cholecystokinin and Dyspepsia

Numerous hormones secreted by the gut, during both the fasted state and in response to a meal, influence gastrointestinal motor and/or sensory function, and appear to contribute to the pathogenesis of delayed gastric emptying associated with gastroparesis, functional dyspepsia (FD) and feed intolerance in critical illness. Gut hormones are, accordingly, potential targets for the management of these patients.. This article will discuss the hypersensitivity to enteral fat and endogenous (nutrient-stimulated) and exogenous cholecystokinin (CCK) in patients with FD, and the elevation in both fasting and postprandial CCK levels evident in this group. It will review the use of pharmacological agonists of motilin and ghrelin, which accelerate gastric emptying, in the management of gastroparesis and FD. The frequent finding of markedly delayed gastric emptying in the critically ill will be examined; this is associated with elevated plasma CCK and peptide YY in both the fasted and postprandial states, which may account for the increase in small intestinal nutrient inhibitory feedback on gastric motility in this group. The concepts that the rate of gastric emptying is a major determinant of postprandial glycemic excursions in diabetes, and that modulation of gastric emptying may improve glycemic control, will be addressed; in type 1 and insulin-treated type 2 diabetic patients, co-ordination of insulin administration with nutrient delivery and absorption should be optimized, while type 2 patients who are not on insulin are likely to respond to dietary and/or pharmacological interventions which slow gastric emptying.

Topics: Adipose Tissue; Blood Glucose; Cholecystokinin; Critical Illness; Diabetes Mellitus; Dyspepsia; Gastric Emptying; Gastroparesis; Ghrelin; Glucagon-Like Peptide 1; Humans; Insulin; Peptide YY; Postprandial Period

Functional dyspepsia (FD) is a common disorder of yet uncertain etiology. Dyspeptic symptoms are usually meal related and suggest an association to gastrointestinal (GI) sensorimotor dysfunction. Cholecystokinin (CCK) is an established brain-gut peptide that plays an important regulatory role in gastrointestinal function. It inhibits gastric motility and emptying via a capsaicin sensitive vagal pathway. The effects on emptying are via its action on the proximal stomach and pylorus. CCK is also involved in the regulation of food intake. It is released in the gut in response to a meal and acts via vagal afferents to induce satiety. Furthermore CCK has also been shown to be involved in the pathogenesis of panic disorder, anxiety and pain. Other neurotransmitters such as serotonin and noradrenaline may be implicated with CCK in the coordination of GI activity. In addition, intravenous administration of CCK has been observed to reproduce the symptoms in FD and this effect can be blocked both by atropine and loxiglumide (CCK-A antagonist). It is possible that an altered response to CCK may be responsible for the commonly observed gastric sensorimotor dysfunction, which may then be associated with the genesis of dyspeptic symptoms.

Topics: Atropine; Cholecystokinin; Dyspepsia; Efferent Pathways; Food Hypersensitivity; Gastrointestinal Motility; Gastrointestinal Tract; Humans; Norepinephrine; Proglumide; Receptors, Adrenergic; Receptors, Serotonin; Serotonin; Stress, Psychological

Functional dyspepsia (FD) refers to unexplained pain or discomfort in the upper abdomen and is commonly seen in gastroenterology practice. The underlying pathophysiologic mechanisms associated with FD are unclear, although traditionally, delayed gastric emptying, visceral hypersensitivity to acid or mechanical distention, and impaired gastric accommodation have been implicated as putative physiologic disturbances. It also remains uncertain whether FD and irritable bowel syndrome are different presentations of the same disorder. Recent data on pathophysiologic mechanisms of FD have focused on postprandial motor disturbances (accelerated gastric emptying, antral-fundic incoordination, and abnormal phasic contractions), alterations of neurohormonal mechanisms in response to a meal, and previous acute infection. Pharmacologic therapies for FD may be guided by these novel mechanisms, as current available therapeutic options are limited. Novel prokinetics and gastric accommodation modulators, visceral analgesics, and agents targeting the neurohormonal response to food ingestion are the next therapeutic frontiers in FD. This review summarizes traditional knowledge and more recent advances in the pathophysiology of FD and potential therapeutic opportunities.

