Prandial lactate infusion inhibits spontaneous feeding in rats

To investigate the acute effects of lactate on spontaneous feeding, we infu sed lactate in the hepatic portal Vein (0.5, 1.0, and 1.5 mmol lactate/meal ) or in the vena cava (1.0 and 1.5 mmol lactate/meal) of ad libitum-fed rat s during their first spontaneous nocturnal meal. Infusions (5 min, 0.1 ml/m in) were remotely controlled, and a computerized feeding system recorded me al patterns. In separate crossover tests, meal size decreased independent o f the infusion route after 1.0 and 1.5 mmol but not after 0.5 mmol lactate. The subsequent intermeal interval (IMI) tended to decrease only after vena cava infusion of 1.0 mmol lactate. The size of the second nocturnal meal i ncreased after the 1.0 mmol lactate infusion. Hepatic portal infusion of 1. 5 mmol lactate increased the satiety ratio [subsequent IMI (min)/meal size (g)] by 175%, which was higher than the insignificant 43% increase after ve na cava infusion. Hepatic portal infusion of 1.5 mmol lactate also increase d systemic plasma lactate but not glucose concentration at 1 min after the end of infusion. The results are consistent with the idea that meal-induced increases in circulating lactate play a role in the control of meal size ( satiation). Moreover, the results suggest that lactate also contributes to postprandial satiety and that the liver is involved in this effect. The exa ct mechanisms of lactate's inhibitory effects on feeding and the site(s) wh ere lactate acts to terminate meals remain to be identified.