Postprandial insulin action relies on meal composition and hepatic parasympathetics: dependency on glucose and amino acids: Meal, parasympathetics & insulin action.

Abstract Insulin sensitivity (IS) increases following a meal. Meal composition affects postprandial glucose disposal but still remains unclear which nutrients and mechanisms are involved. We hypothesized that gut-absorbed glucose and amino acids stimulate hepatic parasympathetic nerves, potentiating insulin action. Male Sprague–Dawley rats were 24 h fasted and anesthetized. Two series of experiments were performed. (A) IS was assessed before and after liquid test meal administration (10 ml.kg −1 , intraenteric): glucose + amino acids + lipids (GAL, n =6); glucose ( n =5); amino acids ( n =5); lipids ( n =3); glucose + amino acids (GA, n =9); amino acids + lipids ( n =3); and glucose + lipids ( n =4). (B) Separately, fasted animals were submitted to hepatic parasympathetic denervation (DEN); IS was assessed before and after GAL ( n =4) or GA administration ( n =4). (A) Both GAL and GA induced significant insulin sensitization. GAL increased IS from 97.9±6.2 mg glucose/kg bw (fasting) to 225.4±18.3 mg glucose/kg bw ( P P To achieve maximal insulin sensitization following a meal, it is required that gut-absorbed glucose and amino acids trigger a vagal reflex that involves hepatic parasympathetic nerves.