Topics: Analgesics; Antidepressive Agents; Cholecystokinin; Dyspepsia; Gastric Acid; Gastric Emptying; Gastrointestinal Agents; Gastrointestinal Tract; Humans; Proton Pump Inhibitors; Serotonin Agents

The main factors involved in the pathophysiology of fat induced dyspepsia were investigated by reviewing a series of controlled double blind randomised studies which sought to determine the role of nutrient fat and the postprandial release of cholecystokinin (CCK) in the development of dyspeptic symptoms in healthy volunteers and in patients with functional dyspepsia. The studies showed that during distension of the stomach, lipids are a major trigger of dyspeptic symptoms such as nausea, bloating, pain, and fullness, and that they modulate upper gastrointestinal sensations and symptoms in a dose related fashion. CCK is a major mediator of the sensitisation of gastric perception by lipids in patients with functional dyspepsia as the CCK-A receptor antagonist dexloxiglumide markedly diminishes this effect. The studies provide important insights into the mechanisms underlying gastrointestinal perception in response to fat and the role of CCK in patients with functional dyspepsia.

Topics: Anesthetics, Local; Benzocaine; Cholecystokinin; Dietary Fats; Duodenum; Dyspepsia; Humans; Pentanoic Acids; Postprandial Period; Randomized Controlled Trials as Topic; Receptors, Cholecystokinin; Sensation; Visceral Afferents

In patients who present with chronic unexplained upper abdominal pain or discomfort (functional dyspepsia), therapy should ideally be targeted on correcting the individual's disturbed pathophysiology. Here, putative mechanisms implicated in functional dyspepsia and potential approaches to therapy are critically reviewed in order to determine if targeting treatment is of value. Pharmacological therapies reviewed include those that aim to correct disordered gastric emptying (e.g. cisapride, dopaminergic receptor antagonists, macrolides), reduce visceral hypersensitivity (e.g. somatostatin analogues, cholecystokinin antagonists, opioid agonists, serotonin type 3 receptor antagonists), reduce gastric acid secretion (e.g. H2-blockers, acid pump inhibitors), cure Helicobacter pylori infection, enhance muscosal defence (e.g. sucralfate, bismuth) or modify central nervous system processes. It is concluded that the imperfectly understood pathophysiology of functional dyspepsia contributes to the paucity of established efficacious therapies.

Topics: Abdominal Pain; Antidepressive Agents; Bismuth; Calcium Channel Blockers; Cholecystokinin; Dyspepsia; Gastric Emptying; Helicobacter Infections; Humans; Narcotics; Nitric Oxide; Prostaglandins, Synthetic

and aims: Dietary fat plays a role in the pathophysiology of symptoms in functional dyspepsia (FD). In healthy subjects, cognitive factors enhance postprandial fullness; in FD patients, attention increases gut perception. We hypothesised that the information given to patients about the fat content of a meal would affect dyspeptic symptoms.. Fifteen FD patients were each studied on four occasions in a randomised double blind fashion. Over two days they ingested a high fat yoghurt (HF) and over the other two days a low fat yoghurt (LF). For each yoghurt, the patients received the correct information about its fat content on one day (HF-C, LF-C) and the opposite (wrong) information on the other day (HF-W, LF-W). Dyspeptic symptoms, plasma cholecystokinin (CCK) concentrations, and gastric volumes were evaluated.. Both the fat content and information about the fat content affected fullness and bloating scores-both were higher after HF-C compared with LF-C, and LF-W compared with LF-C, with no differences between HF-C and HF-W. Nausea scores were higher after HF compared with LF, with no effect of the information about fat content. No differences between discomfort and pain scores were found between study conditions. Plasma CCK and gastric volumes were greater following HF compared with LF, with no effect of the information given to the patients. All differences are p<0.05.. Cognitive factors contribute to symptom induction in FD. Low fat foods may also elicit symptoms if patients perceive foods as high in fat, while CCK and gastric volumes do not appear to be affected by cognitive factors.

