[Acute pancreatitis, a protocol for diagnosis and treatment].
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Biomedical subjects
Publications and source records attributed to R J Lieverse.
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A married couple affected by necrotizing enterocolitis is described. Both had the same toxin-producing Staphylococcus aureus which was considered to be responsible for the necrotizing enterocolitis.
A 77 year-old woman developed severe hepatitis. No cause was found apart from alendronate medication. The hepatitis resolved after alendronate was stopped.
OBJECTIVE: The aim of this study was to investigate whether infusion of bombesin, when combined with a gastric preload, influence satiety and foot intake in obese and lean healthy women. DESIGN: Double blind, placebo controlled study. SETTING: Department of Gastroenterology, Leiden University Medical Center, The Netherlands. SUBJECTS: Obese (n = 7) and lean (n = 7) healthy women. INTERVENTIONS: Intravenous infusion of bombesin (0.09 nmol/kg ideal weight/h) or placebo for 165 min. Gastric preload of banana slices was administered at time 60 min. Meal ingestion started at time 75 min (banana slices). Food intake was calculated and satiety was measured by visual analog scales. RESULTS: During infusion of bombesin the amount of food eaten by the lean individuals (193+/-37 g) was significantly reduced compared to saline infusion (365+/-42 g, P < 0.05). However, bombesin induced no significant feeding suppression in obese women when compared to saline (241+/-46 vs 301+/-45 g, respectively). The decrease in food intake during bombesin infusion compared to saline was significantly greater in lean subjects (173+/-30 g) than in obese subjects (59+/-35 g; P < 0.05). Only in lean subjects subjective preprandial hunger feelings were significantly affected by bombesin infusion. CONCLUSIONS: Infusion of bombesin, when combined with a gastric preload, inhibits food intake and increases satiety in lean women. Obese women are less sensitive for these bombesin induced satiety effects.
The risk of developing gallstones is increased in obese subjects. We have investigated whether gallbladder motility in obese subjects is different from that in lean control subjects. In 25 healthy non-diabetic obese subjects and 20 age- and sex-matched lean controls, fasting gallbladder volumes, gallbladder contraction in response to cephalic vagal cholinergic stimulation by modified sham feeding (MSF) and to hormonal stimulation with cholecystokinin (CCK) were studied. Gallbladder volumes were measured during a 30-min MSF period followed 1 h later by a 1-hour continuous i.v. infusion of 0.5 IDU/kg ideal weight of CCK-33. Fasting gallbladder volumes were significantly (p < 0.001) larger in obese (47 +/- 4 cm3) compared to lean subjects (24 +/- 2 cm3). Fasting gallbladder volume was correlated with body mass index (p < 0.01). Gallbladder contraction during MSF was significantly (p < 0.01) reduced in obese (12 +/- 2%) compared to lean subjects (22 +/- 3%). CCK infusion, leading to physiological post-prandial plasma CCK levels, induced a significantly (p < 0.001) greater absolute gallbladder contraction in obese (27 +/- 3 cm3) compared to lean subjects (15 +/- 1 cm3) but the percentage gallbladder contraction was in the same range (64 +/- 3% vs. 67 +/- 4%, respectively). In addition, residual gallbladder volumes after CCK infusion were significantly (p < 0.001) larger in obese (15 +/- 2 cm3) than in lean subjects (7 +/- 1 cm3). Two groups of obese subjects were identified: one with increased (>40 cm3) and one with normal (< or = 40 cm3) fasting gallbladder volumes. Only obese subjects with increased fasting volumes showed abnormal gallbladder motility.
Several studies have demonstrated that administration of cholecystokinin (CCK) reduces food intake in several species, including humans. In animal studies CCK-receptor antagonists have been reported to increase food intake, suggesting a physiological satiety effect of CCK in these animals. In a double-blind, placebo-controlled study, we investigated the effect of the specific CCK-A receptor antagonist loxiglumide on food intake (carbohydrate-rich meal) and on subjective hunger feelings scored with visual analogue scales and food selection lists in seven healthy obese women and in seven healthy lean women. Loxiglumide was administered intravenously in a dose of 10 mg/kg ideal weight/h. For the whole group, food intake during loxiglumide (359 +/- 39 g) was not significantly different from food intake during saline infusion (333 +/- 31 g). Also, when the lean and obese subgroups were analyzed separately, no significant influence of loxiglumide on food intake was found. In addition, no significant differences in satiety scores were seen using the food selection lists or visual analogue scales. In conclusion, in the present study during infusing the CCK-A receptor antagonist loxiglumide we found no increase in preprandial satiety nor in food intake of a carbohydrate-rich meal nor in postprandial satiety in lean and obese women.
