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Acta Physiologica 2012; Volume 206, Supplement 693
Joint FEPS and Spanish Physiological Society Scientific Congress 2012
9/8/2012-9/11/2012
Santiago de Compostela, Spain
CYSTEINE ACTIVATION OF MEAL-INDUCED INSULIN SENSITIZATION IS DEPENDENT OF THE PARASYMPATHETIC NERVES
Abstract number: O318
Gaspar1 Joana M., Afonso1 Ricardo A., Martins2 Fátima O., Macedo3 M. P.
1CEDOC, 1Centro de Estudos de Doenas Crnicas (CEDOC), Faculdade Cincias Mdicas, Universidade Nova de Lisboa, 1169-056 Lisbon,
2CEDOC, CNC, Centro de Estudos de Doenas Crnicas (CEDOC), Faculdade Cincias Mdicas, Universidade Nova de Lisboa, 1169-056 Lisbon;Centre for Neurosciences and Cell Biology, University of Coimbra,
3CEDOC; APDP-ERC, Centro de Estudos de Doenas Crnicas (CEDOC), Portuguese Diabetes Association (APDP-ERC), Lisbon, Portugal Faculdade Cincias Mdicas, Universidade Nova de Lisboa, 1169-056 Lisbon;
Objectives:
The increment in hypoglycemic insulin action following a meal, ie, meal-induced insulin sensitization (MIS)regulates postprandial glucose homeostasis. We have described that peripheral postprandial glucose disposal requires the presence of glucose and amino acids in the intestine to trigger MIS. MIS is abolished if hepatic parasympathetic nerves are ablated. However it remains to be clarified which specific amino acids are involved in MIS activation.
Cysteine is a semi-essential amino acid and a substrate for glutathione synthesis, playing a role in postprandial glucose homeostasis. Our hypothesis is that cysteine is a vital amino acid for the feeding signal that induces the MIS.
Materials:
After 24h fast, female Wistar rats with 9-weeks old were used. N-acetyl-cysteine (NAC, 1mmol/kg; 15ml/h) was administered intra-enterically, as a source of cysteine. Immediately after, each animal was submitted to an intra-enteric glucose tolerance test (IEGTT). Insulin sensitivity was assessed 120 min after administration of the glucose (10 ml/kg, 60 ml/h), using a rapid euglycaemic clamp. In a separate set of experiments hepatic parasympathetic denervation was done in the fasted state and then NAC and glucose were administered. Blood samples were collected to assess glucose, insulin and C-peptide plasma levels.
Results:
NAC administration did not affect plasma glucose excursions throughout the IEGTT. However, NAC induced significant increase in MIS: insulin sensitivity increased from 117.45 ± 12.23 mg/kg (glucose alone) to 227.29± 17.75 mg/kg (NAC+glucose). When hepatic parasympathetic denervation was performed it prevented the increment of insulin sensitization after NAC and glucose administration (129.25 %± 14.72 mg/k). NAC administration has no effect on insulin or C-peptide.
Conclusions:
Our results suggest that cysteine is an important amino acid, which can function as a feeding signal and requires the activation of the hepatic parasympathetic nerves to induce MIS, contributing to regulation of postprandial insulin action.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 693 :O318