Topics: Adult; Analysis of Variance; Cholecystokinin; Dietary Fats; Dyspepsia; Female; Humans; Male; Middle Aged; Perception; Postprandial Period; Stomach; Yogurt

We aimed to evaluate the role of fat and cholecystokinin (CCK) in the pathophysiology of functional dyspepsia (FD) by investigating symptoms and plasma CCK levels following increasing doses of duodenal lipid during gastric distension, and the effect of CCK-A receptor blockade.. In study A, six FD patients were studied on three occasions during duodenal infusion of saline or lipid (1.1 (L-1) or 2 kcal/min (L-2)) and proximal gastric distensions. Six healthy subjects were also studied as controls during L-2 only. In study B, the effect of the CCK-A antagonist dexloxiglumide (5 mg/kg/h) on L-2 induced symptoms was studied in 12 FD patients. Changes in gastric volume at minimal distending pressure and plasma CCK (study A) were assessed, gastric distensions were performed using a barostat, and dyspeptic symptoms were monitored.. Lipid increased gastric volume compared with saline (DeltaV (ml): saline 15 (20), L-1 122 (42), L-2 114 (28)) in patients and even more so in controls (221 (37); p<0.05). During distensions, symptoms were greater during L-2 than during saline or L-1, and greater in patients than in controls, while gastric compliance was smaller in patients than in controls (p<0.05). Lipid increased plasma CCK levels in patients and controls (p>0.05). Dexloxiglumide abolished the increase in gastric volume (DeltaV (ml): dexloxiglumide 17 (9), placebo 186 (49)) and dyspeptic symptoms (sum of scores: dexloxiglumide 24 (7), placebo 44 (19)) during duodenal lipid infusion. Dexloxiglumide also reduced gastric compliance (ml/mm Hg: dexloxiglumide 51 (7), placebo 72 (11)) and symptoms (sum of scores: dexloxiglumide 101 (17), placebo 154 (21)) during gastric distension.. CCK-A receptors are involved in the generation of dyspeptic symptoms by duodenal lipid during gastric distension.

Topics: Adult; Analysis of Variance; Case-Control Studies; Cholecystokinin; Dose-Response Relationship, Drug; Double-Blind Method; Duodenum; Dyspepsia; Female; Gastric Mucosa; Gastrointestinal Agents; Humans; Lipids; Male; Manometry; Middle Aged; Pentanoic Acids; Receptors, Cholecystokinin

Cholecystokinin (CCK) had been the first gastrointestinal hormone known to exert anorexic effects. CCK had been inferred to contribute to the onset of functional dyspepsia (FD) symptoms. To understand the pathophysiology of FD, the roles of stress have to be clarified. In this study, we aimed to clarify the influence of stress on the action of cholecystokinin (CCK) on appetite and gastric emptying. Using rats, stress was simulated by giving restraint stress or intraperitoneal injection of the stress-related peptide hormone urocortin 1 (UCN1). The effects of CCK and restraint stress, alone or in combination, on food intake and gastric motility were examined, and c-Fos expression in the neurons of appetite control network in the central nervous system was assessed by immunohistochemical staining. CCK inhibited food intake and gastric emptying in a dose-dependent manner. Food intake for 1 h was significantly lower with UCN1 (2 nmol/kg) than with the saline control. Restraint stress amplified the suppressive effects of CCK on food intake for 1 h and on gastric emptying. With regard to brain function, the CCK induced c-Fos expression in the neurons of the nucleus tractus solitarius and paraventricular nucleus of the hypothalamus was markedly and significantly amplified by the addition of restraint stress with CCK. The results suggested that stress might amplify the anorexic effects of CCK through activation of the nuclei that comprise the brain neuronal network for satiation; this might play a role in the pathogenesis of the postprandial distress syndromes of functional dyspepsia.

