A possible central opiate mechanism involved in the inhibition of food intake and reticular motility by duodenal DL-lactic acid infusion in sheep.
Intraduodenal infusion of DL-lactic acid was performed in sheep fitted with a permanent cannula into the lateral cerebral ventricle and nichrome electrodes on the reticulum in order to record its electrical activity during periods of controlled food intake in a series of experiments subsequently repeated in animals fasted for 12 hours. A solution of 0.2M DL-lactic acid was infused at a rate of 1 ml/min during the 1st hour of a 3-hour period of feeding with or without previous intracerebroventricular (ICV) or IV administration of naloxone (2.4 and 10 micrograms/kg). During lactic acid infusion, the food intake and the frequency of reticular contraction (measured during eating) were reduced by 48% and 19%, respectively--these effects being prolonged for the 1st hour after infusion. Previous ICV administration of naloxone (2.4 micrograms/kg) partially blocked the effects of lactic acid on food intake (63%) and frequency of reticulum contractions (58%). These effects were abolished for the largest dose of naloxone (10 micrograms/kg) administered ICV, whereas its IV administration did not affect significantly the effects of lactic acid. It is concluded that the duodenal lactic acid concentration may have a role in the control of food intake by a mechanism involving central opiate mediation.