Satiety effects of a physiological dose of cholecystokinin in humans.

Lieverse, R. J.; Jansen, J. B. M. J.; Masclee, A.A.M.; Lamers, C. B. H. W.

doi:10.1136/gut.36.2.176

Cited by 158 publications

(141 citation statements)

References 21 publications

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“…Duodenal infusion of lipids, like triglycerides 20 or fatty acids, 21 induces early satiety and causes both gastric relaxation and reduction of gastric emptying at least by the release of cholecystokinin. These relationships suggest that satiety mediated by cholecystokinin 22 and PYY 23 administration is related to motility changes of the gastrointestinal tract. Inhibition of the motility of the stomach could be effective in reducing food intake.…”

Section: Discussionmentioning

confidence: 97%

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study

et al. 2006

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Objective: The stomach is the main target organ for bariatric surgery, but no medical treatment has been developed to increase satiety and decrease food intake via gastric pathways. The aim of our study was to investigate whether or not the intraparietogastric administration of botulinum toxin A (BTX), able to modify the motility patterns of the stomach, could be useful for treatment of obesity. Design: Double blind controlled study. Subjects: Twenty-four morbidly obese patients (mean weight (s.e.m.) 116.174.89 kg, mean body mass index (BMI) 43.671.09 kg/m 2 ) were blindly randomized to receive 200 IU BTX or placebo into the antrum and fundus of the stomach by intraparietal endoscopic administration. Measurements: We evaluated weight loss, BMI changes, satiety score, the maximal gastric capacity for liquids and the gastric emptying time (octanoic acid breath test). Results: The two groups were homogeneous for anthropometric characteristics. Eight weeks after treatment, BTX patients had significantly higher weight loss (1171.09 vs 5.771.1 kg, Po0.001) and BMI reduction (470.36 vs 270.58 kg/m 2 , Po0.001) and a higher satiety score on a visual analogic scale (7.6370.38 vs 4.7270.44, Po0.001) than controls. Furthermore, BTX patients showed a significantly greater reduction in maximal gastric capacity for liquids (266.6748 vs 139731, Po0.001) and a greater prolongation in gastric emptying time ( þ 18.9378 vs À2.276.9 min, Po0.05). No significant side effects or neurophysiologic changes were found. Conclusions: Topical intragastric BTX was effective in reducing food intake and body weight in morbidly obese patients.

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Section: Discussionmentioning

confidence: 97%

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study

et al. 2006

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“…We and others have previously reported on the satiating effects of CCK. 13,19,[27][28][29] There is consensus that CCK suppresses food intake on the short term. Our study confirms the correlation between satiety scores and plasma CCK secretion.…”

Section: Discussionmentioning

confidence: 99%

“…A second aim was to evaluate the effect of ileal lipid administration on gut peptide secretion, more specifically on cholecystokinin (CCK), as a more proximal gut peptide with well-known satiety effects, 13 and peptide YY, as a distal gut peptide and proposed biomarker for the activation of the ileal brake. 10 We constructed the following hypotheses: compared with oral ingestion of 3 g of lipid added to a liquid meal, delivery of the same amount of lipid through postprandial (after ingestion of the fat-free breakfast) perfusion into the ileum will (1) lead to an increase in postprandial satiety, (2) be dose dependent (9 g vs 3 g in the ileum) and (3) lead to distal gut hormone secretion.…”

Section: Introductionmentioning

confidence: 99%

Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

et al. 2008

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Objective: The ileal brake is a feedback mechanism activated by nutrients, especially fat, with marked effects on satiety. The effects of low doses of ileal fat on satiety are largely unknown. We therefore studied the effect of ileal vs oral delivery of low doses of fat on satiety and gut peptide secretion. Design: Randomized, single-blind crossover design. Subjects: Sixteen healthy, normal-weight volunteers (6 male; mean age 26 years, mean body mass index 22.4). Intervention: Participants were intubated with a 290-cm-long nasoileal tube and consumed, on 3 consecutive days, either a liquid breakfast with 3 g fat followed by an ileal placebo infusion at t ¼ 105-150 min (treatment C) or a fat-free liquid breakfast followed by an ileal infusion of either an emulsion of 3 g (treatment I3g) or 9 g (treatment I9g) fat (safflower oil). Measurements: Satiety parameters by visual analog scales and plasma concentrations of CCK and PYY. Results: C significantly increased satiety and CCK secretion compared with the fat-free breakfast. Ileal fat perfusion of both 3 and 9 g (I3g and I9g) significantly increased satiety during and after fat perfusion, without differences in satiety between I3g and I9g. During ileal fat infusion, CCK increased dose dependently, whereas PYY concentrations increased significantly only after 9 g of fat. Secretion of CCK but not of PYY correlated to satiety levels. Conclusion: Postprandial satiety following a liquid breakfast can be effectively and significantly increased by small amounts (as little as 3 g) of fat perfused into the ileum. Ileal fat dose-dependently increased CCK but not PYY secretion. The satiating effect of ileal fat may be partly mediated by CCK.

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“…This coordinate system (Kissileff et al 1981;Stacher et al 1982;Liddle, 1995;Herzig et al 1996;Miyasaka & Funakoshi, 1997;Gibbs & Smith, 1998) can regulate cholecystokinin levels in the gastrointestinal tract. When injected parenterally CCK-8 produces a dose-related reduction in sham-feeding in experimental animals and in lean and obese human subjects (Table 2; Kissileff et al 1981;Stacher et al 1982;Baile & Della-Fera, 1984;Boosalis et al 1992;Smith & Gibbs, 1994;Lieverse et al 1995a;Gibbs & Smith, 1998). There are two cholecystokinin receptors, CCK A and CCK B .…”

Section: Cholecystokininmentioning

confidence: 99%

Afferent signals regulating food intake

2000

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Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. β-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.

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Satiety effects of a physiological dose of cholecystokinin in humans.

Cited by 158 publications

References 21 publications

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study

Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

Afferent signals regulating food intake

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