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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
NUTRIENT COMPOSITION AFFECTS POSTPRANDIAL GLUCOSE DISPOSAL, WHICH RELIES ON INSULIN ACTION RATHER THAN INSULIN SECRETION
Abstract number: P40
A Afonso1 R, M Gaspar2 J, Lamarao2 I, P Macedo2 M
1CEDOC, Physiology, Faculdade de Cincias Mdicas, Universidade Nova de Lisboa, Portugal,
2CEDOC, Faculdade de Cincias Mdicas, Universidade Nova de Lisboa, Portugal
Objectives:
We previously reported that peripheral hypoglycaemic insulin action increases from fasted to the fed state - meal-induced insulin sensitization (MIS). MIS is triggered at the intestine and requires hepatic parasympathetic nerves. Our hypothesis was that carbohydrates and aminoacids are required in the gut to fully activate hepatic parasympathetic nerves and thus induce MIS.
Materials:
Fasting (24 h-fast)Sprague-Dawley rats were used. Surgery involved enteric cannulation for meal administration. Two series of experiments were performed. 1) To test the effect of meal composition on insulin sensitivity (IS), IS was assessed in the 24h-fasted state and 2h after intra-enteric (IE) liquid meals (10ml/kg): glucose+aminoacids+lipids (GAL); glucose+aminoacids (GA); aminoacids+lipids (AL); glucose+lipids; glucose; aminoacids; and lipids. 2) In a 2nd protocol, fasted animals were submitted to hepatic parasympathetic denervation (DEN); afterwards, IS was assessed before and after GAL or GA administration.
Results:
1) GAL induced significant MIS activation: IS increased from 97.9±6.2 mg/kg (fasted state) to 225.4±18.3 mg/kg (p< 0.001; 133.7±23.5% potentiation of insulin action). GA also induced MIS activation (IS increased from 115.3±15.3 to 241.6 ± 35.2 mg/kg, after GA; p<0.05; 109.6 ± 9.1% potentiation). None of the other meals tested induced significant MIS. 2) In the DEN animals, neither GAL nor GA induced MIS (IS potentiation: GAL, 19.3±15.2 %; GA, 15.7±15.9 %). Insulin, C-peptide and glycemia profiles were similar after all the test meals studied. DEN and control animals also presented similar pst-meal (GAL and GA) glycemia profiles; however DEN animals showed higher C-peptide and insulinemia, which explain the similar glycemia profiles obtained following both meals.
Conclusions:
Glucose and aminoacids are required in the gut for hepatic parasympathetic activation and to fully trigger the MIS, therefore regulating postprandial glycemia.
Work supported by FCT (grants POCI/SAU-OBS/56716/2004; PIC/IC/82956/2007).
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 693 :P40