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Objective:Prevalence of non-alcoholic fatty liver disease is rising in the Western world and reaches up to 90% in patients undergoing bariatric surgery. Fibroscan®as a non-invasive tool for liver stiffness measurement (LSM) has several limitations in morbidly obese patients. Only few data exist about the technical feasibility and accuracy of LSM in these patients. We aimed to analyse the feasibility of LSM by Fibroscan®in bariatric patients. Materials and methods:In morbidly obese patients, LSM was performed using XL probe. Measurements were termed reliable if 10 successful measurements with a success rate ≥60% and an interquartile range/median (IQR/M) <0.3 were obtained, unreliable if 10 successful measurements were obtained but the IQR/M was >0.3, and they were termed failed if they were neither reliable nor unreliable. Results:A total of 149 patients were included (87 with liver biopsies); mean BMI was 51.6 ± 8.5 kg/m2. In 41% LSM using XL-probe was reliable, in 22% unreliable and in 37% failed. Failed LSM was significantly more frequent in patients with higher BMI compared to reliable and unreliable measurements (p < 0.05). In patients with failed measurement, sonographic paramedian and intercostal distances were significantly higher compared to reliable measurements. All three patients with F4 fibrosis could successfully be differentiated by LSM from patients without fibrosis. Conclusions:LSM with XL probe is feasible in almost two-thirds of morbidly obese patients with a BMI ≥50 kg/m2. Reliable prediction of advanced fibrosis appears to be possible even if formal criteria of successful measurements are not met. [ABSTRACT FROM PUBLISHER]

Background: Cholecystokinin (CCK) exerts trophic effects on the exocrine pancreas. Total parenteral nutrition (TPN) results in hypotrophy of the pancreas. The present study aimed to examine the effect of exogenous and endogenous CCK during TPN., Methods: Seventy-two Sprague-Dawley rats were orally fed or given TPN after pancreaticobiliary diversion (PBD) and were infused with CCK-8S or the CCK-receptor antagonist devazepide for 7 days., Results: Infusion of CCK and PBD caused hyperCCKemia, whereas TPN did not influence the concentration of plasma CCK. The reduced pancreatic contents during TPN could be reversed by CCK but not by PBD. The hyperplastic response to CCK in orally fed rats was abolished during TPN. Devazepide did not influence the pancreatic variables in orally fed and TPN-treated rats., Conclusion: TPN reduces the hyperplastic response of the exocrine pancreas to CCK, and CCK reverses the hypotrophy seen during TPN. The effects of CCK on the exocrine pancreas seems to need enteral nutrition for the full expression.

Background: The purpose of the study was to evaluate the trophic effects of endogenous hypergastrinemia and hypercholecystokininemia on intact and regenerating rat liver. We also examined the effects on the liver of portacaval shunting (PCS) alone or together with hypergastrinemia or hyperCCKemia. PCS is known to enhance the trophic effects of gastrin on the so-called enterochromaffin-like cells of the stomach and of CCK on the pancreas., Methods: Hypergastrinemia was induced by treatment with omeprazole (400 mumol/kg/day) or extirpation of the acid-producing part of the stomach (fundectomy). HyperCCKemia was induced by pancreaticobiliary diversion (PBD). After 4 weeks half of the rats were killed; the rest underwent partial hepatectomy and were killed 60 h later. PCS rats were killed 4 weeks after start of omeprazole treatment or after PBD. The concentrations of circulating gastrin and CCK were measured by radioimmunoassay. The liver weight and DNA content were analyzed., Results: Endogenous hypergastrinemia and hyperCCKemia failed to stimulate growth of either intact or regenerating liver. There were no differences in liver weight and DNA content between rats subjected to PCS and to combinations of PCS and omeprazole treatment, on the one hand, and PCS and PBD, on the other., Conclusion: Gastrin and CCK are unlikely to be physiologically important in the regulation of liver growth and regeneration in the rat.

Background: Studies in humans and rodents indicate that gallstone development may be prevented by inhibiting gallbladder mucus hypersecretion with non-steroidal anti-inflammatory drugs or by preventing stasis of gallbladder bile with administration of cholecystokinin., Methods: The effect of oral aspirin and pancreaticobiliary diversion with endogenous hypercholecystokininemia on crystal and gallstone formation was studied in Syrian golden hamsters fed a lithogenic diet for 8 weeks., Results: None of the control animals fed a normal diet developed gallstones or crystals in gallbladder bile. Gallstones developed in 67% of the animals fed a lithogenic diet only. The gallstone prevalence did not differ significantly in animals on a lithogenic diet and a daily aspirin dose of 6 mg/kg (gallstone prevalence, 60%) or 100 mg/kg (gallstone prevalence, 70%), whereas it was significantly lower in animals with endogenous hypercholecystokininemia on a lithogenic diet (gallstone prevalence, 29%). The prevalence of crystals in gallbladder bile did not differ significantly between any of the experimental groups., Conclusions: It is concluded that in hamsters on a lithogenic diet, aspirin does not prevent gallstone formation, whereas endogenous hypercholecystokininemia reduces the prevalence of stones without affecting the occurrence of crystals in gallbladder bile.

