[Diagnosis of hereditary hemochromatosis].
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Biopsy↗
Biomedical subjects
C Niederau
Publications and source records attributed to C Niederau.
Cholecystokinin's role in regulation of colonic motility in health and in irritable bowel syndrome.
Colonic motor activity and plasma concentrations of cholecystokinin (CCK) both increase after oral intake of a meal. Thus, CCK had been thought to mediate the postprandial increase in colonic motor activity, which is termed gastrocolonic response. The present study used the substance loxiglumide, which acts as a specific antagonist at the CCK-A receptor, to evaluate this hypothesis. In the first set of experiments, eight healthy subjects were studied four times on separate days. A multilumen catheter was endoscopically placed with its tip lying in the descending colon. Motor activity was recorded by a low-compliance perfusion manometry system at six locations 60-45 cm from the anus. Basal activity was recorded for at least 2 hours to achieve steady-state conditions. The order of the following four experiments was randomized: (a) intravenous infusion of the CCK analogue cerulein at increasing doses (7.5, 15, 30, and 60 ng/kg.h, each given for 30 minutes); (b) intravenous cerulein plus 5 mg/kg.h loxiglumide; (c) a 1000-kcal solid/liquid meal consisting of regular German food; and (d) a meal plus 5 mg/kg.h loxiglumide. In the second set of experiments, eight patients with irritable bowel syndrome were studied twice on two separate days, and two experiments were performed n randomized order: (a) a 1000-kcal solid/liquid meal consisting of regular German food; or (b) a meal plus 5 mg/kg.h loxiglumide. The motor index was calculated as the area under contractions by a computerized system. The 1000-kcal meal markedly increased colonic motor activity. This gastrocolonic response was significantly greater in patients with irritable bowel syndrome than in healthy volunteers. Cerulein stimulated motor activity only at pharmacological doses (30-60 ng/kg.h), which resulted in plasma CCK levels markedly exceeding postprandial values. Loxiglumide abolished the effects of cerulein even at pharmacological doses. However, loxiglumide did not inhibit the gastrocolonic response to a regular meal either in healthy volunteers or in patients with irritable bowel syndrome. Loxiglumide also failed to alter the interdigestive colonic motor activity. Therefore, effects mediated by the CCK-A receptor do not play a major physiological role in the regulation of the interdigestive and postprandial motility of the left colon.
Adult↗
Effects of cholecystokinin receptor blockade on circulating concentrations of glucose, insulin, C-peptide, and pancreatic polypeptide after various meals in healthy human volunteers.
This study used a cholecystokinin (CCK) antagonist to evaluate whether CCK that is released after regular meals regulates meal-stimulated insulin secretion. Several experiments were performed in eight to 10 healthy male volunteers, each in duplicate. The subjects received different meals either with or with i.v. infusion of 5 mg/kg/h of the CCK antagonist loxiglumide (Rotta, Italy). The mixed solid-liquid meals of 600, 800, or 1,000 kcal consisting of regular German food were given orally. In addition, studies were carried out in which a liquid test meal of 750 kcal was infused into the duodenum over a 2-hour period to exclude effects of the CCK antagonist on gastric emptying. Finally, the subjects received an oral load of 100 g glucose either with or without i.v. infusion of loxiglumide. Loxiglumide at the dose used completely abolishes the actions of endogenous CCK and of exogenous CCK when given at doses that mimic postprandial circulating concentrations of this peptide at various target organs such as gallbladder, pancreas, stomach, and intestine. Loxiglumide also markedly reduced the increase in pancreatic polypeptide seen after the intraduodenal infusion of nutrients. However, loxiglumide at this dose did not alter the increase in circulating concentrations of glucose, insulin, and C-peptide after any of the various oral meals, after the intraduodenal administration of nutrients, and after the oral load of glucose. Although the present study does not rule out that in some conditions CCK may increase insulin secretion in humans, the results do rule out that CCK acts as a major physiologic incretin in healthy humans.
Administration, Oral↗
Diagnosis of pancreatic carcinoma. Imaging techniques and tumor markers.
