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

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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+/-183 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. (B) 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. (C) 2015 Elsevier Inc. All rights reserved.
Original languageEnglish
Pages (from-to)70-78
JournalJournal of Nutritional Biochemistry
Volume27
Issue numberNA
DOIs
Publication statusPublished - 1 Jan 2016

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Meals
Insulin
Amino Acids
Glucose
Insulin Resistance
Liver
Chemical analysis
Lipids
Parasympathectomy
Animals
Dependency (Psychology)
Denervation
Sprague Dawley Rats
Reflex
Fasting
Nutrients
Rats
Food
Liquids

Cite this

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title = "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+/-183 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. (B) 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. (C) 2015 Elsevier Inc. All rights reserved.",
keywords = "Glucose, HEART-RATE-VARIABILITY, NITRIC-OXIDE, PANCREATIC-SECRETION, Parasympathetic nerves, Protein intake, Insulin sensitivity, Insulin action, EUGLYCEMIC CLAMP, IMPROVES GLUCOSE, DIABETES-MELLITUS, TOLERANCE-TEST, OBESE ZUCKER RAT, BRAIN-GUT AXIS, Nutritional modulation of insulin sensitivity, Meal composition, VAGUS NERVE",
author = "Gaspar, {Joana Margarida Navalho} and Macedo, {Maria Paula Borges de Lemos} and Afonso, {Ricardo Alexandre da Silva Santos}",
year = "2016",
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language = "English",
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T1 - Postprandial insulin action relies on meal composition and hepatic parasympathetics: dependency on glucose and amino acids Meal, parasympathetics & insulin action

AU - Gaspar, Joana Margarida Navalho

AU - Macedo, Maria Paula Borges de Lemos

AU - Afonso, Ricardo Alexandre da Silva Santos

PY - 2016/1/1

Y1 - 2016/1/1

N2 - 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+/-183 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. (B) 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. (C) 2015 Elsevier Inc. All rights reserved.

AB - 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+/-183 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. (B) 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. (C) 2015 Elsevier Inc. All rights reserved.

KW - Glucose

KW - HEART-RATE-VARIABILITY

KW - NITRIC-OXIDE

KW - PANCREATIC-SECRETION

KW - Parasympathetic nerves

KW - Protein intake

KW - Insulin sensitivity

KW - Insulin action

KW - EUGLYCEMIC CLAMP

KW - IMPROVES GLUCOSE

KW - DIABETES-MELLITUS

KW - TOLERANCE-TEST

KW - OBESE ZUCKER RAT

KW - BRAIN-GUT AXIS

KW - Nutritional modulation of insulin sensitivity

KW - Meal composition

KW - VAGUS NERVE

U2 - 10.1016/j.jnutbio.2015.08.023

DO - 10.1016/j.jnutbio.2015.08.023

M3 - Article

VL - 27

SP - 70

EP - 78

JO - Journal of Nutritional Biochemistry

JF - Journal of Nutritional Biochemistry

SN - 0955-2863

IS - NA

ER -