Postprandial but not fasting insulin resistance is an early identifier of dysmetabolism in overweight subjects.

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Abstract

The dynamic response to insulin is highly potentiated after meal ingestion, and this meal-induced insulin sensitization (MIS) in healthy subjects is dependent on cholinergic mechanisms. The main objective of this study was to test the hypothesis that the reduced response to insulin observed in moderately overweight subjects, in comparison with control lean subjects, is due to MIS impairment and not to a reduction in the direct hypoglycemic action of insulin. Both lean and overweight male subjects were recruited. Insulin sensitivity (IS) was assessed by the rapid insulin sensitivity test (RIST) performed after a 24 h fast, as well as after a standardized meal. Fasting glucose disposal was similar between lean and overweight subjects. Following the meal, glucose disposal increased more extensively in lean than overweight subjects. The insulin profiles, in both fasted and fed states, were superimposable, suggesting that the absence of a factor other than insulin is responsible for the decreased postprandial insulin sensitivity observed in overweight subjects. Our data suggest that in overweight subjects, MIS contribution is decreased, which is responsible for the postprandial impaired IS observed and is suggested to be the cause, not effect, of mild adiposity.
Original languageEnglish
Pages (from-to)923-931
Number of pages9
JournalCanadian Journal Of Physiology And Pharmacology
Volume90
Issue number7
DOIs
Publication statusPublished - 2012

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Insulin Resistance
Fasting
Insulin
Meals
Glucose
Adiposity
Hypoglycemic Agents
Cholinergic Agents
Healthy Volunteers
Eating

Cite this

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title = "Postprandial but not fasting insulin resistance is an early identifier of dysmetabolism in overweight subjects.",
abstract = "The dynamic response to insulin is highly potentiated after meal ingestion, and this meal-induced insulin sensitization (MIS) in healthy subjects is dependent on cholinergic mechanisms. The main objective of this study was to test the hypothesis that the reduced response to insulin observed in moderately overweight subjects, in comparison with control lean subjects, is due to MIS impairment and not to a reduction in the direct hypoglycemic action of insulin. Both lean and overweight male subjects were recruited. Insulin sensitivity (IS) was assessed by the rapid insulin sensitivity test (RIST) performed after a 24 h fast, as well as after a standardized meal. Fasting glucose disposal was similar between lean and overweight subjects. Following the meal, glucose disposal increased more extensively in lean than overweight subjects. The insulin profiles, in both fasted and fed states, were superimposable, suggesting that the absence of a factor other than insulin is responsible for the decreased postprandial insulin sensitivity observed in overweight subjects. Our data suggest that in overweight subjects, MIS contribution is decreased, which is responsible for the postprandial impaired IS observed and is suggested to be the cause, not effect, of mild adiposity.",
keywords = "SENSITIZATION, SENSITIVITY, RESPONSES, insulin resistance, overweight, meal-induced insulin sensitivity, hepatic insulin sensitizing substance, rapid insulin sensitivity test, meal tolerance test, insulin secretion, NITRIC-OXIDE, DYSFUNCTION, OBESITY, SECRETION, EXTRACTION, IMPAIRED GLUCOSE-TOLERANCE, GLUTATHIONE",
author = "Macedo, {Maria P} and Fernandes, {Ana B} and Afonso, {Ricardo A} and Rita Patarr{\~a}o and Ribeiro, {Rog{\'e}rio T} and Boavida, {Jos{\'e} M}",
year = "2012",
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journal = "Canadian Journal Of Physiology And Pharmacology",
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T1 - Postprandial but not fasting insulin resistance is an early identifier of dysmetabolism in overweight subjects.

AU - Macedo, Maria P

AU - Fernandes, Ana B

AU - Afonso, Ricardo A

AU - Patarrão, Rita

AU - Ribeiro, Rogério T

AU - Boavida, José M

PY - 2012

Y1 - 2012

N2 - The dynamic response to insulin is highly potentiated after meal ingestion, and this meal-induced insulin sensitization (MIS) in healthy subjects is dependent on cholinergic mechanisms. The main objective of this study was to test the hypothesis that the reduced response to insulin observed in moderately overweight subjects, in comparison with control lean subjects, is due to MIS impairment and not to a reduction in the direct hypoglycemic action of insulin. Both lean and overweight male subjects were recruited. Insulin sensitivity (IS) was assessed by the rapid insulin sensitivity test (RIST) performed after a 24 h fast, as well as after a standardized meal. Fasting glucose disposal was similar between lean and overweight subjects. Following the meal, glucose disposal increased more extensively in lean than overweight subjects. The insulin profiles, in both fasted and fed states, were superimposable, suggesting that the absence of a factor other than insulin is responsible for the decreased postprandial insulin sensitivity observed in overweight subjects. Our data suggest that in overweight subjects, MIS contribution is decreased, which is responsible for the postprandial impaired IS observed and is suggested to be the cause, not effect, of mild adiposity.

AB - The dynamic response to insulin is highly potentiated after meal ingestion, and this meal-induced insulin sensitization (MIS) in healthy subjects is dependent on cholinergic mechanisms. The main objective of this study was to test the hypothesis that the reduced response to insulin observed in moderately overweight subjects, in comparison with control lean subjects, is due to MIS impairment and not to a reduction in the direct hypoglycemic action of insulin. Both lean and overweight male subjects were recruited. Insulin sensitivity (IS) was assessed by the rapid insulin sensitivity test (RIST) performed after a 24 h fast, as well as after a standardized meal. Fasting glucose disposal was similar between lean and overweight subjects. Following the meal, glucose disposal increased more extensively in lean than overweight subjects. The insulin profiles, in both fasted and fed states, were superimposable, suggesting that the absence of a factor other than insulin is responsible for the decreased postprandial insulin sensitivity observed in overweight subjects. Our data suggest that in overweight subjects, MIS contribution is decreased, which is responsible for the postprandial impaired IS observed and is suggested to be the cause, not effect, of mild adiposity.

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KW - NITRIC-OXIDE

KW - DYSFUNCTION

KW - OBESITY

KW - SECRETION

KW - EXTRACTION

KW - IMPAIRED GLUCOSE-TOLERANCE

KW - GLUTATHIONE

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SN - 0008-4212

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