In view of the increasing number of new imaging techniques and serum tumor markers, it is not well established which combination or which order of tests may provide the most information for diagnosis of pancreatic carcinoma. This review determines the diagnostic value of the various tests and evaluates which combination of tests may provide the most information and what may be considered to be a current rational approach to the diagnosis of pancreatic carcinoma. In the present analysis endoscopic retrograde cholangiopancreatography (ERCP) provided a 92% sensitivity that exceeded the 83% and 74% sensitivities calculated for computed tomography (CT) and ultrasound, respectively. The specificity of all three imaging techniques exceeded 90%. Serum determination of CA 19-9 yielded an 83% sensitivity, which was considerably higher than sensitivities of carcinoembryonic antigen and various other tumor markers. The combination of CA 19-9 and ultrasound improved the sensitivity of each test performed alone by 10-15%. Fine-needle biopsy allows diagnosis of pancreatic carcinoma with a sensitivity of 83% and an almost perfect specificity of 99%. On the basis of these data, the combination of ultrasound and determination of CA 19-9 is recommended as the initial tests when pancreatic carcinoma is suspected. CT also must be performed if ultrasound is indeterminant or inconsistent with the clinical evaluation, as well as in patients with negative ultrasound but abnormal CA 19-9. Negative results of CT, ultrasound, and CA 19-9 will exclude pancreatic carcinoma in most patients. A positive ultrasound or CT result usually leads to fine-needle biopsy, which helps avoid most diagnostic laparotomies. ERCP must be performed in patients where ultrasound, CT, and fine-needle biopsy do not clarify the diagnosis. In the majority of patients with pancreatic carcinoma, noninvasive imaging techniques such as ultrasound and CT also allow adequate staging. In some patients, however, laparoscopy and angiography may need to be performed for strategic planning of further therapy. Although modern imaging techniques and serum tumor markers allow diagnosis of pancreatic carcinomas as small as 2-3 cm and help avoid most diagnostic laparotomies, this improvement in diagnostic capability has as yet not significantly improved the prognosis.
Angiography↗
Effects of antioxidants and free radical scavengers in three different models of acute pancreatitis.
The present studies were done to evaluate the therapeutic potential of several antioxidants and free radical scavengers in three different models of acute pancreatitis. (a) Edematous pancreatitis with acinar cells necrosis was induced by seven hourly intraperitoneal injections of 50 micrograms of caerulein per kg in mice. (b) Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet in mice. (c) Hemorrhagic pancreatitis was induced by retrograde infusion of 0.6 ml of 5% sodium taurocholate into the pancreatic duct in rats. The following antioxidants and free radical scavengers were given at various doses intravenously, subcutaneously, or intraperitoneally before the onset of pancreatitis: Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one], superoxide dismutase, catalase, deferoxamine (Desferal), dimethyl sulfoxide, or allopurinol. The severity of pancreatitis was assessed at various times after its onset by determination of serum amylase and pancreatic weight (edema), by grading of histological alterations, and by determination of survival (survival determined in models of hemorrhagic pancreatitis). In general, free radical scavengers and antioxidants ameliorated edema and inflammation to a greater degree than necrosis and the increase in serum amylase. Superoxide dismutase (as did Ebselen in previous studies) exerted beneficial effects on survival in diet-induced pancreatitis in the absence of marked effects on pancreatic necrosis, suggesting that these beneficial effects are due to amelioration of extrapancreatic complications that often contribute to mortality in acute pancreatitis. None of the antioxidants had major beneficial effects in taurocholate-induced hemorrhagic pancreatitis. Thus, formation of free radicals may be important for progression and outcome in diet-induced and, to a lesser degree, in caerulein-induced pancreatitis but not at all in taurocholate-induced pancreatitis. Different models of pancreatitis may, therefore, involve different degrees and mechanisms of free radical formation. Despite the amelioration of edema and the beneficial effects on mortality seen for some antioxidants in some of the models, antioxidants and free radical scavengers appear to have only a limited potential for treatment of acute pancreatitis.
Acute Disease↗
Acute experimental hemorrhagic-necrotizing pancreatitis induced by feeding a choline-deficient, ethionine-supplemented diet. Methodology and standards.
