Insulin sensitivity predicts glycemia after a protein load

Citation
Jc. Brand-miller et al., Insulin sensitivity predicts glycemia after a protein load, METABOLISM, 49(1), 2000, pp. 1-5
Citations number
17
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
METABOLISM-CLINICAL AND EXPERIMENTAL
ISSN journal
00260495 → ACNP
Volume
49
Issue
1
Year of publication
2000
Pages
1 - 5
Database
ISI
SICI code
0026-0495(200001)49:1<1:ISPGAA>2.0.ZU;2-P
Abstract
Protein ingestion results in small but distinct changes in plasma glucose a nd insulin. We hypothesized that the glycemic and/or insulin response to pr otein might be related to the degree of insulin sensitivity. Our aim was to determine the relationships between insulin sensitivity (assessed by eugly cemic-hyperinsulinemic clamp) and postprandial glucose, insulin, C-peptide, and glucagon responses to a 75-g protein meal and a 75-g glucose load. Six teen lean healthy Caucasian subjects (mean +/- SD age, 25 +/- 6 years; body mass index [BMI], 23.1 +/- 1.7 kg/m(2)) participated in the study. After t he protein meal, the mean plasma glucose declined gradually below fasting l evels to a nadir of -0.36 +/- 0.46 mmol/L from 60 to 120 minutes, showing w ide intraindividual variation. Insulin sensitivity (M value) was 1.1 to 3.9 mmol/L/m(2) min in the subjects and correlated inversely with the plasma g lucose response to the protein meal (r = -.58, P = .03), ie, the most insul in-sensitive subjects showed the greatest decline in plasma glucose. In con trast, there was no correlation between insulin sensitivity and the insulin or glucagon response to the protein load, or between the M value and the m etabolic responses (glucose, insulin, C-peptide, and glucagon) to the gluco se load. Our study suggests that the net effect of insulin and glucagon sec retion on postprandial glucose levels after a protein meal might depend on the individual's degree of insulin sensitivity. Gluconeogenesis in the live r may be less susceptible to inhibition by insulin in the more highly resis tant subjects, thereby counteracting a decline in plasma glucose. Copyright (C) 2000 by W.B. Saunders Company.