Meal-induced insulin sensitization and its parasympathetic regulation in humans

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Abstract

In animal studies, the whole-body glucose disposal effect of insulin is low in the fasted state or after atropine infusion, but doubles after a meal, consistent with the hepatic insulin-sensitizing substance (HISS) hypothesis. We tested how a standardized test meal and atropine affected the dynamic response to insulin in humans. Insulin sensitivity was assessed in healthy male subjects (aged 28.9 +/- 1.9 years, body mass index 23.3 +/- 0.8 kg.m(-2)) by using the rapid insulin sensitivity test (RIST), which is a transient euglycemic clamp. After a 24-hour fasting period, dynamic insulin sensitivity was assessed and then repeated 100 min after the test meal. In a second protocol, the volunteers were fed the standardized test meal and intravenous atropine (0.5 mg) or saline (control group) was administered 50 min before insulin sensitivity assessment. Insulin sensitivity increased in the fed state (232.1% +/- 46.3%, n = 7) in comparison with the 24-hour fasted state. In the atropine protocol, the drug partially blocked (56.5% +/- 11.6%, n = 6) insulin sensitivity. In humans, feeding resulted in increased insulin sensitivity. The low dose of atropine in humans lead to a partial HISS-dependent decrease in insulin sensitivity. Meal- induced insulin sensitization occured in humans by a similar mechanism as that reported in other species. The sensitization process was regulated by a cholinergic 'feeding signal.'
Original languageEnglish
Pages (from-to)880-888
Number of pages9
JournalCanadian Journal Of Physiology And Pharmacology
Volume86
Issue number12
DOIs
Publication statusPublished - 2008

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Meals
Insulin Resistance
Insulin
Atropine
Glucose Clamp Technique
Liver
Cholinergic Agents
Volunteers
Fasting
Healthy Volunteers
Body Mass Index
Glucose
Control Groups
Pharmaceutical Preparations

Cite this

@article{4d701b1e7246465d8bae4444821ee641,
title = "Meal-induced insulin sensitization and its parasympathetic regulation in humans",
abstract = "In animal studies, the whole-body glucose disposal effect of insulin is low in the fasted state or after atropine infusion, but doubles after a meal, consistent with the hepatic insulin-sensitizing substance (HISS) hypothesis. We tested how a standardized test meal and atropine affected the dynamic response to insulin in humans. Insulin sensitivity was assessed in healthy male subjects (aged 28.9 +/- 1.9 years, body mass index 23.3 +/- 0.8 kg.m(-2)) by using the rapid insulin sensitivity test (RIST), which is a transient euglycemic clamp. After a 24-hour fasting period, dynamic insulin sensitivity was assessed and then repeated 100 min after the test meal. In a second protocol, the volunteers were fed the standardized test meal and intravenous atropine (0.5 mg) or saline (control group) was administered 50 min before insulin sensitivity assessment. Insulin sensitivity increased in the fed state (232.1{\%} +/- 46.3{\%}, n = 7) in comparison with the 24-hour fasted state. In the atropine protocol, the drug partially blocked (56.5{\%} +/- 11.6{\%}, n = 6) insulin sensitivity. In humans, feeding resulted in increased insulin sensitivity. The low dose of atropine in humans lead to a partial HISS-dependent decrease in insulin sensitivity. Meal- induced insulin sensitization occured in humans by a similar mechanism as that reported in other species. The sensitization process was regulated by a cholinergic 'feeding signal.'",
keywords = "hepatic insulin-sensitizing substance, SENSITIVITY TEST RIST, NITRIC-OXIDE, RAT, REPRODUCIBILITY, atropine, liver, RESISTANCE, EUGLYCEMIC CLAMP, insulin resistance, meal-induced insulin sensitivity, GLUCOSE CLAMP, INTERRUPTION, rapid insulin sensitivity test, feeding, COMPLICATIONS, POSTPRANDIAL HYPERGLYCEMIA",
author = "Afonso, {Ricardo A.} and Boavida, {Jos{\'e} Manuel} and Ribeiro, {Rog{\'e}rio T.} and Fernandes, {Ana B.} and Rita Patarr{\~a}o and MP Guarino and MP Macedo",
year = "2008",
doi = "10.1139/Y08-080",
language = "English",
volume = "86",
pages = "880--888",
journal = "Canadian Journal Of Physiology And Pharmacology",
issn = "0008-4212",
publisher = "National Research Council Canada",
number = "12",

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TY - JOUR

T1 - Meal-induced insulin sensitization and its parasympathetic regulation in humans

AU - Afonso, Ricardo A.

