Glucose is the major component controlling irregular spike activity after feeding in primates.

The aim of this study was to examine the caloric components responsible for the postprandial increase in small intestinal electrical spike activity. Monopolar electrodes were surgically placed on the jejunum and on the ileum of 8 cynomolgus monkeys 2 wk before study. Myoelectric activity was measured after a 14-h fast, and was compared with activity seen either after feeding or after intragastric injection of test solutions [MCT oil (100 kcal), Crisco oil (100 kcal), glucose (40 kcal), glucose polymer (100 kcal), or an equivalent volume of saline control]. Data were analyzed by a spike train analysis program to provide activity front cycle length, quantitative measurements of the activity, front spike activity, and frequency of irregular spike activity before and after feeding. Oral feeding of a predominantly carbohydrate banana meal or an intragastric solution resulted in a significant delay in periodic activity fronts and a significant increase in jejunal postprandial spike activity over fasted irregular spike activity. Increases in postprandial spike activity appeared to parallel increases in the serum glucose concentration. These studies demonstrate that phasic fasting spike activity occurs in the primate small intestine and that this activity is disrupted by oral feeding. Carbohydrates were responsible for the increased postprandial spike activity and for the disruption of regular spike activity after meals. A local effect of the carbohydrate is the most likely explanation. With carbohydrate or fat solutions, changes can occur in postprandial spike activity independent of the delay in periodic activity front activity. The increase in postprandial spike activity and the postprandial delay in periodic activity front activity appear to be controlled through separate mechanisms.