Cholecystokinin abnormalities in coeliac disease

Expression of cholecystokinin in the duodenum of patients with coeliac disease: respective role of atrophy and lymphocytic infiltration

“…Previous results in the literature are at variance with this finding with reports of increased CCK cell counts in coeliac mucosa [15,16,31] and decreased amounts of CCK in duodenal extracts [6,14]. These discrepancies could be related to the site where the pathological specimen was taken (duodenum, Treitz angle or proximal jejunum), to methodological difficulties in counting endocrine cells in atrophic or non-atrophic mucosa, to the method used to relate the CCK-positive cells to the epithelial surface area, to the various antisera used (recognition of smaller and larger CCK forms), to differences in the degree of mucosal lesions, or to the type of coeliac patients studied (on a normal diet or a gluten-free diet).…”

“…These discrepancies could be related to the site where the pathological specimen was taken (duodenum, Treitz angle or proximal jejunum), to methodological difficulties in counting endocrine cells in atrophic or non-atrophic mucosa, to the method used to relate the CCK-positive cells to the epithelial surface area, to the various antisera used (recognition of smaller and larger CCK forms), to differences in the degree of mucosal lesions, or to the type of coeliac patients studied (on a normal diet or a gluten-free diet). The size of the cells could also account for some discrepancy, since CCK cells were shown to be more numerous but smaller in one report [31] and larger in another study [15]. We studied 19 patients, divided into three groups according to the severity of their mucosal lesion, and we could not show any significant differences in the number of CCK cells in specimens taken from the distal duodenum.…”

“…Lower intestinal concentrations of CCK have been reported in coeliac atrophic mucosa by means of CCK extraction and radioimmunoassay [6,14]. These observations are contrary to immunocytochemistry reports showing an increased number of CCK cells in the coeliac mucosa [15,16]. Impaired release could also be explained by decreased stimulation of the mucosal CCK cells due to impaired intraduodenal hydrolysis of nutrients observed with mucosal atrophy [17].…”

“…Between-group comparison showed a significant decrease in CCK concentration in patients from group A with atrophic changes (P l 0.006), but surprisingly also in patients from group B with an infiltrative pattern (P l 0.01). PCR products were separated using 1.5 % agarose gel electrophoresis and exposed to X-ray film for 1 h. Duodenal extracts were obtained from controls (Control, lanes 1-4), coeliac patients with atrophic mucosa (Group A, lanes 5-8), IEL infiltration (Group B, lanes 9-12), and completely restored duodenal mucosa (Group C, lanes [13][14][15][16]. PCR results were calculated as the CCK/RPL19 ratio and averaged for four dilutions (1 : 10, 1 : 5, 1 : 2.5 and 1 : 1).…”

Effect of predigested fat on intestinal stimulation of plasma cholecystokinin and gall bladder motility in coeliac disease.

“…(Gut 1995;36: [17][18][19][20][21] Keywords: gall bladder motility, coeliac disease, lipid digestion, cholecystokinin. Cholecystokinin (CCK) is a major factor in mediating the gall bladder contraction in response to intestinal fat.1l4 The cells that produce CCK are located in the mucosa of the upper small intestine.5 In patients with a flat jejunal mucosa as a result of untreated coeliac disease, plasma CCK and gall bladder responses to oral or intestinal fat are abolished,67 and intestinal concentrations of CCK have been reported to be lower in patients with coeliac disease than in healthy subjects.8 The finding of an increased number of CCK producing cells in duodenal biopsy specimens from patients with coeliac disease seems to contradict the absence of gall bladder emptying and plasma CCK release in response to the appropriate stimulus in this disorder.9 10 Little is known of the mechanisms by which fatty nutrients stimulate CCK producing cells. In dogs with gastric and pancreatic fistulas, fat did not stimulate pancreatic protein secretion unless the triglycerides were mixed and incubated with bile and lipase active pancreatic juice."…”