Topics: Animals; Appetite; Brain; Cholecystokinin; Dyspepsia; Eating; Gastric Emptying; Male; Neurons; Proto-Oncogene Proteins c-fos; Rats, Sprague-Dawley; Stress, Psychological; Urocortins

Topics: Appetite; Cholecystokinin; Dipeptides; Dyspepsia; Ghrelin; Humans; Intestinal Mucosa

Dyspeptic symptoms are frequently induced, or exacerbated, by fatty food ingestion. Excessive release of, and/or hypersensitivity to, cholecystokinin (CCK) may explain the exaggerated response to lipid in patients with functional dyspepsia (FD). Thus far, plasma CCK response has been evaluated. However, stimulation of CCK1 receptors on duodenal vagal afferents occurs in a paracrine manner, suggesting that mucosal CCK concentrations are relevant to quantify. Apolipoprotein A-IV stimulates mucosal CCK release.. To investigate the hypothesis that fat-induced release of CCK and apolipoprotein A-IV (apoA-IV) is enhanced in the duodenum of FD patients.. Sixteen symptomatic FD patients and 10 healthy volunteers (HV) underwent duodenal perfusion with intralipid 20%, 2 kcal/min, for 60 min. Symptoms were scored and blood samples were collected every 15 min during lipid perfusion and 15 min after discontinuation when duodenal biopsies were taken. Plasma and mucosal concentrations of CCK and apoA-IV were quantified.. Abdominal discomfort (P=0.001), nausea (P=0.05), and fullness (P=0.005) in response to duodenal lipid increased significantly only in FD patients. Following lipid infusion, the mean mucosal CCK concentration was lower in FD patients compared with HV (P<0.0001). Fasting concentrations and plasma response of CCK were comparable in FD patients and HV. Plasma apoA-IV response appeared to differ between patients and HV, whereas mucosal apoA-IV concentrations were similar.. Our results suggest excessive local release of CCK in response to duodenal lipid in FD. This likely causes exaggerated stimulation of duodenal vagal afferents, explaining dyspeptic symptom generation. The mechanisms underlying elevated mucosal CCK release warrant further investigation.

Topics: Adult; Apolipoproteins A; Biomarkers; Biopsy; Case-Control Studies; Cholecystokinin; Down-Regulation; Duodenum; Dyspepsia; Emulsions; Female; Humans; Intestinal Mucosa; Male; Middle Aged; Netherlands; Phospholipids; Predictive Value of Tests; Soybean Oil; Time Factors

Functional dyspepsia is predominantly attributed to gastric sensorimotor dysfunctions. The contribution of intestinal chemosensitivity to symptoms is not understood. We evaluated symptoms and plasma hormones during enteral nutrient infusion and the association with impaired glucose tolerance and quality-of-life (QOL) scores in patients with functional dyspepsia vs. healthy controls.. Enteral hormonal responses and symptoms were measured during isocaloric and isovolumic dextrose and lipid infusions into the duodenum in 30 patients with functional dyspepsia (n=27) or nausea and vomiting (n=3) and 35 healthy controls. Infusions were administered in randomized order over 120 min each, with a 120-min washout. Cholecystokinin, glucose-dependent insulinotropic peptide, glucagon-like peptide 1 (GLP1), and peptide YY were measured during infusions.. Moderate or more severe symptoms during lipid (4 controls vs. 14 patients) and dextrose (1 control vs. 12 patients) infusions were more prevalent in patients than controls (P≤0.01), associated with higher dyspepsia symptom score (P=0.01), worse QOL (P=0.01), and greater plasma hormone concentrations (e.g., GLP1 during lipid infusion). Moderate or more severe symptoms during enteral infusion explained 18%, and depression score explained 21%, of interpatient variation in QOL. Eight patients had impaired glucose tolerance, associated with greater plasma GLP1 and peptide YY concentrations during dextrose and lipid infusions, respectively.. Increased sensitivity to enteral dextrose and lipid infusions was associated with greater plasma enteral hormone concentrations, more severe daily symptoms, and worse QOL in functional dyspepsia. These observations are consistent with the hypothesis that enteral hormones mediate increased intestinal sensitivity to nutrients in functional dyspepsia.