The present work evaluates the methodology and standards of acute hemorrhagic-necrotizing pancreatitis induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet to mice. The diet model appears to be a good approximation of severe necrotizing human pancreatitis. Both the gross and histological appearance of the pancreatic and peripancreatic inflammation as well as the clinical and biochemical course of diet-induced pancreatitis resemble human disease. By limiting the period of feeding the diet, one can control the mortality at any desired level between 0 and 100%. Ascites, acidosis, hypoxia and hypovolemia occur in this model as well as in human pancreatitis. The time course of the morphological and biochemical alterations have extensively been studied and are, thus, well defined in this model. Despite the differences in pathogenesis of pancreatitis induced in this model versus human disease, the experimental pancreatitis and clinical pancreatitis share several pathophysiologic features. Therefore, the model is suitable to study pathophysiologic aspects of this disease. The diet model is particularly well suitable to study the potential for new therapeutic substances. The small size of the animals used, however, is a limitation for the evaluation of surgical procedures and of new diagnostic tools. Several pitfalls and problems have to be considered in order to obtain valuable data. The amount of injury produced by the CDE diet depends critically on sex, age and weight of the mice. Special care has to be taken to guarantee that the intake of the CDE diet is identical between different experimental groups. Therefore, each set of experiments needs to include a separate control group of mice which receive the CDE diet without any other special treatment. The potential benefit of an experimental therapy can be assessed by measuring survival, various biochemical and histological features, and alterations in hematocrit, pH and blood gases.
Acute Disease↗
Treatment of pain with pancreatic extracts in chronic pancreatitis: results of a prospective placebo-controlled multicenter trial.
According to the theory of negative feedback regulation of pancreatic enzyme secretion by proteases, treatment with pancreatic extracts has been proposed to lower pain in chronic pancreatitis by decreasing pancreatic duct pressure. We conducted a prospective placebo-controlled double blind multicenter study to investigate the effect of porcine pancreatic extracts on pain in chronic pancreatitis. 47 patients with pain (41 males, 6 females) due to chronic pancreatitis documented by sonography, endoscopic retrograde cholangiopancreatography, and CT were included. Exclusion criteria were steatorrhea above 30 g/day, gastric or pancreatic resections in the history, and serum bilirubin above 1.5 mg/dl. Patients received pancreatic extracts (acid-protected microtablets; Panzytrat -20,000; 5 x 2 capsules/day; proteases/capsule 1,000 Pharmacopoea europaea units) for 14 days followed by treatment with placebo for another 14 days or vice versa. Pain (graded from 0 to 3) and concomitant use of analgesics (N-butylscopolaminiumbromide and tramadol) were recorded by diary. Physical examination and blood chemistry were done at day -1, 15 and 29. Quantitative stool fat was determined at days -2/-1, 13/14 and 27/28. 43 patients completed the studies. Pain improved in most patients irrespective of whether they started with placebo or verum. There was no significant difference between both treatment arms. We conclude that pancreatic extracts are not very efficient in lowering pain.
Adult↗
Prospective randomized controlled trial of sequential treatment with corticoids and alpha-interferon versus treatment with interferon alone in patients with chronic active hepatitis B.
OBJECTIVES: A randomized controlled trial was conducted to prospectively compare the efficacy of sequential treatment with corticoids and alpha-interferon versus treatment with interferon (IFN) alone in patients with chronic hepatitis B. METHODS: Sixty patients with chronic active hepatitis B and positive serum HBV-DNA were randomized into two treatment groups (n = 20, respectively) and one control group (no treatment; n = 20). In one treatment group, patients received first an oral corticoid (2 weeks 40 mg/day and further 2 weeks 20 mg/die prednisolone); thereafter interferon-alpha (Intron A, Essex) was given as three subcutaneous injections of 2 million units per week for 3 months. In patients in whom therapy did not eliminate HBe-Ag and HBV-DNA two months after its end, a similar sequential treatment was given with the same corticoid dose but a higher IFN dose of 5 MU. In the other treatment group patients were given three subcutaneous injections of 5 MU IFN per week for 4 months. The sequential corticoid/IFN treatment at a dose of 3 x 2 MU IFN resulted in seroconversion of HBe-Ag in only 4 of 20 patients (20%). Of the remaining 16 patients 14 subjects received a repetitive corticoid/IFN therapy with the same corticoid dose but with a 3 x 5 MU dose of IFN. RESULTS: With the higher IFN dose, 6 of 14 patients had a seroconversion of HBe-Ag. Therapy with 3 x 5 MU IFN without prior corticoids resulted in a seroconversion in 8 of 20 patients (40%). Calculated for both doses, the sequential corticoid/IFN therapy eliminated HBe-Ag and HBV-DNA in 10/20 patients (50%); therapy with IFN alone was almost as effective (40% seroconversion) (p > 0.05 for comparison of seroconversion rates by chi 2-test). Seroconversion of HBe-Ag and elimination of HBV-DNA occurred in parallel and were associated with a decrease of serum transaminases and a regression of inflammatory activity on rebiopsy. In the control group there was no spontaneous seroconversion of HBs-Ag, HBe-Ag or HBV-DNA. CONCLUSIONS: The present results show that in many patients who failed to respond to a sequential therapy with corticoids and 2 MU IFN, the higher IFN dose of 5 MU effectively eliminated HBe-Ag and HBV-DNA. Sequential corticoid/IFN therapy and therapy with IFN alone eliminated HBe-Ag and HBV-DNA in a similar percentage of patients. Further statistical analysis showed that, in particular, patients with low transaminases benefit from prior corticoid treatment. In all groups, patients with low serum HBV-DNA and a short history of infection had the best treatment results.
