Introduction: One of the etiological causes of nonulcer dyspepsia (NUD) is H. pylori infection. The role of H. pylori infection in dyspepsia and its accompaniment with hormonal disorders remain controversial. We studied the association between existence of H. pylori and variation of Colecystokinin (CCK) and gastrin in NUD patients.Methods: One hundred consecutive out patients with NUD that referred to Taleghani Hospital in Tehran from May 2002 to January 2003 were studied. Demographic and clinical examinations were fulfilled and basal serum gastrin and CCK level and IgG anti H. pylori were measured. After through endoscopic evaluation, gastric mucosal biopsies were taken from all patients for investigation of H. pylori (Rapid urease test (R.U.T), direct exam and IgG Anti H. pylori tests) and histological assessment.Results: 100 NUD patients including 48 (48%) male and 52(52%) female were studied. 11 patients were smoker. Fullness (62%) was the predominant symptoms in them. 59% of patients complained of abdominal pain, 57% of early satiety, 42% of anorexia, 17% of dysphagia, 46% of nausea and 20% of vomiting. 78 (78%) of patients were H. Pylori positive.In H. pylori positive group, the mean± SD of CCK was 1.06± 0.40 and gastrin was 6.68 ± 7.82. In H. pylori negative group the mean ± SD of CCK was 0.92 ± 0.31 and gastrin 8.20 ± 12.58. There was no significant difference in gastrin and CCK serum level between H. pylori positive and H. pylori negative in nonulcer dyspeptic patients. Conclusion: According to high frequency of H. pylori in NUD patients, the investigation of patients for the presence of H. pylori in patients is recommended. We didn’t find any relation between H. pylori infection and the serum level of gastrin and CCK in NUD patients.

In the present study the effects of both CCK receptor agonists and antagonists on antinociception induced by morphine in the tail-flick test have been evaluated.Morphine induced dose-dependent antinociceptionin mice. The response of morphine was potentiated by sulfated cholecystokinin-8 (CCK-8S) but not by unsulfated cholecystokinin-8 (CCK-8U). The CCK receptor antagonists MK-329 and L-365, 260 decreased the potentiation of morphine antinociception induced by CCK-8S. The antagonists even decreased the response induced by morphine in the presence of CCK-8U. High doses of MK-329 and L-365, 260 also potentiated morphine's antinociception. Single administration of the CCK receptor agonists CCK-8 and CCK-8U or CCK receptor antagonists did not elicit any response in the tail-flick test. It is concluded that CCK receptor mechanisms are involved in the modulation of pain response and/or morphine antinociception.

Background and purpose: Obesity disrupts the secretion of appetite-regulating hormones, such as peptide YY (PYY) and cholecystokinin (CCK), which disrupts natural appetite control mechanisms and promotes excessive food intake and weight gain. Over time, these disturbances elevate the risk of metabolic disorders. This study aimed to investigate the effects of eight weeks of core stability training combined with chitosan supplementation on anthropometric indices, lipid profiles, and gastrointestinal hormones (CCK and PYY) in obese women. Materials and methods: This clinical trial was conducted on 60 obese women (BMI: 30.83±1.43), who were randomly assigned to three intervention groups and one control group. Participants in the exercise-only group performed core stability training three times per week for eight weeks. The supplement-only group consumed two 500 mg chitosan capsules daily for the same duration. The combined intervention group simultaneously engaged in both the exercise protocol and chitosan supplementation. Measurements of study variables were taken twice before and after the intervention. Data analysis was performed using two-way ANOVA in SPSS (version 27) with a significance level of α = 0.05. Results: The findings revealed significant differences in PYY and CCK levels among the intervention groups (exercise, supplement, and combined intervention) (P< 0.05), whereas no significant changes were observed in the control group (P> 0.05). Additionally, the intervention groups demonstrated significant improvements in anthropometric indices and lipid profiles (P< 0.05). Conclusion: Core stability training, chitosan supplementation, and their combined implementation positively influenced anthropometric measures, plasma lipid profiles, and gastrointestinal hormones (PYY and CCK). These findings suggest that combining exercise with supplementation may be an effective strategy for improving metabolic health and supporting weight management in obese women. (Clinical Trials Registry Number: IRCT20221120056548N6)

Objective(s): Cholecystokinin (CCK) has been proposed as a mediator in stress. However, it is still not fully documented what are its effects. We aimed to evaluate the effects of systemic administration of CCK exactly before induction of stress on spatial memory and synaptic plasticity at CA1 in rats. Materials and Methods: Male Wistar rats were divided into 4 groups: the control, the control-CCK, the stress and the stress-CCK. Restraint stress was induced 6 hr per day, for 24 days. Cholecystokinin sulfated octapeptide (CCK-8S) was injected (1. 6 μ g/kg, IP) before each session of stress induction. Spatial memory was evaluated by Morris water maze test. Long-term potentiation (LTP) in Schaffer collateral-CA1 synapses was assessed (by 100 Hz tetanization) in order to investigate synaptic plasticity. Results: Stress impaired spatial memory significantly (P<0. 01). CCK in the control rats improved memory (P<0. 05), and prevented the impairments in the stress group. With respect to the control group, both fEPSP amplitude and slope were significantly (P<0. 05) decreased in the stress group. However, there were no differences between responses of the control– CCK and Stress– CCK groups compared to the control group. Conclusion: The present results suggest that high levels of CCK-8S during induction of stress can modulate the destructive effects of stress on hippocampal synaptic plasticity and memory. Therefore, the mediatory effects of CCK in stress are likely as compensatory responses.