Topics: Adult; Blood Glucose; C-Peptide; Case-Control Studies; Cholecystokinin; Duodenum; Dyspepsia; Enteral Nutrition; Female; Gastric Inhibitory Polypeptide; Ghrelin; Glucagon-Like Peptide 1; Glucose; Glucose Intolerance; Humans; Lipids; Male; Peptide YY; Quality of Life; Severity of Illness Index

It has been suggested that there could be three possible mechanisms of gastric dysfunction in patients with FD: (i) delayed gastric emptying, (ii) impaired gastric accommodation of food intake, and (iii) hypersensitivity to gastric distention. Postprandial fullness seems to be the most severe symptom in patients who report aggravation of their symptoms after meals. Therefore, it has been assumed that delayed gastric emptying and consequent prolonged antral distension could reduce hunger, increase satiety, and even cause gastric discomfort, all of which would pose a significant barrier to adequate nutrition. We previously reported that postprandial water intake inhibits gastric antral motility along with an increase of cholecystokinin (CCK) in normal subjects. We assumed that the rapid increase of CCK after water intake was initiated by a feedback mechanism related to the inflow of fatty chyme into the duodenum that inhibits gastric antral activity. This duodeno-gastric interaction is known as the "duodenal break." We also reported that total gastric emptying was more rapid after the intake of a high-viscosity liquid meal than after a low-viscosity meal, because the low-viscosity liquid meal inhibits gastric emptying after rapid initial inflow into the duodenum. Considering these results, we hypothesized that rapid gastric emptying, rather than delayed gastric emptying, could be a cause of FD. In some patients with postprandial distress syndrome (PDS), we have found a significant correspondence between PDS-related dyspepsia and accelerated gastric emptying in the early postprandial period. It is worth emphasizing that the duodenum and the duodeno-gastric interaction (duodenal break) could have an important role in the pathophysiology of FD. We consider that rapid gastric emptying might be a more important factor than delayed gastric emptying in patients with FD.

Topics: Abdominal Pain; Cholecystokinin; Diet; Drinking; Duodenum; Dyspepsia; Eating; Feedback, Physiological; Gastric Emptying; Humans; Postprandial Period; Viscosity

Post-infectious irritable bowel syndrome (PI-IBS) and functional dyspepsia (FD) have been described after both Campylobacter jejuni gastroenteritis and Giardia infection. After C. jejuni, there is increased rectal serotonin (5-HT)-containing EC cells and postprandial plasma 5-HT, while a pilot study suggested increased plasma cholecystokinin (CCK) after Giardia infection.. To determine changes in plasma and duodenal mucosal 5-HT and CCK in Giardia-induced PI-IBS.. A total of 32 patients previously infected with Giardia and 19 who had recovered fully (controls) completed symptom questionnaires. Endoscopic duodenal biopsies were obtained from all subjects and immunohistochemically stained for CCK, 5-HT and CgA containing entero-endocrine cells and mast cells. 5-HT content was also assessed. Twenty-one of 32 patients and 19 controls consumed a high-carbohydrate meal, while fasting and postprandial plasma CCK and 5-HIAA were measured.. Post-infectious irritable bowel syndrome patients had increased numbers of CCK cells (P = 0.02), but lower numbers of EC cells (P = 0.009). Plasma CCK did not differ significantly between the groups, but correlated significantly with postprandial dyspepsia scores (r = 0.5, P = 0.05). PI-IBS patients had significantly lower plasma 5-HIAA, before and after meal (P = 0.05) as well as more dyspepsia (P < 0.0001) compared with recovered subjects.. Post-infectious bowel dysfunction following Giardia infection is associated with increased duodenal mucosal CCK. Postprandial dyspeptic symptoms correlate better with CCK than measures of 5-HT metabolism.