Adolescent↗
[Liver function tests in a clinical comparison].
Various liver function tests were evaluated in regard to a quantitative estimation of the impairment of liver function related to the Child-Pugh classification in 32 patients with cirrhosis. Only the ICG-test revealed significant differences between healthy subjects and cirrhotic patients in stadium Child A, B and C. When ICG-dye retention values were plotted as a function of the individual score units of the Child-Pugh classification, a linear relationship with a correlation coefficient of 0.7 was obtained. In contrast to the ICG-test, the MEGX- and galactose elimination capacity (GEC)-test as well as static parameters of liver function (cholinesterase activity, prealbumin concentration, coagulation factor V and VII) resulted in less significant differentiation of the various Child classes. The MEGX-test, GEC, concentration of prealbumin, coagulation factor V and VII were only weakly correlated to the score units of the Child-Pugh index. The results of this study indicate that of all evaluated parameters only the ICG-test is suitable for objective and graduated analysis of liver function in patients with cirrhosis.
Cholinesterases↗
[Gastrointestinal diseases in perioperative risk assessment].
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Diagnostic Tests, Routine↗
[Applicability of CCK receptor antagonists in physiologic and therapeutic studies].
The development of potent and specific CCK-receptor antagonists made it possible to evaluate the physiological role of CCK for various gastrointestinal functions. The results of these studies show that CCK is the hormone which principally mediates meal-induced gallbladder emptying. In addition, CCK appears to play an important role in maintaining the fasting muscular tone of the gallbladder. In contrast, CCK-antagonists could inhibit only about 50% of the meal-stimulated pancreatic exocrine secretion. Because of their marked relaxing effect on the gallbladder, CCK-antagonists might become an important clinical tool for treatment of gallbladder spasms and colics. On the other hand, long-term application of CCK-antagonists will increase the risk of stone formation in the gallbladder. CCK-antagonists also had beneficial effects in some animal models of acute pancreatitis. As yet, it is unclear whether CCK-antagonists might become useful for the treatment of human pancreatitis. Since CCK-antagonists only slightly inhibited pancreatic growth, it is unlikely that they will exert major inhibitory effects against growth of pancreatic carcinoma. CCK-antagonists failed to alter gastric emptying of a normal mixed solid-liquid meal, but accelerated gastric emptying of purely liquid meals. Thus, CCK-antagonists are not likely to become useful agents to treat alterations of gastric emptying. The studies with CCK-antagonists further showed that CCK plays only a minor role in the regulation of the motility of the small and large intestine. CCK is probably not involved in the regulation of the gastrocolonic response after a meal. Some reports indicate that CCK-antagonists might increase colonic transit and might therefore be useful to treat constipation.
Animals↗
Involvement of free radicals in the pathophysiology of chronic pancreatitis: potential of treatment with antioxidant and scavenger substances.