Gastrin and possibly cholecystokinin (CCK) control the activity and growth of the histamine-containing endocrine cells, the enterochromaffin-like (ECL) cells, in the oxyntic mucosa of the rat. Portacaval shunting (PCS) is known to activate the ECL cells through as yet unknown mechanisms. PCS also exaggerates the ECL cells' response to gastrin, whereas antrectomy causes hypotrophy and hypoplasia of the ECL cells. A recent study showed that the ECL cells failed to respond to sustained hyperCCKemia caused by pancreaticobiliary diversion (PBD). In the present study we investigated whether PBD-produced hyperCCKemia influenced the effects of PCS or antrectomy on the ECL cells. The results show 1) that hyperCCKemia raised the histidine decarboxylase (HDC) activity of the ECL cells in PCS rats but not in control rats, and the CCK-A receptor blockade failed to prevent the enzyme activation; and 2) that PBD prevented the ECL cell hypoplasia and the decrease in HDC activity induced by antrectomy. The findings suggest that under special circumstances endogenous CCK may stimulate the ECL cells.

The purpose of the present study was to examine the weight, DNA content, and enzyme mRNA levels in the pancreas in response to endogenous hypercholecystokininemia produced by pancreaticobiliary diversion (PBD) in starved rats. The results showed that PBD, which is known to increase the circulating cholecystokinin (CCK) concentration, prevented the reduction in the weight and DNA content of the pancreas after 3 days of starving, and that PBD increased the mRNA levels of amylase, chymotrypsinogen B, and procarboxypeptidase A in the pancreas of starved rats. The findings support the view that endogenous CCK plays an important role in maintaining the weight of the normal pancreas of starved rats and that it stimulates the transcription of genes coding for pancreatic exocrine enzymes.

The trophic effect of cholecystokinin (CCK) on the pancreas was examined in portacava-shunted (PCS) rats. Exogenous CCK-8s and the CCK-A receptor antagonist devazepide were infused continuously by means of osmotic minipumps. HyperCCKemia of endogenous origin was induced by pancreaticobiliary diversion (PBD), which is known to cause growth of the pancreas. The results showed that PCS as such was without a trophic effect on the pancreas, whereas the combination of CCK-8s and PCS or PBD and PCS increased the trophic effects on the pancreas compared with CCK-8s or PBD alone. Moreover, the trophic effects of PBD and of the combination of PBD and PCS could be prevented by CCK-A receptor blockade (devazepide infusion). The results suggest that the capacity of the pancreas to respond to CCK is exaggerated--for as yet unknown reasons--after PCS.

The histamine-producing enterochromaffin-like (ECL) cells in the oxyntic mucosa are controlled by gastrin. An acute gastrin challenge induces release and accelerated resynthesis of ECL cell histamine. Long-term stimulation with gastrin causes ECL cell hyperplasia. We set out to study whether the ECL cells respond not only to gastrin but also to cholecystokinin (CCK). A wide dose range of gastrin-14 sulfated and -17 non-sulfated and CCK-8 sulfated (CCK-8s) and non-sulfated (CCK-8) was infused intravenously to rats for 3 h. The activity of the histamine-forming enzyme was measured at termination of infusion. Gastrins and CCK-8s were equally effective in activating the enzyme, whereas sulfated CCK-8 was notably less potent than the other three peptides. Clearly, the receptor responsible for activation of the ECL cells distinguishes poorly between gastrin-17 and CCK-8s, which is in line with the characteristics of the CCK-B receptor. Moreover, neither the response to gastrin-17 nor that to CCK-8s was affected by concomitant infusion of devazepide (200 micrograms/kg/h), a selective CCK-A-receptor antagonist. One group of rats received CCK-8s continuously via a minipump. Another group of rats was subjected to pancreaticobiliary diversion (PBD), which increases the plasma CCK concentration 10- to 20-fold. The rats were killed 7 or 10 weeks later, respectively, and the stomachs were analyzed with regard to mucosal growth and ECL cell hyperplasia. HyperCCKemic rats had increased pancreatic weights but showed no signs of growth stimulation in the stomach and no ECL cell hyperplasia.(ABSTRACT TRUNCATED AT 250 WORDS)

To ascertain whether the increase in cholecystokinin (CCK) level associated with pancreaticobiliary diversion has a cytoproliferative effect on the liver similar to that on the pancreas, we studied three groups of rats: group I (n = 19) had a pancreaticobiliary diversion and 4 weeks later a 70% liver resection, group II (n = 13) had a liver resection only, and group III (n = 6) underwent a sham liver operation. Tissue samples were taken from the liver and pancreas 48 h after the liver operation. Liver regeneration was evaluated on the basis of continuous incorporation of tritiated thymidine into hepatocytes, liver weight, and DNA content. For confirmation of the increase in CCK levels the effects on the pancreas was studied by measuring wet weight, total protein, and total DNA content. The results showed trophic effects on the pancreas, as expected, but no effects whatsoever on liver regeneration. CCK does not seem to have any role in the regulation of liver regeneration.