Topics: Adult; Cholecystokinin; Dyspepsia; Giardiasis; Humans; Intestinal Mucosa; Irritable Bowel Syndrome; Middle Aged; Norway; Serotonin; Young Adult

The actions of cholecystokinin (CCK) on gastrointestinal functions occur mainly via paracrine effects on peripheral sensory vagal fibers, which engage vago-vagal brain stem circuits to convey effector responses back to the gastrointestinal tract. Recent evidence suggests, however, that CCK also affects brain stem structures directly. Many electrophysiological studies, including our own, have shown that brain stem vagal circuits are excited by sulfated CCK (CCK-8s) directly, and we have further demonstrated that CCK-8s induces a remarkable degree of plasticity in GABAergic brain stem synapses. In the present study, we used fasted, anesthetized Sprague-Dawley rats to investigate the effects of brain stem administration of CCK-8s on gastric tone before and after activation of the esophageal-gastric reflex. CCK-8s microinjected in the dorsal vagal complex (DVC) or applied on the floor of the fourth ventricle induced an immediate and transient decrease in gastric tone. Upon recovery of gastric tone to baseline values, the gastric relaxation induced by esophageal distension was attenuated or even reversed. The effects of CCK-8s were antagonized by vagotomy or fourth ventricular, but not intravenous, administration of the CCK-A antagonist lorglumide, suggesting a central, not peripheral, site of action. The gastric relaxation induced by DVC microinjection of CCK-8s was unaffected by pretreatment with systemic bethanecol but was completely blocked by NG-nitro-L-arginine methyl ester, suggesting a nitrergic mechanism of action. These data suggest that 1) brain stem application of CCK-8s induces a vagally mediated gastric relaxation; 2) the CCK-8s-induced gastric relaxation is mediated via activation of nonadrenergic, noncholinergic pathways; and 3) CCK-8s reverses the esophageal-gastric reflex transiently.

Topics: Animals; Brain Stem; Cholecystokinin; Dose-Response Relationship, Drug; Dyspepsia; Esophagus; Fasting; Male; Microinjections; Neural Inhibition; Peptide Fragments; Rats; Rats, Sprague-Dawley; Reflex; Stomach; Vagus Nerve

In patients with functional dyspepsia (FD), symptoms are frequently triggered, or exacerbated, by fatty foods. We hypothesized that in FD patients, a high-fat (high-FAT) meal would induce more symptoms than a high-carbohydrate (high-CHO) meal, associated with an altered secretion of cholecystokinin (CCK), peptide-YY (PYY), and ghrelin and an increased antral size, when compared to healthy subjects (HS).. FD symptoms, appetite perceptions, plasma hormones, and antral area were measured in 8 FD patients and 8 HS on three separate days after the ingestion of high-CHO or high-FAT (500 kcal/400 g) meals, or a low-nutrient control (180 kcal/400 g); the energy intake was quantified 60 min later.. Nausea (P < 0.01) and pain (P= 0.05) were greater in FD after the high-FAT, when compared to high-CHO and control meals and in HS. Discomfort was greater after all meals in FD when compared to HS (P < 0.05). Fasting CCK and stimulation of CCK by the high-FAT (P < 0.01) meal were greater in FD, while fasting and postprandial PYY were lower (P < 0.001) in FD than in HS, with no differences in fasting, or postprandial, plasma ghrelin between FD and HS. Fasting antral area was greater in FD (P < 0.05), with no differences postprandially between FD and HS. There were no differences in the energy intake between the two groups.. In FD patients: (a) a high-FAT meal induces more symptoms than an isocaloric high-CHO meal, and (b) fasting and postprandial plasma CCK concentrations are greater and PYY concentrations are less. Our findings have important implications for the development of diet-based therapies for the treatment of FD.

