Postprandial insulin action relies on meal composition and hepatic parasympathetics: dependency on glucose and amino acids
Meal, parasympathetics & insulin action
Ricardo A. Afonso, Joana M. Gaspar, Iva Lamarão, W. Wayne Lautt, M. Paula Macedo
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. 1) IS was assessed before and after liquid test meal administration (10 ml.kg-1, intra-enteric): 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). 2) Separately, fasted animals were submitted to hepatic parasympathetic denervation (DEN); IS was assessed before and after GAL (n=4) or GA administration (n=4).
1) 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< 0.001; 143.6±26.0% potentiation of IS); GA increased IS from 109.0±6.6 to 240.4±18.0 mg glucose/kg bw (p<0.001; 123.1±13.4% potentiation). None of the other meals potentiated IS. 2) GAL and GA did not induce a significant insulin sensitization in DEN animal.
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.