The present work reviews the evidence for an involvement of free radicals in the pathophysiology of chronic pancreatitis and the potential of treatment with antioxidant and scavenger substances. Preliminary results indicate that exposure of isolated pancreatic acinar cells to a reaction mixture containing hypoxanthine, xanthine oxidase, and chelated iron causes cell damage and death probably due to generation of superoxide anion and hydrogen peroxide. It still needs to be analyzed which scavengers and antioxidants are able to ameliorate the damage due to oxidant stress in cell models. Such knowledge from cellular studies might help to plan therapeutical trials to evaluate potentially effective antioxidants and scavengers in the experimental animal and in patients with pancreatitis. As yet there are no published studies about the role of free radicals in animal models of chronic pancreatitis. This fact is probably due to the shortcomings of the animal models available. Recent studies presented evidence that activation of oxygen-derived free radicals occurs in patients with chronic pancreatitis. There is also some evidence that the dietary intake of antioxidants may be reduced in patients with chronic pancreatitis. It was suggested that such reduction of antioxidant defenses in the face of an increased demand due to heightened induction of P450 activities may facilitate lipid peroxidation. However, as yet, there is no direct evidence that a reduction of dietary antioxidants with a simultaneous increase in P450 activity is the primary mechanism which initiates chronic pancreatitis without contribution of other factors.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Wilson disease: clinical presentation, treatment, and survival.
OBJECTIVE: To evaluate the diagnostic features, clinical course, and overall long-term survival of patients with Wilson disease. DESIGN: Retrospective cohort study with a mean follow-up period of 14.2 years. SETTING: A university medical center and a community hospital. PATIENTS: Fifty-one consecutive patients with Wilson disease were evaluated between 1957 and 1989. INTERVENTIONS: Patients were treated with D-penicillamine (600 to 1800 mg/d). Two patients with end-stage liver disease had liver transplantation. MAIN RESULTS: Initial symptoms occurred at a mean age of 15.5 years. At diagnosis, the most common neurologic signs were dysarthria, tremor, writing difficulties, and ataxia followed by hypersalivation and headache. Somatic symptoms included abdominal pain, hepatomegaly, splenomegaly, cirrhosis of the liver, and thrombocytopenia. The mean serum concentrations of ceruloplasmin and copper were 44 mg/L and 4.7 mumol/L, respectively. The mean basal urinary copper excretion was 5.5 mumol/d, and the mean hepatic copper concentration was 19.6 mumol/g dry weight. Free serum copper concentration (mean, 2.7 mumol/L) was a reliable indicator of disease and was useful in assessing the effectiveness of therapy (values less than 1.6 mumol/L). Treatment with D-penicillamine improved most of the hematologic and neurologic abnormalities but had little effect on hepatomegaly and splenomegaly and did not reverse cirrhosis. Two patients died of fulminant hepatic failure during the observation period, whereas two others with end-stage liver disease had successful liver transplantation and remain asymptomatic. Long-term survival of patients with Wilson disease was similar to that of age- and sex-matched controls. CONCLUSION: Our results suggest that long-term treatment of patients with Wilson disease with D-penicillamine can relieve symptoms and improve prognosis.
Adolescent↗
[Serum ferritin and hemochromatosis].
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Adult↗
Effects of cholecystokinin-receptor blockade on pancreatic and biliary function in healthy volunteers.
This study used the specific cholecystokinin (CCK)-receptor antagonist loxiglumide to evaluate whether endogenous CCK, which is released after a meal, regulates pancreatic and biliary functions. Eight healthy volunteers were studied twice on separate days. The subjects received a continuous intraduodenal infusion of a 750-kcal liquid test meal for 2 hours either with or without IV infusion of 5 mg.kg-1.h-1 of loxiglumide. Loxiglumide at this dose abolishes the actions of CCK at various target organs including gallbladder and pancreas, when given at doses that mimic postprandial plasma concentrations of CCK. Loxiglumide markedly decreased the meal-stimulated outputs of amylase, trypsin, and chymotrypsin by 55%-70% of control values but only slightly decreased duodenal volume (25% inhibition of mean integrated secretion). Loxiglumide abolished gallbladder emptying induced by infusion of nutrients and even increased gallbladder volumes when compared with prior fasting values. Correspondingly, loxiglumide almost abolished the output of bilirubin after infusion of nutrients. However, loxiglumide failed to alter the increase in circulating concentrations of glucose, insulin, and C peptide after infusion of nutrients. The present results show that CCK is one of several factors that regulate pancreatic protein secretion after absorption of nutrients. However, CCK is probably not involved in regulation of pancreatic secretion of fluid. In contrast, gallbladder function is mainly regulated by CCK, both in terms of its emptying after intestinal absorption of nutrients and in terms of maintenance of its fasting volume. Cholecystokinin does not play a major physiological role as an insulinotropic factor.