Background and Objectives: Opioids are an important group of analgesics that are used extensively to control sever pains. Physical dependence to these drugs is a major problem. There are a few studies regarding the involvement of cholecyctokinin (CCK) in the withdrawal syndromes of opioids. In the present study, the effects of CCK agonist and antagonist on the number of jumping of morphine dependent mice were evaluated.Materials and Methods: In this experimental study, the effects of CCK-8 and LY225910 (selective CCK2 receptor antagonist) on jumpings of mice after morphine dependence were evaluated. Mice were injected with morphine three times a day (50, 50 and 75 mg/kg) for three days; at the forth day they received 50 mg/kg morphine. Injection of naloxone (5 mg/kg) induced withdrawal signs such as jumping. The experimental groups received different doses of CCK-8 (0.1, 0.3 and 0.6 mg/kg) and LY225910 (0.01, 0.5 and 1 mg/kg) with each injection of morphine.Results: Injection of CCK-8 significantly decreased the naloxone-induced jumpings, while LY225910 did not have any significant effects on these jumpings.Conclusions: Based on the results of the present study, activation of CCK1 receptors probably is involved in morphine dependence. The results also confirm that injection of CCK but not CCK2 selective antagonist probably decreases the jumpings of mice following withdrawal syndrome of morphine.

Cholecystokinin (CCK), a peptide hormone found in the gut, is the most abundant peptide neurotransmitters in the brain, and its acute effects on the brain activity have been shown. In this study we aimed to evaluate the acute effects of CCK on short-term synaptic plasticity in the dentate gyrus (DG) of the rat hippocampus. Via stereotaxic surgery, the stimulating and the recording electrodes were placed in the perforant pathway and dentate gyrus, respectively and 30 min after intraperitoneal (i.p.) injection of CCK octapeptide sulfated (CCK-8S, 1.6 mg/kg), evoked responses were recorded after delivering of paired-pulse stimulations at 10 to 500 ms inter-stimulus intervals. With respect to the control group that received saline instead of CCK, in baseline responses, slope of field excitatory postsynaptic potential (fEPSP) 5 min and 10 min after injection of CCK-8S (p<0.05) and population spikes (PS)-amplitudes 5 min after injection of CCK-8S (p <0.05) were significantly increased. In paired pulse responses, PS amplitudes were increased in the CCK group, but these enhancements only were significant at inter-stimulus interval 40 ms (p<0.05). However fEPSP slopes were decreased at inter-stimulus intervals 70 ms (p <0.05), 120 ms (p <0.01), 150 ms (p <0.001) and 300 ms (p <0.001). The results showed that CCK-8S has a transient excitatory effects on baseline responses, but it inhibits paired pulse indices in acute. Therefore, in a short period of time, effect of CCK on the function of synapses is time dependent, and it has stimulatory or inhibitory effects at different time periods.

Introduction: It has been demonstrated that cholecystokinin sulfated octapeptide (CCK-8s) can affect synaptic transmission in the hippocampus. Because one of the major experimental models to understand the events happening in synaptic plasticity is To Study the long-term potentiation (LTP), we decided to investigate the effect of concomitant administration of CCK-8s and tetanic stimulation of Schaffer collateral path-CA1 synapses on LTP induction and maintenance. Materials and Methods: Experimental groups were control, CCK-5min and CCK-30min. CCK-8s was injected 5 or 30 min (1.6 g/kg, i.p.) prior to induction of LTP. The stimulating and the recording electrodes were placed in the Schaffer collateral pathway and hippocampal CA1, respectively. LTP was induced by 100 Hz tetanization and field excitatory postsynaptic potentials (fEPSP) slope, area and amplitude were measured and compared during 30 minutes Interval before, and 90 minutes Interval after LTP induction in each group. Results: The results showed that maintenance of the induced LTP was significantly improved in the CCK-30min group comparing to the control group. This improvement was particularly visible in the fEPSP slope (p<0.001) and the fEPSP area (p<0.001). Seventy minutes after the LTP induction, fEPSP was similar in both the CCK-5min and the CCK-30min groups and there was Also a significant difference between the treated groups comparing to the control group (p<0.05). Conclusion: These results indicated that LTP induction and maintenance is carried out effectively, at higher levels of CCK in the brain. The data suggest that CCK-8s has pronounced effects on synaptic plasticity in the hippocampus and the consequent cognitive functions.

The effects of cholecystokinin (CCK) receptor antagonists on hypothermia induced by cocaine or morphine have been studied in mice. In the present work, subcutaneous (SC) injection of cocaine (50-150 mg/kg) or morphine (125-500 mg/kg) induced hypothermia in mice. Administration of CCKA receptor antagonist MK-329 (0.5-1.5 mg/kg), CCKB receptor antagonist L-365, 260 (0.5-1.5 mg/kg) and CCK receptor antagonist proglumide (15-45 mg/kg) 60 min. prior to cocaine injection reduced hypothermia induced by cocaine. MK-329 or proglumide also reduced the morphine response. Single administration of MK-329 and L-365, 260 to mice decreased mice core body temperature. It is concluded that the hypothermic effect of cocaine and morphine may be mediated through CCKA and CCKB receptor mechanism(s).