Role of cholecystokinin as a regulator of solid and liquid gastric emptying in humans

Borovicka, Jan; Kreiss, Christianna; Asal, Korhan; Remy, Bernadette; Mettraux, Christine; Wells, Anita S.; Read, N. W.; Jansen, J.; D’Amato, Maura; Delaloye, Angelika Bischof; Fried, Michael; Schwizer, Werner

doi:10.1152/ajpgi.1996.271.3.g448

Cited by 27 publications

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“…Similarly, 5-HT 3 receptor participation in the control of gastric emptying has also been demonstrated to be mediated along capsaicin-sensitive extrinsic afferent nerve fibers (4). In view of the fact that CCK and 5-HT activate distinct separate populations of vagal afferent fibers (23), the present findings suggest that CCK-induced suppression of sham feeding is mediated along vagal afferent fibers not directly originating from 5-HT 3 receptors.…”

Section: Discussionsupporting

confidence: 59%

“…One such response is the mediation of nutrient-induced inhibition of gastric emptying (49). Similar to 5-HT, one mechanism by which CCK suppresses food intake is through its ability to inhibit gastric emptying (3,12,19,36,40,43,55).Previous studies have shown an interaction between the serotonergic and cholecystokinergic systems in the control of food intake (7,8,47). Although original exploration of this interaction focused on central serotonergic activity, recent reports (11), including those from our own laboratory (22), have shown that systemic administration of a selective 5-HT 3 receptor antagonist attenuates CCK-induced satiation.…”

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confidence: 99%

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“…25). Systemic serotonergic activity has been shown to induce an anorectic response through activation of 5-HT 3 receptors under a number of paradigms (1,21). One such response is the mediation of nutrient-induced inhibition of gastric emptying (49).…”

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confidence: 99%

“…Although original exploration of this interaction focused on central serotonergic activity, recent reports (11), including those from our own laboratory (22), have shown that systemic administration of a selective 5-HT 3 receptor antagonist attenuates CCK-induced satiation. Furthermore, peripheral 5-HT 3 and CCK A receptors cooperate interdependently in the control of CCK-induced suppression of food intake (22).…”

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5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Hayes¹,

Moore²,

Shah³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Hayes, Matthew R., Rachael L. Moore, Samit M. Shah, and Mihai Covasa. 5-HT 3 receptors participate in CCK-induced suppression of food intake by delaying gastric emptying. Am J Physiol Regul Integr Comp Physiol 287: R817-R823, 2004. First published June 10, 2004 10.1152/ajpregu.00295.2004.-Serotonin type 3 (5-HT 3) receptors have been shown to participate in the negative-feedback control of food intake. We previously reported that cholecystokinin (CCK)-induced suppression of food intake is partly mediated through 5-HT 3 receptors when rats were tested on a preferred liquid diet, but whether such an effect occurs when they are tested on a solid maintenance diet is unknown. In the present study, we examined the effects of ondansetron, a selective 5-HT 3 antagonist, on CCK-induced suppression of solid chow intake. Intraperitoneal administration of ondansetron significantly attenuated 30-and 60-min CCK-induced reduction of food intake, with suppression being completely reversed by 120 min. It is not known whether 5-HT 3 receptors directly mediate CCK-induced satiation or whether their participation depends on CCK acting as part of a feedback cascade to inhibit ongoing intake. Because CCKinduced inhibition of sham feeding does not depend on additive gastric/postgastric-feedback signals, we examined the ability of ondansetron to reverse CCK-induced satiation in sham-feeding rats.Ondansetron did not attenuate reduction of sham feeding by CCK, suggesting that ondansetron does not directly antagonize CCK-satiation signals. CCK suppresses real feeding through a delay in gastric emptying. Ondansetron could attenuate CCK-induced reduction of food intake by reversing CCK-induced inhibition of gastric emptying. We found that blockade of 5-HT3 receptors attenuates CCK-induced inhibition of gastric emptying of a solid meal, as well as saline and glucose loads. We conclude that 5-HT 3 receptors mediate CCKinduced satiation through indirect mechanisms as part of a feedback cascade involving inhibition of gastric emptying. ondansetron; serotonin; osmotic; glucose; satiety GASTRIC EMPTYING IS ONE MECHANISM involved in the regulation of food intake (33, 43). A delay in gastric emptying limits the rate of absorption by reducing the rate of nutrient delivery to the small intestine (5, 15, 58) and is associated with suppression of food intake (43). Inhibition of gastric emptying is mediated by peripheral vagal and sympathetic nerves and by the release of a variety of peptides and neurotransmitters (43,54). Cholecystokinin (CCK) and serotonin [5-hydroxytryptamine (5-HT)] are two humoral signals thought to exert control on gastric emptying and are released in response to nutrients entering the duodenum (6,28,30,43,49,60). Both of these satiety signals bind to receptors on terminals of vagal afferent fibers, resulting in a delay in gastric emptying (4, 24, 49).Considerable evidence indicates that the serotonergic system participates in the negative-feedback control of food intake (for review see Ref. 25). Systemic serotonergic activity h...

