Type II diabetic patients with no clinical evidence of neuronal dysfunction have a significantly more rapid rate of gastric emptying of a solid high-carbohydrate meal when compared with nondiabetic control subjects.
SUMMARYThe effect of jejunal bypass on pancreatic growth and plasma cholecystokinin (CCK) was investigated in rats. Rats underwent bypass of jejunum or sham operation. Rats with jejunal bypass were further divided into three groups; one group received a continuous infusion of a partially hydrolysed liquid diet (Vital) into the bypassed jejunum; a second group received the nutrient solution mixed with trypsin and infused into the bypassed jejunum; the third bypass group did not receive infusion of nutrient or trypsin into the jejunum. Jejunal bypass alone did not significantly stimulate pancreatic growth or DNA content at one or two weeks postoperative. Infusion of nutrient solution into the bypassed jejunum stimulated pancreatic growth and DNA content, with maximal increases of 185 % and 181 % for pancreatic weight and DNA content, respectively, at two weeks. This coincided with significant increases in postabsorptive plasma CCK concentrations. Infusion of pancreatic proteases into the bypassed jejunum partially reversed the effects of nutrient infusion. These results suggest that exclusion of bile-pancreatic juice or pancreatic proteases from the jejunum does not lead to maximal release of CCK unless the jejunum receives luminal nutrients. It is proposed that CCK release from rat jejunum occurs spontaneously in the absence of pancreatic proteases, and that luminal nutrients in bypassed jejunum increase plasma CCK and stimulate pancreatic growth by maintaining synthesis of CCK.Exclusion of bile-pancreatic juice (BPJ) from the proximal small intestine stimulates pancreatic secretion and growth,' and increases plasma cholecystokinin (CCK) in the rat.23 These phenomena are attributed to loss of feedback inhibition of CCK release by luminal pancreatic proteases.45 Transposition of the duodenum to lie between the jejunum and ileum also stimulates pancreatic growth in the rat.6 We suggested that this was caused by the consequent diversion of BPJ from the jejunum to the ileum, resulting in loss of protease induced inhibition of CCK release from the jejunum.I The results of this latter study6 indicated that the jejunum may be the major site of feedback control of CCK release in the proximal small intestine in the rat, because in that model BPJ was diverted from the jejunum, but not
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