Topics: Adult; Cholecystokinin; Dietary Carbohydrates; Dietary Fats; Disease Progression; Dyspepsia; Fasting; Female; Follow-Up Studies; Humans; Middle Aged; Peptide YY; Postprandial Period; Prognosis; Surveys and Questionnaires

Symptoms of functional dyspepsia are characterized by upper abdominal discomfort or pain, early satiety, postprandial fullness,bloating, nausea and vomiting. It is a chronic disorder, with symptoms more than 3 mo per year,and no evidence of organic diseases. Dysfunctional motility, altered visceral sensation, and psychosocial factors have all been identified as major pathophysiological mechanisms. It is believed that these pathophysiological mechanisms interact to produce the observed symptoms. Dyspepsia has been categorized into three subgroups based on dominant symptoms. Dysmotility-like dyspepsia describes a subgroup of patients whose symptom complex is usually related to a gastric sensorimotor dysfunction. The brain-gut peptide cholecystokinin (CCK) and serotonin (5-HT) share certain physiological effects. Both have been shown to decrease gastric emptying and affect satiety. Furthermore the CCK induced anorexia depended on serotonergic functions probably acting via central pathways. We believe that abnormalities of central serotonergic receptors functioning together with a hyper responsiveness to CCK or their interactions may be responsible for the genesis of symptoms in functional dyspepsia (FD).

Topics: Cholecystokinin; Dyspepsia; Gastric Emptying; Gastrointestinal Motility; Humans; Psychomotor Performance; Receptors, Cholecystokinin; Receptors, Serotonin; Satiety Response; Serotonin; Signal Transduction; Stress, Physiological

There is no general agreement as regards the effect of Helicobacter pylori infection on gastric emptying in patients with functional dyspepsia. Food releases several gastrointestinal hormones, and some of these are known to contribute to the regulation of gastric emptying. The aim of this study was to investigate the influence of H. pylori on gastric emptying in dyspeptic and healthy subjects and to verify whether different hormone secretion patterns are affected by the presence of the bacterium. Twenty-seven patients affected by functional dyspepsia and 30 asymptomatic healthy subjects entered the study. H. pylori presence was assessed in controls by IgG antibodies to H. pylori and [13C] urea breath test, and that in patients by Warthin-Starry stain on gastric biopsies. After ingesting a standard solid-liquid meal, an ultrasound examination of gastric emptying was performed. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were measured in the fasting and postprandial period for 4 hours. The incidence of H. pylori infection was not higher in functional dyspepsia patients than in controls. As regards gastric emptying, no difference was detected between patients and controls with and without H. pylori infection. On the contrary, the presence of H. pylori infection determined alterations in gastrin levels, which were higher in controls than in patients. Basal CCK levels were higher in the H. pylori-negative patients than H. pylori-positive patients and controls. In conclusion, H. pylori infection seems not to cause alterations in gastric emptying, but rather alterations in gastrin levels. In contrast, the altered levels of CCK account for its involvement in the pathophysiology of H. pylori-negative dyspepsia.

Topics: Adolescent; Adult; Cholecystokinin; Dyspepsia; Female; Gastric Emptying; Gastrins; Gastrointestinal Hormones; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pancreatic Polypeptide

Early satiety and postprandial epigastric fullness are common symptoms in functional dyspepsia. Cholecystokinin (CCK), a mediator of satiety in humans, may be responsible for these symptoms through an increased effect on delaying gastric emptying.. In five normal subjects and in five patients, gastric emptying of inert liquid mixed with technetium (Tc99m) was studied during i.v. perfusion of normal saline and of physiological concentrations of CCK octapeptide.. Administration of CCK significantly delayed emptying of inert liquid in patients and in normal subjects, and the effect was of similar magnitude in the two groups: residual gastric volumes at 90 min increased from 9.9 +/- 6.1 to 32.1 +/- 6.2% (p < 0.025) in controls and from 9.8 +/- 4.4 to 32.2 +/- 4.7% (p < 0.005) in patients during saline infusion in comparison with CCK infusion; also, prolongation of half emptying time was not different between the two groups (19.4 +/- 1.9 min to 39.4 +/- 15.2 min in controls and 19.5 +/- 3.0 min to 31.4 +/- 7.9 min in patients).. We conclude that CCK at physiological concentrations acts similarly in normal subjects and in patients with functional dyspepsia; this suggests that, if this hormone is normally released after a meal, a peripheral action of CCK through delayed gastric emptying is not responsible for increased postprandial satiety in functional dyspepsia.