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confidence: 59%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Hayes¹,

Moore²,

Shah³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Postprandial hyperglycemia was ameliorated by taking metformin 30 min before a meal than taking metformin with a meal; a randomized, open-label, crossover pilot study

et al. 2015

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Taking metformin with a meal has been shown to decrease bioavailability of metformin. We hypothesized that taking metformin 30 min before a meal improves glucose metabolism. As an animal model, 18 Zucker-rats were divided into three groups as follows: no medication (Control), metformin (600 mg/kg) with meal (Met), and metformin 10 min before meal (pre-Met). In addition, five diabetic patients were recruited and randomized to take metformin (1000 mg) either 30 min before a meal (pre-Met protocol) or with a meal (Met protocol). In the animal model, the peak glucose level of pre-Met (7.8 ± 1.5 mmol/L) was lower than that of Control (12.6 ± 2.5 mmol/L, P = 0.010) or Met (14.1 ± 2.9 mmol/L, P = 0.020). Although there was no statistical difference among the three groups, total GLP-1 level at t = 0 min of pre-Met (7.4 ± 2.7 pmol/L) tended to be higher than that of Control (3.7 ± 2.0 pmol/L, P = 0.030) or Met (3.9 ± 1.2 pmol/L, P = 0.020). In diabetic patients, the peak glucose level of pre-Met protocol (7.0 ± 0.4 mmol/L) was lower than that of Met protocol (8.5 ± 0.9 mmol/L, P = 0.021). Total GLP-1 level at t = 30 min of pre-Met protocol (11.0 ± 6.1 pmol/L) was higher than that of Met protocol (6.7 ± 3.9 pmol/L, P = 0.033). Taking metformin 30 min before a meal ameliorated postprandial hyperglycemia. This promises to be a novel approach for postprandial hyperglycemia.

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Intestinal Cholecystokinin Controls Glucose Production through a Neuronal Network

et al. 2009

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Cholecystokinin (CCK) is a peptide hormone that is released from the gut in response to nutrients such as lipids to lower food intake. Here we report that a primary increase of CCK-8, the biologically active form of CCK, in the duodenum lowers glucose production independent of changes in circulating insulin levels. Furthermore, we show that duodenal CCK-8 requires the activation of the gut CCK-A receptor and a gut-brain-liver neuronal axis to lower glucose production. Finally, duodenal CCK-8 fails to lower glucose production in the early onset of high-fat diet-induced insulin resistance. These findings reveal a role for gut CCK that lowers glucose production through a neuronal network and suggest that intestinal CCK resistance may contribute to hyperglycemia in response to high-fat feeding.

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Role of cholecystokinin as a regulator of solid and liquid gastric emptying in humans

Cited by 27 publications

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5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Postprandial hyperglycemia was ameliorated by taking metformin 30 min before a meal than taking metformin with a meal; a randomized, open-label, crossover pilot study

Intestinal Cholecystokinin Controls Glucose Production through a Neuronal Network

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Role of cholecystokinin as a regulator of solid and liquid gastric emptying in humans

Cited by 27 publications

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5-HT3receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

5-HT3receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Postprandial hyperglycemia was ameliorated by taking metformin 30 min before a meal than taking metformin with a meal; a randomized, open-label, crossover pilot study

Intestinal Cholecystokinin Controls Glucose Production through a Neuronal Network

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5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying