No abstract available.
Cholecystokinin ; Colon

No abstract available.
Cholecystokinin* ; Gallbladder Emptying* ; Gallbladder* ; Meals*

Fenofibrate is a selective peroxisome proliferator-activated receptor alpha (PPARalpha) activator and is prescribed to treat hyperlipidemia. The mechanism through which PPARalpha agonists reduce food intake, body weight, and adiposity remains unclear. One explanation for the reduction of food intake is that fenofibrate promotes fatty acid oxidation and increases the production of ketone bodies upon a standard experimental dose of the drug (100~300 mg/kg/day). We observed that low-dose treatment of fenofibrate (30 mg/kg/day), which does not cause significant changes in ketone body synthesis, reduced food intake in Long-Evans Tokushima (LETO) rats. LETO rats are the physiologically normal controls for Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which are obese and cholecystokinin (CCK)-A receptor deficient. We hypothesized that the reduced food intake by fenofibrate-treated LETO rats may be associated with CCK production. To investigate the anorexic effects of fenofibrate in vivo and to determine whether CCK production may be involved, we examined the amount of food intake and CCK production. Fenofibrate-treated OLETF rats did not significantly change their food intake while LETO rats decreased their food intake. Treatment of fenofibrate increased CCK synthesis in the duodenal epithelial cells of both LETO and OLETF rats. The absence of a change in the food intake of OLETF rats, despite the increase in CCK production, may be explained by the absence of CCK-A receptors. Contrary to the OLETF rats, LETO rats, which have normal CCK receptors, presented a decrease in food intake and an increase in CCK production. These results suggest that reduced food intake by fenofibrate treatment may be associated with CCK production.
Adiposity ; Animals ; Body Weight ; Cholecystokinin ; Diethylpropion ; Eating ; Epithelial Cells ; Fenofibrate ; Hyperlipidemias ; Ketone Bodies ; PPAR alpha ; Rats ; Rats, Inbred OLETF ; Receptor, Cholecystokinin A ; Receptors, Cholecystokinin

BACKGROUND/AIMS: At present, the gallbladder dysfunction implies a disorder of decreased gallbladder contractility. Other motor disorder such as overactive gallbladder which shows excessive contraction cannot be excluded in the motility disorder of gallbladder. Thus, this study was done to define the diagnostic criteria and to develop the techniques to induce the excessive contraction of gallbladder. METHODS: CCK-op at 20 ng/kg by slow continuous infusion for 30minutes, that is known as most physiologic method for gallbladder contraction, was given for assessment of gallbladder emptying in 12 normal volunteers. Also, rapid bolus injection of cholecystokinin octapeptide (CCK-op) at 20 ng/kg or 40 ng/kg was performed to induce the excessive contraction of gallbladder. Gallbladder contractility was represented as the ejection fraction (GBEF) measured by cholecystokinin-cholescintigraphy. RESULTS: 1. With a slow continuous infusion of CCK-op, the mean GBEF was 78.2+/-5.6% (mean+/-SD). 2. With a rapid bolus injection of CCK-op, GBEF showed variable results (10-86%) among subjects who had normal gallbladder. 3. Based on the results obtained by slow continuous infusion of CCK-op in normal volunteers, overactive gallbladder was defined when GBEF approached more than 70% within 15minutes after bolus injection of CCK-op. The overactive gallbladder was noted in 6 (50%) subjects who received rapid bolus injection of CCK-op (40 ng/kg). 4. Abdominal pain developed only in high-dose (40 ng/kg) bolus injection group (6/12, 50%), concomitantly with increased bowel movements, irrespective of excessive gallbladder contractility. CONCLUSION: Excessive gallbladder contraction had no clinical significance in the experimentally induced clinical model.
Abdominal Pain ; Cholecystokinin ; Gallbladder Emptying ; Gallbladder* ; Healthy Volunteers ; Sincalide

Functional dyspepsia (FD) is a heterogeneous disorder associated with diverse pathophysiologic mechanisms. Studies have shown duodenal implications in the pathophysiology of FD. Duodenal hypersensitivity to acid, increased duodenal acid exposure, and abnormal responses to duodenal lipids or released cholecystokinin have been observed in patients with FD. Moreover, there is evidence indicating duodenal immune activation in FD. Alterations in the number of duodenal eosinophils or intraepithelial lymphocytes have been reported in a subset of FD patients, particularly in patients with post-infectious FD. Whether these abnormalities in the duodenum play a crucial role in the generation of dyspeptic symptoms needs to be elucidated. Further investigations on the relationship between duodenal abnormalities and well-known pathophysiologic mechanisms of FD are required. Furthermore, the causative factors related to the development of duodenal abnormalities in FD warrant further study.
Cholecystokinin ; Duodenum ; Dyspepsia ; Eosinophilia ; Eosinophils ; Humans ; Hypersensitivity ; Lymphocytes

Hesperetin (3',5,7-trihydroxy 4'-methoxyflavanone) and its glycoside hesperidin (hesperetin 7-rhamnoglucoside) in oranges have been reported to possess pharmacological effects related to anti-obesity. However, hesperetin and hesperidin have not been studied on suppressive effects on appetite. This study examined that hesperetin and hesperidin can stimulate the release of cholecystokinin (CCK), one of appetite-regulating hormones, from the enteroendocrine STC-1 cells, and then examined the mechanisms involved in the CCK release. Hesperetin significantly and dose-dependently stimulated CCK secretion with an EC50 of 0.050 mM and increased the intracellular Ca2+ concentrations ([Ca2+]i) compared to the untreated control. The stimulatory effect by hesperetin was mediated via the entry of extracellular Ca2+ and the activation of TRP channels including TRPA1. These results suggest that hesperetin can be a candidate biomolecule for the suppression of appetite and eventually for the therapeutics of obesity.
Appetite ; Cholecystokinin* ; Citrus sinensis ; Enteroendocrine Cells ; Hesperidin ; Obesity

BACKGROUND/OBJECTIVES: Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release. MATERIALS/METHODS: STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular Ca2+ ([Ca2+]i) were measured after incubation of cells with naringenin and naringin for 1 h. RESULTS: Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in [Ca2+]i, influx of extracellular Ca2+, at least in part, and activation of TRP channels, including TRPA1. CONCLUSION: Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.
Appetite ; Appetite Regulation ; Body Weight ; Cholecystokinin* ; Enteroendocrine Cells ; Intestines ; Neuropeptides

Photodynamic action, due to the rather limited lifetime (1 μs) and effective reactive distance of singlet oxygen (< 10 nm), could subcellular-specifically regulate different cellular functions. Photodynamic action could activate permanently cholecystokinin (CCK) 1 receptors, and sensitize or desensitize other G protein-coupled receptors. The emergence in recent years of genetically- encoded protein photosensitisers has enabled more precisely-targeted photodynamic modulation of subcellular organelles and functional proteins. Protein photosensitisers (such as KillerRed, miniSOG or SOPP) expressed on the plasma membrane, mitochondria, lysosomes or endoplasmic reticulum can modulate photodynamically subcellular functions and fine-tune protein activity by targeted photooxidation. With the newly emerged active illumination technique, simultaneous photodynamic action localized at multiple sites is now possible, and the contribution of subcellular regions to the whole cell or individual cells to a cell cluster could be quantitated. Photodynamic action with protein photosensitiser will be a powerful tool for nano-manipulation in cell physiology research.
Endoplasmic Reticulum ; Light ; Mitochondria ; Photosensitizing Agents ; Receptors, Cholecystokinin

Cholecystokinin is known to be involved in the modulation of nociception and to reduce the efficacy of morphine analgesia. This study investigated the effects of intrathecal administration of morphine and the cholecystokinin type B antagonist CI-988 on below-level neuropathic pain after spinal cord injury in rats. We also examined the interaction of morphine and CI-988 in the antinociceptive effect. Both morphine and CI-988 given individually increased the paw withdrawal threshold to mechanical stimulation in a dose-dependent manner. The combination of ineffective doses of intrathecally administered CI-988 and morphine produced significant analgesic effects and the combination of effective doses resulted in analgesic effects that were greater than the sum of the individual effects of each drug. Thus, morphine showed a synergistic interaction with CI-988 for analgesia of central neuropathic pain.
Analgesia ; Animals ; Cholecystokinin ; Morphine* ; Neuralgia* ; Nociception ; Rats* ; Spinal Cord Injuries*

OBJECTIVE: This study aimed to test the possible association between Cholecystokinin B receptor (CCKBR) promoter gene and panic disorder. METHODS: 262 patients with panic disorder and 76 healthy controls participated in this study. Genotyping was performed by polymerase chain reaction-based method. RESULTS: Allele distribution of CT repeat polymorphism in patients with panic disorder was not different from those of the controls. However, after excluding the patients with panic disorder comorbid with major depressive disorder and other anxiety disorder, we found out the significant association of CCKBR (CT)n repeat with the panic disorder without comorbidities. And we analysed the data as a di-allelic polymorphism with a short (140-162 bp) and a long (164-180 bp) allele. In the di-allelic analysis, there was an excess of the shorter allele in patients with panic disorder. CONCLUSION: The present study suggested that the CCKBR promoter dinucleotide polymorphism may have a potential role for susceptibility to panic disorder in the Korean population and thus calls for consecutive studies in order to pile up the data with larger different ethnic background.
Alleles ; Anxiety Disorders ; Cholecystokinin* ; Comorbidity ; Depressive Disorder, Major ; Diagnosis* ; Drug Therapy* ; Humans ; Panic Disorder* ; Panic* ; Receptor, Cholecystokinin B*