Topics: Adult; Case-Control Studies; Cholecystokinin; Dyspepsia; Female; Gastric Emptying; Humans; Sincalide; Sodium Chloride; Technetium Tc 99m Sulfur Colloid; Time Factors; Water

The aim of the present study was to clarify the effects of Helicobacter pylori infection and its eradication on gastric emptying.. Out of a total of 52 patients with non-ulcerative dyspepsia, 34 H.pylori-positive patients were enrolled. Antimicrobial drugs for the eradication of H. pylori were administered to 19 out of the 34 H. pylori-positive patients. Gastric emptying was evaluated according to the acetaminophen method. Inflammatory changes and intracellular periodic acid-Schiff-positive substances in the antral mucosa were examined in biopsy specimens.. Although gastric emptying was significantly prolonged in the patients with non-ulcerative dyspepsia compared with the control group (P < 0.01), there was no difference in gastric emptying between H. pylori-positive and -negative patients, with all patients showing significantly less gastric emptying than the control group. The H. pylori eradication rate was 58% (11 out of 19) and gastric emptying improved significantly in seven patients whose infection was eradicated and whose dyspeptic symptoms disappeared. The ammonia concentration in gastric juice, inflammatory changes in the gastric mucosa and the index of periodic acid-Schiff-positive substances improved significantly when H. pylori was successfully eradicated compared with patients in whom eradication was unsuccessful. As gut hormones may affect gastroduodenal motility associated with H. pylori infection, we also studied the levels of serum gastrin and cholecystokinin. In the patients whose infection was eradicated, serum gastrin decreased significantly, but the cholecystokinin level did not change significantly, although there was a non-significant trend for cholecystokinin to increase.. These results suggest that delayed gastric emptying is partly associated with H. pylori infection and that the infection may contribute to the development of non-ulcerative dyspepsia.

Topics: Adult; Aged; Amoxicillin; Cholecystokinin; Dyspepsia; Female; Gastric Emptying; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Penicillins

Eleven patients (8 male, 3 female, age 21-53 years) with dyspeptic symptoms and no gastrointestinal organic diseases were studied for their gallbladder contractile function. A comparative sonographic study of gallbladder contraction was performed after exogenous and endogenous stimulation. On day 1, ceruletide was infused at a dose of 2.5 ng/kg/min about 10 minutes. On day 2, a semi-liquid test meal of 1450 kJ (44 kJ% carbohydrates, 24 kJ% protein, 32 kJ% fat) was administered. Gallbladder volume was determined for 30 minutes before and 5, 10, 20, 30, 40, 60, 80, 100 and 120 minutes after both stimulations by means of realtime ultrasonography. Three diameters in two plains were measured for calculation of gallbladder volume. Following ceruletide, peak gallbladder contraction (range 7-48% of initial volume) was observed within 10 (n = 5) or 20 (n = 6) minutes. Following the test meal, peak gallbladder contraction ranged from 27-80% and was observed within 30 to 100 minutes. Variations in time and amount of peak gallbladder contraction does hardly allow to establish normal values. No significant correlation was found between both types of stimulation concerning peak gallbladder contraction or time to peak contraction. We conclude that for the assessment of gallbladder contractility, ceruletide infusion and determination of gallbladder volume after 20 minutes (upper range 48% of initial volume) is the most valuable procedure. Impaired gallbladder contractility can be diagnosed with certainty only after exogenous stimulation.

Topics: Adult; Ceruletide; Cholecystokinin; Diagnosis, Differential; Dyspepsia; Eating; Female; Gallbladder Diseases; Gallbladder Emptying; Gastric Emptying; Humans; Male; Middle Aged; Ultrasonography

Topics: Adult; Asthenia; Cholecystectomy; Cholecystography; Cholecystokinin; Cholelithiasis; Colon; Colon, Sigmoid; Constipation; Desensitization, Immunologic; Diarrhea; Dyspepsia; Female; Headache; Histamine H1 Antagonists; Humans; Hypersensitivity; Middle Aged; Pain; Postoperative Complications; Sleep Wake Disorders; Stomach