Adult↗
Effects of the seleno-organic substance Ebselen in two different models of acute pancreatitis.
This study evaluated the effects of the seleno-organic substance Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one] in two models of acute hemorrhagic and acute edematous pancreatitis. Ebselen is known to catalyze glutathione peroxidase-like reactions and to inhibit lipid peroxidation. Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet to mice for 66 h. Edematous pancreatitis was induced by 7-h subcutaneous injections of 50 micrograms/kg of cerulein in mice. Ebselen was given from the beginning of the CDE diet either as a subcutaneous injection of 100 mg/kg at 6-h intervals or was mixed in with the CDE diet to yield a daily dose of 100 mg/kg of Ebselen. In further experiments, Ebselen was given at various time intervals after the beginning of the CDE diet as subcutaneous injections of 100 mg/kg at 6-h intervals. In the cerulein model, Ebselen was given 5 min prior to each cerulein injection at doses from 10-500 mg/kg. Prophylactic administration of Ebselen given orally or subcutaneously significantly improved survival from 38.5% in the control group of saline-injected CDE-fed mice to 61.9 and 65.0%, respectively. Ebselen also reduced increases in serum amylase and pancreatic weight in the diet model. Therapeutic administration of Ebselen significantly increased survival only when injections were started 20 h after the beginning of the CDE diet (64%), but not when started after 40 h (44%). Similarly, increases in serum amylase and pancreatic weight due to the CDE diet were significantly reduced by Ebselen only when injections were started after 20 h but not when started after 40 h.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Effects of CCK receptor blockade on intestinal motor activity in conscious dogs.
This study employed a cholecystokinin (CCK) antagonist to evaluate whether endogenous CCK regulates fasted and fed motor patterns of the small intestine. Experiments were performed in six conscious dogs, each in duplicate. Motor activity was recorded by six strain-gauge transducers implanted along the small intestine. The effects of the CCK analogue caerulein and the CCK antagonist loxiglumide were studied in fasted and fed states. Computer analysis determined contractile frequency and area under contractions. Caerulein given as an intravenous bolus 30 min after phase III dose dependently caused a burst of phasic contractions preceded by a retrograde giant contraction. Continuous intravenous infusion of 10 mg.kg-1.h-1 loxiglumide completely abolished the effects of 10 ng/kg caerulein, which increases plasma CCK immunoreactivity to postprandial levels. Loxiglumide, at 10 mg.kg-1.h-1, markedly reduced the increase in phasic contractions due to a supraphysiological dose of 50 ng/kg caerulein to 14 +/- 6(SD)% of the control without loxiglumide (P less than 0.01). The motor activity stimulated by the cholinesterase inhibitor neostigmine (10 micrograms/kg) was not altered by loxiglumide. Loxiglumide given in the fasted state decreased contractile frequency from 9.5 +/- 0.7 to 8.1 +/- 0.6/min and reduced the area under contractions during phase II to 81 +/- 5% of the control without loxiglumide (P less than 0.05). Loxiglumide also decreased contractile frequency during the fed state from 9.7 +/- 0.6 to 8.3 +/- 0.5/min and reduced the area under contractions to 78 +/- 6% of the control without loxiglumide (P less than 0.05). Thus loxiglumide acts as a specific antagonist of the actions of CCK on small intestinal motor activity in the dog. Loxiglumide, at a dose that abolishes actions of endogenous CCK, significantly decreased fasting motor activity during phase II. Loxiglumide also significantly reduced motor responses to feeding but did not prevent interruption of migrating motor complex cycle by a meal. CCK plays a physiological role in regulation of fasting and fed motor activity of small intestine, although other factors in addition to CCK mediate meal-induced motor activity.
Animals↗
[Inhibition of pancreatic growth by exogenous and endogenous factors].
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Animals↗