Cholecystokinin (CCK) is the major hormonal stimulus of gallbladder contraction. Both somatostatin and CCK-A receptor antagonists inhibit stimulation of the gallbladder by CCK. The aim of this study was to compare the effect of somatostatin and the CCK-A receptor antagonist loxiglumide (CR 1505) on gallbladder volume at baseline and after feeding. In random order nine healthy subjects received somatostatin (IV loading dose 125 micrograms, followed by IV infusion of 125 micrograms.h-1), loxiglumide (10 mg.kg-1.h-1) and control saline. Gallbladder volumes and plasma CCK levels were measured basally and during stimulation by an intraduodenal infusion of fat using, respectively, ultrasound and a sensitive and specific radioimmunoassay. Mean basal gallbladder volume was similar prior to the saline control (28.5 ml), loxiglumide (28.7 ml) and somatostatin (23.4 ml) experiments. In the control experiment, intraduodenal fat led to a significant increase in plasma CCK from 2.6 to 4.8 pmol.1-1, accompanied by contraction of the gallbladder to 2.0 ml. Loxiglumide induced dilatation of the gallbladder to 40 ml and prevented the any contraction in response to intraduodenal fat. During the somatostatin infusion, gallbladder volume remained the same both basally and during fat stimulation. The plasma CCK response to intraduodenal fat was exaggerated by loxiglumide and was abolished by somatostatin.
Hyperplastic colonic polyps are considered to be benign. We report the case of a man with multiple hyperplastic colon polyps who developed a colonic adenocarcinoma. The literature on the relation between hyperplastic colon polyps and adenocarcinoma is discussed.
Cholecystokinin 33 (CCK) was infused intravenously to eight healthy obese women and 10 healthy lean women of the same age, in doses that elicited plasma cholecystokinin concentrations in the physiological range. The effect of these infusions after a standardised banana 'shake' (preload) on food intake and satiety signals was compared with the effect of saline infusions in the same subjects. For the whole group food intake (mean (SEM)) (282 (29 g)) was significantly less during CCK than during saline (346 (31) g, p < 0.05). Hunger feelings tended to be less during CCK infusions. Examination of the separate subgroups showed no differences between lean and obese subjects in the satiety effects of CCK. In conclusion, under the conditions of this study, CCK significantly decreases food intake in humans, and this effect is similar for lean and obese subjects.
Somatostatin (ST) inhibits gastrointestinal motility and exocrine and endocrine secretions. In animals, ST has been demonstrated to decrease food intake. We investigated, in a randomized double-blind investigation in 10 healthy humans, the effects of an intravenous ST infusion compared to saline on subjective hunger feelings. After 1 h, a low dose of fat was given intraduodenally to induce the release of endogenous upper-intestinal satiety factors. Ninety minutes later sandwiches were served and eaten until satiation. In the first hour, when no intraduodenal fat was given, there was a significant decrease in feelings of hunger with ST (p < 0.05). During the intraduodenal fat infusion this pattern reversed with a trend towards less satiety with ST. Food intake during intraduodenal fat infusion tended to be higher during ST (305 +/- 42 g) than during saline (205 +/- 36 g) although not significantly. In the 5 h after the experiment hunger feelings were significantly less after ST. In conclusion, we found evidence for a satiety effect of ST in humans which reversed towards less satiety when intraduodenal intralipid, which presumably produced endogenous satiety factors, was given. Postmeal satiety is higher after ST.
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BACKGROUND/AIMS: Cholecystokinin (CCK) inhibits gastric emptying and may exert satiety effects in several species, including humans. Because the effects of physiological doses of CCK on satiety in humans is unclear, the satiety effects of CCK-33 in physiological levels in lean and obese subjects were studied. METHODS: CCK-33 was infused intravenously to 32 healthy men or women (14 obese, all women; 18 lean, 4 men and 14 women) in doses that elicited plasma CCK concentrations in the physiological range. The effects of these infusions on feelings of hunger, wish to eat, fullness, and prospective feeding intentions were measured on visual analogue scales and compared with saline during a 1-hour infusion period. RESULTS: The CCK infusions induced significant decreases in hunger feelings, wish to eat, and prospective feeding intentions (P < 0.05), whereas fullness tended to be increased (P = 0.054). No clear differences between lean and obese subjects were observed apart from a more marked decrease in fullness and increase in prospective feeding intentions during the 1-hour saline infusion in the lean group (P < 0.05). CONCLUSIONS: CCK infusion leading to physiological plasma levels significantly increases satiety in humans.
