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. (Gut 1995; 36: 176-179)

No abstract

In the rat model, polyunsaturated vegetable oil has been shown to stimulate pancreatic secretion and promote pancreatic carcinogenesis, whereas dietary fish oil has been found to protect against carcinogenesis. Because cholecystokinin (CCK), a hormonal polypeptide secreted from the upper small intestine after food stimulation, is the most important known humoral stimulus of pancreatic secretion and also because this gut hormone has been shown to promote pancreatic carcinogenesis in the rat, we decided to study the effects of various triglycerides on CCK secretion in this species. Small amounts (2.5 mL) of corn oil, beef tallow, fish oil, medium-chain triglyceride (MCT) oil or saline (control) were administered to groups of five fasted rats. Plasma CCK levels were measured using a specific and sensitive radioimmunoassay. The maximal CCK increments for corn oil, beef tallow, fish oil and MCT oil were 3.0 +/- 0.5, 2.1 +/- 0.6 and 7.2 +/- 0.4 pmol/L, respectively. All the increments were significantly greater (p less than 0.05) than the change found after saline administration (-0.8 +/- 0.3 pmol/L). In another experiment, plasma CCK levels after intragastric administration of MCT oil reached a peak increment of 6.4 +/- 0.4 pmol/L after 240 min and continued to be significantly increased for the entire 480-min study period. It was concluded that all four triglycerides caused a significant CCK release in the rat and that the MCT oil was the most powerful stimulator of CCK secretion among the triglycerides studied.

Cholecystokinin (CCK) has been shown to promote pancreatic growth and azaserine-induced pancreatic carcinogenesis in rats. The present study was carried out to determine effects of CCK on pancreatic growth and carcinogenesis in the N-nitrosobis(2-oxopropyl)amine (BOP) hamster model. One hundred male Syrian golden hamsters were injected s.c. once weekly with 20 mg BOP/kg body wt at 6, 7 and 8 weeks of age, and divided into four groups of 25 animals each, which received one of the following treatments (once daily, 3 days/week for 16 weeks): gelatin; CR-1409, a potent CCK-receptor antagonist; CCK-8, 2.5 micrograms/kg body wt; or CCK-8 in combination with CR-1409 (30 min before CCK treatment). The animals were killed after 19 weeks. The growth of the pancreas but not the incidence of pancreatic (pre)neoplastic lesions was enhanced by CCK-8. CR-1409 did not influence the effect of CCK on pancreatic growth.

The effect of cholecystokinin-33 on gastric emptying was studied in eight healthy men. The test meal was a firm custard pudding, labelled with 99mTc-Chelex-100 particles. Gastric emptying rate was measured, using a dual-headed gamma camera, and was expressed as the half time of the emptying curve. Plasma cholecystokinin concentrations were determined by radioimmunoassay. Subjects were studied three times: (i) during infusion of saline; during cholecystokinin infusion, (ii) 0.375 IDU kg-1 h-1 and (iii) 0.75 IDU kg-1 h-1. Furthermore, plasma cholecystokinin was determined after a regular meal. During saline, plasma cholecystokinin increased minimally. After the regular meal it increased from 1.6 to 6.5 pmol l-1 at 30 min, decreasing to 5.3 pmol l-1 at 60 min. During the lower and higher doses of cholecystokinin it increased from 1.0 and 1.4 to 4.5 and 7.3 pmol l-1, respectively. The lower and higher doses significantly (P less than 0.05) increased half emptying time, from 45 +/- 8 to 86 +/- 17 and 198 +/- 50 min, respectively. Cholecystokinin is most likely a physiological hormonal mediator of fat-induced inhibition of gastric emptying.