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Biomedical subjects

R J Lieverse

Publications and source records attributed to R J Lieverse.

26 records · Page 2Linked to original sources

Bombesin reduces food intake after a preload in man by a cholecystokinin-independent mechanism.

1. A double-blind study was undertaken to determine whether the infusion of bombesin inhibits the intake of a carbohydrate-rich meal, consumed 15 min after a 300 ml banana shake, in nine lean healthy subjects and whether the possible inhibition of food intake by bombesin is mediated by cholecystokinin. 2. The amount of food eaten during infusion of bombesin (267 +/- 60 g) and bombesin combined with the cholecystokinin-receptor antagonist loxiglumide (269 +/- 39 g) was slightly (P = 0.09) less than during saline infusion (384 +/- 40 g). In addition, preprandial feelings of hunger were significantly less during infusion of both bombesin and bombesin combined with loxiglumide. 3. In conclusion, infusion of bombesin tends to inhibit the intake of a carbohydrate-rich meal after a preload by a cholecystokinin-independent mechanism.

Adult↗

Bombesin reduces food intake in lean man by a cholecystokinin-independent mechanism.

This double blind study was undertaken to determine whether infusion of bombesin (BBS) inhibits the intake of a carbohydrate-rich meal in nine lean healthy subjects and whether inhibition of food intake by BBS is mediated by cholecystokinin (CCK). During infusion of BBS, the amount of food eaten was decreased compared to that after saline infusion (482 +/- 74 vs. 602 +/- 68 g; P < 0.01). Subjective criteria of satiation were also significantly affected by BBS infusion (P < 0.05). Administration of the CCK receptor antagonist loxiglumide (CR1505) to six of the subjects did not prevent the decrease in food intake due to BBS (365 +/- 69 g) or the subjective criteria for satiety. Furthermore, the amount of food eaten during loxiglumide treatment alone (537 +/- 109 g) was not different from that during control saline infusion. In conclusion, infusion of BBS inhibits the intake of a carbohydrate-rich meal by a CCK-independent mechanism.

Adult↗

Gastrointestinal disturbances with obesity.

Steatosis and steatohepatitis are associated with obesity. Despite florid histological changes, patients with non-alcoholic steatohepatitis generally remain asymptomatic, and it usually runs a relatively benign course. An elevated insulin level may be important in the pathogenesis. There is a marked regression of fatty changes after weight reduction. In obese subjects the risk of developing gallstones is increased due to an increased saturation of gallbladder bile with cholesterol and possible gallbladder stasis. During weight reduction with very low calorie diets the incidence in gallstones increases probably because of an increased saturation of bile during the loss of weight. Ursodeoxycholic acid appears to be a promising prophylactic agent. Chenodeoxycholic acid is not useful for these subjects. There is controversy over whether obesity contributes to gastroesophageal reflux and gastric emptying disturbances. There are changes in gastrointestinal peptide plasma levels in obesity but it is not clear if this contributes to its development. The risk for high-risk colorectal adenomas and carcinomas is reported to be increased in obese males. Vertical banded gastroplasty and gastric bypass procedures are nowadays the surgical options for the treatment of obesity. Nutritional deficiencies, particularly of vitamin B12, folate and iron are common after gastric bypass and must be sought and treated. Dumping is another potential complication of this operation. If stenosis and gastric outlet obstruction develop endoscopic dilatation is a good therapeutic option.

Animals↗

Cholecystokinin and satiation.

Peripheral signals from stomach and small intestine are believed to induce satiation. In experimental animals, satiation factors can be transfused pointing to the humoral nature of the signal. Cholecystokinin (CCK) may be an important mediator, since infusion of exogenous CCK has been demonstrated to induce satiation and to inhibit gastric emptying. However, whether this effect of CCK is a physiological or pharmacological event is a matter of controversy. The significance of exogenous CCK or stimulation of endogenous CCK in the possible treatment of obesity requires further study.

Animals↗

Relationship between hunger and plasma cholecystokinin during weight reduction with a very low calorie diet.

Based on a large number of studies in various species, cholecystokinin (CCK) is considered to function as an important regulator of satiety. The present study was undertaken to determine the relationship between hunger score and basal and postprandial plasma CCK secretion, in six obese subjects before and after weight loss with modified fasting. Modified fasting (modifast, 240 kcal/day) for ten weeks induced a mean weight loss of 23 kg. The hunger score was reduced by about 75%. However, basal and plasma CCK release induced by 80 kcal of modifast were not different before and after ten weeks of modifast treatment. Thus, the reduction of hunger during modified fasting is not mediated by circulating CCK.

Adult↗