The aim of the present review is to synthesise and summarise our recent knowledge on the involvement of cholecystokinin (CCK) and gastrin peptides and their receptors in the control of digestive functions and more generally their role in the field of nutrition in mammals. First, we examined the release of these peptides from the gut, focusing on their molecular forms, the factors regulating their release and the signalling pathways mediating their effects. Second, general physiological effects of CCK and gastrin peptides are described with regard to their specific receptors and the role of CCK on vagal mucosal afferent nerve activities. Local effects of CCK and gastrin in the gut are also reported, including gut development, gastrointestinal motility and control of pancreatic functions through vagal afferent pathways, including NO. Third, some examples of the intervention of the CCK and gastrin peptides are exposed in diseases, taking into account intervention of the classical receptor subtypes (CCK1 and CCK2 receptors) and their heterodimerisation as well as CCK-C receptor subtype. Finally, applications and future challenges are suggested in the nutritional field (performances) and in therapy with regards to the molecular forms or in relation with the type of receptor as well as new techniques to be utilised in detection or in therapy of disease. In conclusion, the present review underlines recent developments in this field: CCK and gastrin peptides and their receptors are the key factor of nutritional aspects; a better understanding of the mechanisms involved may increase the efficiency of the nutritional functions and the treatment of abnormalities under pathological conditions.

The present study was conducted to investigate the effects of ghrelin on gastric acid and pepsin secretion, as well as the mRNA expression of gastrin, somatostatin (SS) and receptors for growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in gastric mucosal cells in vitro. Gastric mucosal cells were isolated from 5-week-old weanling piglets and exposed for 4 h to 3×10−2, 3×10−1, 3, 3×10 and 3×102 nmol/l of h-ghrelin, respectively after 30-h incubation in DMEM/F-12. Pepsin activity in culture medium, cell viability and H+-K+-ATPase activity, as well as mRNA expression of gastrin, SS, GHR and IGF-1R in gastric mucosal cells were determined as response criteria. The experiment was repeated three times. Ghrelin significantly (P<0·05) increased H+-K+-ATPase activity of gastric mucosal cells at 3×10−1, 3 and 3×10 nmol/l of h-ghrelin. However, no significant changes were observed either in pepsin activity or the cell viability after ghrelin treatment. The mRNA expression of gastrin and SS was significantly increased in gastric mucosal cells exposed to h-ghrelin at 3×10−1 and 3 nmol/l (P<0·05). H-ghrelin significantly increased IGF-1R but not GHR mRNA expression at 3×10−1, 3 and 3×10 nmol/l of h-ghrelin (P<0·05). Ghrelin acts on gastric mucosal cells from weanling piglets to regulate the H+-K+-ATPase activity and mRNA expression of gastrin, SS, and IGF-1R in vitro.

The aim of this study was to investigate the effect of feeding frequency on total tract digestibility and plasma glucose, insulin, urea, gastrin and cortisol concentrations at rest and following exercise in seven Standardbred horses in race training. The horses were fed every 12 h (twice a day, 2TD) and every 4 h (six times a day, 6TD) for 25 days, in a cross-over design. The diet (64% grass hay, 36% concentrates on weight basis) was fed at twice the maintenance energy requirement. Blood samples were taken every hour for 24 h on day 17, total collection of urine and faeces was made on days 19–21 and an intensive exercise test was performed on day 25. Altering feeding frequency caused small variations in diurnal plasma glucose, urea, gastrin and cortisol concentrations and did not affect total tract nutrient digestibility. There was an increase in the mean diurnal plasma urea concentration on the 2TD regime and low levels of plasma insulin were observed 7 h after feeding 2TD. The response to intensive exercise on heart rate, plasma lactate and plasma glucose was similar on both treatments but the plasma insulin concentration was higher following exercise in the 2TD regime, indicating that post-exercise glucose metabolism was altered. In conclusion, this study shows that feeding athletic horses only 2TD caused metabolic signs resembling those observed during feed deprivation (low levels of plasma insulin and an increased diurnal plasma urea concentration) and an altered post-exercise glucose metabolism, but did not affect the digestive response.

We studied the effects of a fermentable sugar-alcohol (lactitol) on the concentrations of enteroglucagon and gastrin in the blood of rats for 7·5 h after feeding. The control and treatment groups were fed on semi-purified diets containing either non-fermentable cellulose or lactitol respectively, at 100 g/kg. Compared with the cellulose-fed group, the animals fed with lactitol had higher levels of enteroglucagon (5−10 times higher than control; P < 0·05) and lower serum gastrin (70−80% of control; P< 0.·05) for several hours after the withdrawal of feed. In contrast, varying the level of dietary lipid (maize oil) over a range of 8−120 g/kg had no effect on the release of either peptide. These results suggest that poorly absorbed fermentable dietary carbohydrate stimulates postprandial plasma enteroglucagon and inhibits serum gastrin release in the rat. The mechanism is uncertain but an endocrine response by the colon to fermentation products seems probable.

The effect of dietary fats on gastrin in the pyloric antrum and plasma of Wistar rats was examined. Two different age-groups of rats were fed on three different diets in which fat was in the form of menhadenoil (MO), hydrogenated coconut oil (CO) and safflower oil (SO) respectively. Control groups were fed on normal laboratory diet. Each diet was isoenergetic and no group showed significant differences in either food intake or weight gain during the experiment. Weaner rats fed on the MO diet exhibited significant reductions in both antral (P = 0.047) and plasma (P = 0.002) gastrin concentrations when compared with age-matched controls. Likewise, adult rats fed on the MO diet exhibited significant reductions in both antral (P = 0.008) and plasma (P = 0.002) gastrin concentrations. In addition, adult rats fed on the CO diet exhibited significant reductions in both antral (P = 0.047) and plasma gastrin(P = 0.002) concentrations. Rats from both age-groups fed on the SO diet exhibited no significant differences in gastrin concentrations when compared with their respective control groups. These findings indicate that the composition of dietary fat can have profound effects on both tissue and plasma concentrations of gastrin in rats.

The flow pattern of unilateral parotid saliva in sheep was compared when a total of 800 g lucerne (Medicago sativa) hay was offered as one, two, four or eight distinct meals. These patterns were related to changes in the tonicity of rumen fluid and plasma and to plasma concentrations of gastrin and pancreatic polypeptide. Sheep having ad lib access to hay overnight were offered fresh hay from 08.00 to 09.00 hours and were then given one, two, four or eight meals of fresh hay according to a schedule such that the mean deprivation period was 6.5 h for each meal frequency-size. Neither the peak in saliva flow rate nor the time of this peak differed among the different meal sizes. The flow rate decreased rapidly after reaching a maximum at 3.2 min into the meal. After 7 min of eating, the tonicity of plasma and rumen fluid had increased by only 2.2 and 8.2 mosmol/kg respectively. These increases would not cause the rapid decline in parotid flow observed after 3.2 min of eating. There was no postprandial change in the concentration of gastrin in jugular plasma. However, it did increase significantly (P = 0.0043) from 16 to 4 min before eating commenced. There was a postprandial peak in plasma pancreatic polypeptide concentration after 4.5 min of eating. However, the parotid flow rate remained low after the concentration of this peptide returned to prefeeding levels. The rapid decrease in parotid secretion rate observed early in the meal may be due to subsiding central excitation rather than to an inhibitory factor limiting production.