AU - Boavida, José Manuel

AU - Ribeiro, Rogério T.

AU - Fernandes, Ana B.

AU - Patarrão, Rita

AU - Guarino, MP

AU - Macedo, MP

PY - 2008

Y1 - 2008

N2 - In animal studies, the whole-body glucose disposal effect of insulin is low in the fasted state or after atropine infusion, but doubles after a meal, consistent with the hepatic insulin-sensitizing substance (HISS) hypothesis. We tested how a standardized test meal and atropine affected the dynamic response to insulin in humans. Insulin sensitivity was assessed in healthy male subjects (aged 28.9 +/- 1.9 years, body mass index 23.3 +/- 0.8 kg.m(-2)) by using the rapid insulin sensitivity test (RIST), which is a transient euglycemic clamp. After a 24-hour fasting period, dynamic insulin sensitivity was assessed and then repeated 100 min after the test meal. In a second protocol, the volunteers were fed the standardized test meal and intravenous atropine (0.5 mg) or saline (control group) was administered 50 min before insulin sensitivity assessment. Insulin sensitivity increased in the fed state (232.1% +/- 46.3%, n = 7) in comparison with the 24-hour fasted state. In the atropine protocol, the drug partially blocked (56.5% +/- 11.6%, n = 6) insulin sensitivity. In humans, feeding resulted in increased insulin sensitivity. The low dose of atropine in humans lead to a partial HISS-dependent decrease in insulin sensitivity. Meal- induced insulin sensitization occured in humans by a similar mechanism as that reported in other species. The sensitization process was regulated by a cholinergic 'feeding signal.'

AB - In animal studies, the whole-body glucose disposal effect of insulin is low in the fasted state or after atropine infusion, but doubles after a meal, consistent with the hepatic insulin-sensitizing substance (HISS) hypothesis. We tested how a standardized test meal and atropine affected the dynamic response to insulin in humans. Insulin sensitivity was assessed in healthy male subjects (aged 28.9 +/- 1.9 years, body mass index 23.3 +/- 0.8 kg.m(-2)) by using the rapid insulin sensitivity test (RIST), which is a transient euglycemic clamp. After a 24-hour fasting period, dynamic insulin sensitivity was assessed and then repeated 100 min after the test meal. In a second protocol, the volunteers were fed the standardized test meal and intravenous atropine (0.5 mg) or saline (control group) was administered 50 min before insulin sensitivity assessment. Insulin sensitivity increased in the fed state (232.1% +/- 46.3%, n = 7) in comparison with the 24-hour fasted state. In the atropine protocol, the drug partially blocked (56.5% +/- 11.6%, n = 6) insulin sensitivity. In humans, feeding resulted in increased insulin sensitivity. The low dose of atropine in humans lead to a partial HISS-dependent decrease in insulin sensitivity. Meal- induced insulin sensitization occured in humans by a similar mechanism as that reported in other species. The sensitization process was regulated by a cholinergic 'feeding signal.'

KW - hepatic insulin-sensitizing substance

KW - SENSITIVITY TEST RIST

KW - NITRIC-OXIDE

KW - RAT

KW - REPRODUCIBILITY

KW - atropine

KW - liver

KW - RESISTANCE

KW - EUGLYCEMIC CLAMP

KW - insulin resistance

KW - meal-induced insulin sensitivity

KW - GLUCOSE CLAMP

KW - INTERRUPTION

KW - rapid insulin sensitivity test

KW - feeding

KW - COMPLICATIONS

KW - POSTPRANDIAL HYPERGLYCEMIA

U2 - 10.1139/Y08-080

DO - 10.1139/Y08-080

M3 - Article

VL - 86

SP - 880

EP - 888

JO - Canadian Journal Of Physiology And Pharmacology

JF - Canadian Journal Of Physiology And Pharmacology

SN - 0008-4212

IS - 12

ER -