CCK probably acts in conjunction with other peptides and the action of the stomach.
Cholecystokinin and satiety: current perspectives
Nutrition, 2000
In the almost 30 years since the ability of peripheral administration of the brain/gut peptide cholecystokinin (CCK) to inhibit food intake was first demonstrated, significant progress in our overall understanding of the role of CCK in ingestive behavior has been made. A physiologic role for endogenous CCK in the control of meal size has been demonstrated and sites and mechanisms of action for CCK in food intake have been investigated. Recent work has uncovered roles for the CCK satiety pathway in the mediation of the feeding modulatory actions of estradiol, insulin, and leptin. The availability of the Otsuka Long Evans Tokushima Fatty (OLETF) rat, a strain lacking CCK A receptors, provides a unique model for the study of how deficits in a within-meals satiety signaling pathway may result in long-term changes in food intake and body weight.
Elevated plasma cholecystokinin and appetitive ratings after consumption of a liquid meal in humans
Nutrition (Burbank, Los Angeles County, Calif.), 2003
OBJECTIVE: This study had two objectives. The first was to evaluate the possibility that, in a previous study, a soup preload augmented the reduction of food intake in a test meal induced by an exogenous infusion of cholecystokinin (CCK) because the soup also endogenously released CCK. The second was to compare CCK release by soup between men and women to determine whether the increased satiating effectiveness of soup in women as opposed to men could have been partly attributable to differences in CCK release. METHODS: By using a bioassay that measures all of its known isoforms we determined plasma CCK levels at baseline and at several times postprandially in eight healthy, non-obese men and women (four of each sex). Each subject ingested 800 g of tomato soup, which was followed 30 min later by 300 g of a yogurt shake. Appetitive ratings were also collected and related to CCK levels. RESULTS: Ingestion of tomato soup significantly increased plasma CCK levels by 3.81 pmol/L (+/- 1.21 standard error, P = 0.016) over baseline within 30 min in all subjects combined. When CCK concentrations at 5 min after soup and 5 min after yogurt were averaged, the women's mean averaged concentration was 5.58 pmol/L (+/- 1.994, t = 2.80, P = 0.0073) higher than the men's. The elevated levels persisted but did not rise further upon consumption of the yogurt shake. Hunger ratings declined and fullness ratings increased after eating, although patterns of ratings did not match exactly patterns of CCK release. CONCLUSIONS: A large quantity of tomato soup stimulates significant CCK release; therefore, some of the satiating effects of soup preloads could have been mediated by an elevation in endogenous CCK.
AJP: Gastrointestinal and Liver Physiology, 2004
meister. Effect of oral CCK-1 agonist GI181771X on fasting and postprandial gastric functions in healthy volunteers. Am J Physiol Gastrointest Liver Physiol 287: G363-G369, 2004; 10.1152/ ajpgi.00074.2004.-CCK influences satiation and gastric and gallbladder emptying. GI181771X is a novel oral CCK-1 agonist; its effects on gastric emptying of solids, accommodation, and postprandial symptoms are unclear. Effects of four dose levels of the oral CCK-1 agonist GI181771X and placebo on gastric functions and postprandial symptoms were compared in 61 healthy men and women in a randomized, gender-stratified, double-blind, doubledummy placebo-controlled, parallel group study. Effects of 0.1, 0.5, and 1.5 mg of oral solution and a 5.0-mg tablet of GI181771X on gastric emptying of solids by scintigraphy, gastric volume by 99m Tc-single photon emission computed tomographic imaging, maximum tolerated volume of Ensure, and postprandial nausea, bloating, fullness, and pain were studied. On each of 3 study days, participants received their randomly assigned treatment. Adverse effects and safety were monitored. There were overall group effects of GI181771X on gastric emptying (P Ͻ 0.01) and fasting and postprandial volumes (P ϭ 0.036 and 0.015, respectively). The 1.5-mg oral solution of GI181771X significantly delayed gastric emptying of solids (P Ͻ 0.01) and increased fasting (P ϭ 0.035) gastric volumes without altering postprandial (P ϭ 0.056) gastric volumes or postprandial symptoms relative to placebo. The effect of the 5.0-mg tablet on gastric emptying of solids did not reach significance (P ϭ 0.052). Pharmacokinetic profiles showed the highest area under the curve over 4 h for the 1.5-mg solution and a similar area under the curve for the 0.5-mg solution and 5-mg tablet. Adverse effects were predominantly gastrointestinal and occurred in a minority of participants. GI181771X delays gastric emptying of solids and exhibits an acceptable safety profile in healthy participants. CCK-1 receptors can be modulated to increase fasting gastric volume. accommodation; single photon emission computed tomography; satiation; fasting CCK IS A gastrointestinal hormone that is released in response to the ingestion of fat and protein. It plays an important role in stimulation of pancreatic secretion, gallbladder contraction, regulation of gastrointestinal motility, and induction of satiety .