Specific adaptation of gastric emptying to diets with differing protein content in the rat: is endogenous cholecystokinin implicated?

Abstract

Background-Recent studies indicate that gastric emptying may be influenced by patterns of previous nutrient intake. Endogenous cholecystokinin (CCK), whose synthesis and release can be aVected by dietary intake, has a major role in the regulation of gastric emptying. Aims-To evaluate the influence of diets with diVering protein content on gastric emptying of diVering liquid test meals and plasma CCK levels in the rat and to check whether the inhibitory eVect of exogenous CCK on gastric emptying is modified after long term intake of diets with diVering protein content. Methods-Rats were fed for three weeks with high protein, medium protein (regular), or low protein diet. On day 22 gastric emptying of a peptone meal was studied. In addition, basal and postprandial CCK levels after the diVerent dietary regimens were measured by bioassay. The time course of dietary adaptation was studied and its specificity assessed through the use of diVerent (peptone, glucose, and methylcellulose) test meals. The eVect of exogenous CCK-8 on gastric emptying was studied at the end of the adaptation period (three weeks). Results-Feeding the animals with a high protein diet for three weeks resulted in a significant (p<0.05) acceleration (by 21.2 (8.2)%) of gastric emptying while feeding with a low protein diet was followed by a significant (p<0.05) delay (by 24.0 (6.2)%) in the emptying rate. When the time course of the eVect of dietary adaptation on gastric emptying was studied, it appeared that at least two weeks are required for dietary protein to be eVective. The regulatory eVect of dietary protein on gastric emptying proved to be dependent on meal composition. Only the emptying rate of a protein containing meal (40% peptone) was significantly modified by previous dietary intake. No significant (p>0.05) changes were observed with glucose and methylcellulose meals whose emptying rates were similar in rats receiving a high protein or low protein diet. A peptone meal strongly and significantly (p<0.05) increased plasma CCK levels in rats fed a medium protein (regular) diet. Results were similar in rats receiving a low protein diet (p<0.05) but not in rats on a high protein diet (p>0.05). As a consequence, postprandial plasma levels of CCK in rats fed with a medium or low protein diet were significantly (p<0.05) higher than those in rats receiving a high protein diet. In rats on high and low protein diets, dose response curves to CCK-8 were virtually identical, suggesting that dietary protein intake has no influence on the eVect of exogenous CCK. Conclusions-These results clearly show that gastric emptying of a protein containing meal can be modified by previous dietary protein intake. This eVect, which is time dependent and meal specific, may be related to changes in endogenous CCK release which will aVect emptying rate. While the exact mechanisms underlying this adaptive response need to be studied and clarified further, these results emphasise the importance of dietary history in the evaluation and interpretation of gastri...

Influence of low protein diets on gene expression of digestive enzymes and hormone secretion in the gastrointestinal tract of young weaned piglets

“…CCK can stimulate gallbladder contraction, SS release, and pancreatic growth, and its release of enzymes (Wank, 1995), and is the basis for its older name, pancreozymin. The present research confirmed earlier reports (Green et al, 1986;Leray et al, 2003) that low protein diets enhance CCK release but did not support views (Shi et al, 1997;Hara et al, 2001) that low protein diets inhibited pancreatic enzymes including amylase and protease. However, 17% dietary CP stimulated gastric generation of SS and CCK while weakening expression of pepsinogen A and progastricsin and reducing intestinal SS release.…”

“…High protein diets increased cholecystokinin (CCK) release and pancreatic protease secretion (Green et al, 1986), but Shi et al (1997) and Leray et al (2003) argued that a low-protein diet inhibited gastric emptying through modulation of CCK release and gastric muscle sensitivity to CCK, and postprandial plasma levels of CCK were increased significantly. Pancreatic amylase production was suppressed by endogenous CCK (Hara et al, 2001).…”

Adaptation to high-fat diet accelerates emptying of fat but not carbohydrate test meals in humans

“…A high-protein diet has been shown to lead to an acceleration of emptying of a peptone meal but not of glucose or methylcellulose (29). Covasa and Ritter (9) recently demonstrated in rats that the delay in gastric emptying of saline caused by both intestinal oleate infusion and intraperitoneal CCK is attenuated by prior consumption of an HFD (54% energy from fat), whereas the delay in gastric emptying caused by intestinal infusion of maltotriose was unaffected (10).…”

Protein hydrolysate-induced cholecystokinin secretion from enteroendocrine cells is indirectly mediated by the intestinal oligopeptide transporter PepT1

“…CCK is released in response to dietary protein, particularly protein hydrolysates, and stimulates gallbladder contraction (18), pancreatic enzyme secretion (14,21), and activation of the CCK 1 receptor-mediated vagal afferent pathway to inhibit gastric motility and emptying (7,9,32,43) and reduce food intake (1,34). Although neural pathways and functional responses to protein detection by the gut wall are well established, it is unclear precisely how protein hydrolysates are detected by the intestinal I cell to stimulate CCK secretion.…”