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The Role of Fat and Cholecystokinin in Functional Dyspepsia M Fried, C Feinle

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The Role of Fat and Cholecystokinin in Functional Dyspepsia M Fried, C Feinle i54 VISCERAL PERCEPTION Gut: first published as 10.1136/gut.51.suppl_1.i54 on 1 July 2002. Downloaded from The role of fat and cholecystokinin in functional dyspepsia M Fried, C Feinle ............................................................................................................................. Gut 2002;51(Suppl I):i54–i57 The main factors involved in the pathophysiology of fat These studies provide important insights into the induced dyspepsia were investigated by reviewing a mechanisms underlying gastrointestinal percep- tion in response to fat and the role of CCK in series of controlled double blind randomised studies healthy subjects and patients with functional which sought to determine the role of nutrient fat and dyspepsia. the postprandial release of cholecystokinin (CCK) in the INTRODUCTION development of dyspeptic symptoms in healthy Patients with functional dyspepsia exhibit a vari- volunteers and in patients with functional dyspepsia. The ety of symptoms, such as bloating, nausea, and studies showed that during distension of the stomach, early fullness, which generally occur in response to ingestion of a meal. Hypersensitivity of the lipids are a major trigger of dyspeptic symptoms such as stomach to postprandial distension is an essential nausea, bloating, pain, and fullness, and that they pathophysiological characteristic of functional dyspepsia and an important factor in the genera- modulate upper gastrointestinal sensations and 12 tion of dyspeptic symptoms. In healthy subjects symptoms in a dose related fashion. CCK is a major and in patients with functional dyspepsia, percep- mediator of the sensitisation of gastric perception by tion of gastric distension is enhanced by nutrient 3–5 lipids in patients with functional dyspepsia as the CCK-A lipids but not by glucose (fig 1). A number of studies have shown that release of receptor antagonist dexloxiglumide markedly diminishes CCK in response to fat ingestion plays a major this effect. The studies provide important insights into the role in the regulation of upper gastrointestinal function.6–9 Fat induced CCK release inhibits mechanisms underlying gastrointestinal perception in postprandial gastric emptying by altering gastric response to fat and the role of CCK in patients with motility,67 and the products of fat hydrolysis http://gut.bmj.com/ functional dyspepsia. inhibit postprandial gastric acid secretion, prob- ably by modifying CCK release.9 .......................................................................... It can therefore be hypothesised that besides their effects on upper gastrointestinal function, SUMMARY such as gastric emptying, stimulation of pancrea- A subgroup of patients with functional dyspepsia ticobiliary secretion, and gastric acid secretion, fat are characterised by heightened visceral sensitiv- induced CCK release plays an important role in ity to mechanical distension of the stomach with the pathophysiology of functional dyspepsia. on September 29, 2021 by guest. Protected copyright. a balloon. Small intestinal infusion of nutrients, Knowledge of the factors involved in the genera- particularly fat, exacerbates this hypersensitivity tion of fat induced symptoms is essential for the and also modulates sensations, such as hunger development of therapeutic concepts and targets and fullness, in healthy subjects. Previous studies in the treatment of functional dyspepsia. We in healthy subjects suggest that cholecystokinin therefore sought to investigate the main factors (CCK)-A and serotonergic (5-HT3) receptors involved in the pathophysiology of fat induced mediate, at least in part, the effects of lipid on dyspepsia in a series of controlled double blind gastrointestinal sensations. Recent studies have randomised studies. shown that duodenal fat infusion causes a dose In all trials, a standard barostat technique was dependent increase in the intensity of sensations employed to study gastric volume changes and to and symptoms during gastric distension. How- apply ramp distensions of the proximal ever, fat digestion, achieved by using the specific stomach,10 with and without concomitant in- lipase inhibitor tetrahydrolipstatin (THL) is nec- traduodenal infusion of nutrients and drugs. essary to promote the effects of fat on visceral Most studies were performed in healthy sensation, gastric relaxation, and CCK release. volunteers,11–14 and in one trial, patients with The digestion products of fat interact with recep- functional dyspepsia were examined.15 Sensory See end of article for tors in the small intestine. Long chain triglycer- responses were assessed by means of visual authors’ affiliations ....................... ides (LCT) appear to be more potent than medium analogue scales. chain triglycerides (MCT) in inducing symptoms The role of intestinal chemoreceptors thought Correspondence to: of fullness, nausea, and suppression of hunger. to be involved in mediating the effects of lipids Professor M Fried, Gastroenterology Division, The effects of LCT are at least partially mediated University Hospital Zurich, by CCK as MCTs do not cause CCK release. In ................................................. CH-8091 Zurich, patients with functional dyspepsia, gastro- Switzerland; intestinal symptoms induced by duodenal lipid Abbreviations: CCK, cholecystokinin; LCT, long chain [email protected] infusion and gastric distension are alleviated by triglycerides; MCT, medium chain triglycerides; SPE, ....................... sucrose polyester; THL, tetrahydrolipstatin. the CCK-A receptor antagonist dexloxiglumide. www.gutjnl.com The role of fat and cholecystokinin in functional dyspepsia i55 800 intensity of nausea.16 17 These findings suggest that small 700 mucosal chemoreceptors in the small intestine are involved in the effects of duodenal lipids on gastric sensory function. Gut: first published as 10.1136/gut.51.suppl_1.i54 on 1 July 2002. Downloaded from 600 Luminal (duodenal and jejunal) infusion of the local 500 anaesthetic benzocaine or saline combined with duodenal 400 infusion of lipid or saline was used to investigate the role of intestinal chemoreceptors in the induction of gastric sensa- 300 tions by lipid in healthy volunteers. 200 Benzocaine attenuated duodenal lipid induced gastric Gastric bag volume (ml) 100 relaxation and markedly diminished CCK release in the duo- denum but not in the jejunum. Benzocaine also diminished 0 0.9% Lipid 0.9% Glucose the generation of dyspeptic symptoms and nausea that saline saline accompanied duodenal infusion of lipids and gastric disten- sion. During duodenal lipid infusion, gastric perception Figure 1 Gastric bag volumes at which discomfort was appeared to be disassociated from gastric relaxation. These experienced by patients with functional dyspepsia during gastric distension and duodenal infusion of saline, lipid, or glucose (1 studies demonstrate that duodenal receptors activated by lip- kcal/min). Patients tolerated significantly larger volumes during ids play an important modulatory role in the induction of gastric distension when glucose was infused compared with saline, gastrointestinal sensations during gastric distension. Applica- most likely due to the greater gastric relaxation that was observed tion of topical anaesthetic drugs may therefore provide one during glucose infusion. However, despite marked gastric relaxation possible therapeutic approach to the treatment of functional during the lipid infusion, discomfort was experienced during this gastrointestinal disorders. infusion at similar volumes as during saline infusion, indicating heightening of gastric sensitivity to distension by lipid. DOSE-RESPONSE RELATIONS BETWEEN DUODENAL was investigated in healthy volunteers during duodenal infu- LIPID LOADS AND GASTRIC PERCEPTION sion of benzocaine combined with lipids.13 The relationship Duodenal lipids induce nausea during gastric distension and between the energy load of nutrients, in particular fat, and the enhance gastric relaxation. Previous studies suggested that sensory responses to gastric distension was investigated by increasing the dose of lipids increases the severity of nausea.3 administering increasing amounts of intraduodenal It is conceivable therefore that increasing amounts of lipids nutrients.11 The effects of digested (as opposed to undigested) augment gastric relaxation and induce dyspeptic symptoms in fat on induction of dyspeptic symptoms was studied using the a dose dependent fashion. To test this hypothesis, the relation- specific lipase inhibitor orlistat (tetrahydrolipstatin (THL)) to ship between increasing intraduodenal doses of lipids (1–3 inhibit triglyceride hydrolysis during intraduodenal infusion kcal/min) or saline and gastric sensations during gastric baro- of lipids.14 In order to evaluate the role of CCK in the stat distension was studied in healthy volunteers.11 pathophysiology of functional dyspepsia, generation of dys- Nausea and other dyspeptic symptoms were found to peptic symptoms and CCK release was studied in patients increase during gastric distension in relation to the dose of with functional dyspepsia using increasing doses of duodenal lipid administered. Lipid administration simultaneously http://gut.bmj.com/ lipids combined with intravenous dexloxiglumide, a specific caused a dose dependent relaxation of the stomach and an CCK-A receptor antagonist.15 increase in plasma concentrations of CCK. Duodenal lipids without gastric distension did not significantly modulate BLOCKADE OF SMALL INTESTINAL RECEPTORS gastrointestinal
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