Satiation, the process that brings eating to an end, and satiety, the state of inhibition over further eating, may be influenced by cholecystokinin (CCK). In animal and human studies, it has been shown that infusion of exogenous CCK decreases food intake, but the doses given may well have led to supraphysiological plasma concentrations. This study was done to discover if a low dose of intraduodenal fat releasing physiological amounts of endogenous cholecystokinin exerts satiation or satiety effects, or both and if these effects could be inhibited by the CCK receptor antagonist loxiglumide. In 10 healthy lean volunteers (5 F, 5 M, mean age 26) three tests were performed in a randomised blind fashion. Intralipid 20% (6 g/h) (experiments A and C) or saline (experiment B) were given intraduodenally from 1030 until 1300. The subjects received saline (experiments A and B) or loxiglumide (experiment C) a specific CCK-receptor antagonist (10 mg/kg/h) intravenously from 0930 until 1300. At 1200 a meal was served. At regular time intervals hunger feelings were measured using visual analogue scales and food selection lists and plasma CCK was measured by radioimmunoassay. Food intake (mean (SEM)) during intraduodenal fat (206(35)g) was lower than in the control study (269(37)g, p = 0.09). Loxiglumide largely prevented the inhibitory effect of intraduodenal fat on food intake (245(30)g). From 1030 until the meal at 1200 there was a significant satiating effect of intraduodenal fat compared with the control and loxiglumide experiments according to the food selection lists, which was because of the satiating effect for the fat rich items (p<0.05). Also feelings of fullness were significantly higher during intraduodenal fat than in the control or loxiglumide experiments (p<0.05). During intraduodenal fat there was a significant increase of plasma CCK from 2.4(0.3) to 4.8(0.4) pM (p<0.001). Loxiglumide led to an exaggerated CCK release to a peak concentration of 16(2.4) pM before the meal. This study shows that in humans low dose intraduodenal fat increases satiety and satiation, mainly through the effect of CCK.
The aim of this work was to determine whether infusion of bombesin inhibits intake of a carbohydrate-rich meal in lean and obese women. A double blind study was carried out using bombesin or saline infusion. The subjects were nine lean and nine obese women of the same age. Food intake and hunger feelings were measured. During infusion of bombesin, the amount of food eaten by the lean individuals (294 +/- 55 g) was significantly less than during infusion of saline (467 +/- 69 g, P < 0.01). However, bombesin induced no significant feeding suppression in the obese women when compared to saline (431 +/- 60 vs 499 +/- 99 g). Subjective hunger feelings were significantly affected by bombesin infusion in the lean subjects only. It was concluded that bombesin infusion inhibits food intake and increases satiety in lean women, whereas obese women are less sensitive to these bombesin-induced satiety effects.
Disturbed satiety mechanisms may contribute to obesity. There has been speculation that cholecystokinin (CCK) and pancreatic polypeptide (PP) are involved in the regulation of satiety. We have therefore investigated whether there are differences between healthy lean and healthy non-diabetic obese volunteers in plasma CCK or PP release after a neuropeptidergic stimulation with bombesin and after infusion of a mixed meal. There were no differences in plasma CCK between groups either basally or in response to either form of stimulation. However, the plasma PP concentrations after the meal were significantly less in obese (2845 +/- 404 pM.min) than in lean subjects (5569 +/- 997 pM.min), whereas the plasma PP concentrations during bombesin were similar in both groups. We tested two other groups of nine obese and lean subjects to determine whether a disturbed vagal function could be the cause of the diminished plasma PP in obese persons, by studying the effect of modified sham feeding (MSF) on plasma PP. However, there were no significant differences in the plasma PP response to MSF between lean and obese subjects. We conclude that there are no differences between lean and obese persons in plasma CCK secretion in response to infusion of the neuropeptide bombesin or to ingestion of a mixed meal. However, the plasma PP after a mixed meal, is markedly diminished in obese subjects. This could not be attributed to a disturbed vagal cephalic stimulation.
CCK-33 was infused intravenously to groups of 9 lean and 9 obese volunteers in doses that elicited plasma CCK concentrations in the physiological range. The effect of these infusions on food intake and satiety signals was compared with the effect of saline infusions in the same subjects. Food intake (486 +/- 52 g; mean +/- S.E.M.) was slightly, but not significantly decreased (553 +/- 55 g after saline), and hunger and fullness feelings after eating were unaffected, in both of the two groups. We conclude that the infusion of CCK-33 to plasma levels comparable to those observed after a fatty meal does not have a major effect on food intake and postprandial hunger feelings.