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Insulin secretion and incretin hormones after oral glucose in non-obese subjects with impaired glucose tolerance

Rask, E; Olsson, T; Soderberg, S; Holst, JJ; Tura, A; Pacini, G and Ahrén, Bo LU (2004) In Metabolism, Clinical and Experimental 53(5). p.624-631
Abstract
Subjects with impaired glucose tolerance (IGT) are usually overweight and exhibit insulin resistance with a defective compensation of insulin secretion. In this study, we sought to establish the interrelation between insulin secretion and insulin sensitivity after oral glucose in non-obese subjects with IGT and we also examined this interrelation in relation to the 2 main incretins, glucagon-like peptide (GLP-1) and gastric inhibitory polypeptide (GIP). To that end, 13 women with IGT and 17 women with normal glucose tolerance (NGT) underwent an oral glucose tolerance test (OGTT) with measurements of glucose, insulin, C-peptide, GLP-1, and GIP. Insulin secretion (TIS) and insulin sensitivity (OGIS) were assessed using models describing the... (More)
Subjects with impaired glucose tolerance (IGT) are usually overweight and exhibit insulin resistance with a defective compensation of insulin secretion. In this study, we sought to establish the interrelation between insulin secretion and insulin sensitivity after oral glucose in non-obese subjects with IGT and we also examined this interrelation in relation to the 2 main incretins, glucagon-like peptide (GLP-1) and gastric inhibitory polypeptide (GIP). To that end, 13 women with IGT and 17 women with normal glucose tolerance (NGT) underwent an oral glucose tolerance test (OGTT) with measurements of glucose, insulin, C-peptide, GLP-1, and GIP. Insulin secretion (TIS) and insulin sensitivity (OGIS) were assessed using models describing the relationship between glucose, insulin and C-peptide data. These models allowed estimation also of the hepatic extraction of insulin. The age (54.2 +/- 9.7 [mean +/- SD] years) and body mass index (BMI; 26.0 +/- 4.0 kg/m(2)) did not differ between the groups. Subjects with IGT displayed lower TIS during the initial 30 minutes after oral glucose (0.97 +/- 0.17 [mean +/- SEM] v 1.75 +/- 0.23 nmol/L in NGT; P = .018) and lower OGIS (397 21 v 463 12 mL/min/m(2); P = .005). The incremental 30-minute TIS times OGIS (reflecting insulin secretion in relation to insulin sensitivity) was significantly reduced in IGT (359 51 v 774 91 nmol/min/m(2), p = .001). This measure correlated inversely to the 2-hour glucose level (r = -0.71; P < .001). In contrast, TIS over the whole 180-minute period was higher in IGT (26.2 +/- 2.4 v 20.0 +/- 2.0 nmol/L; P = .035). Hepatic insulin extraction correlated linearly with OGIS (r = 0.71; P < .001), but was not significantly different between the groups although there was a trend with lower extraction in IGT (P = .055). Plasma levels of GLP-1 and GIP increased after oral glucose. Total secretion of these incretin hormones during the 3-hour test did not differ between the 2 groups. However, the 30-minute increase in GLP-1 concentrations was lower in IGT than in NGT (P = .036). We conclude that also in non-obese subjects with IGT, when adiposity is controlled for in relation to NGT, defective early insulin secretion after oral glucose is a key factor. This defective beta-cell function is associated with, and may be caused by, a reduced early GLP-1 response. (C) 2004 Elsevier Inc. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Metabolism, Clinical and Experimental
volume
53
issue
5
pages
624 - 631
publisher
Elsevier
external identifiers
  • pmid:15131768
  • wos:000221443500014
  • scopus:2342642148
ISSN
1532-8600
DOI
10.1016/j.metabol.2003.11.011
language
English
LU publication?
yes
id
67798c99-61ed-454c-b5ca-0ed0b1390ad2 (old id 277857)
date added to LUP
2007-10-30 15:32:39
date last changed
2017-10-22 04:32:28
@article{67798c99-61ed-454c-b5ca-0ed0b1390ad2,
  abstract     = {Subjects with impaired glucose tolerance (IGT) are usually overweight and exhibit insulin resistance with a defective compensation of insulin secretion. In this study, we sought to establish the interrelation between insulin secretion and insulin sensitivity after oral glucose in non-obese subjects with IGT and we also examined this interrelation in relation to the 2 main incretins, glucagon-like peptide (GLP-1) and gastric inhibitory polypeptide (GIP). To that end, 13 women with IGT and 17 women with normal glucose tolerance (NGT) underwent an oral glucose tolerance test (OGTT) with measurements of glucose, insulin, C-peptide, GLP-1, and GIP. Insulin secretion (TIS) and insulin sensitivity (OGIS) were assessed using models describing the relationship between glucose, insulin and C-peptide data. These models allowed estimation also of the hepatic extraction of insulin. The age (54.2 +/- 9.7 [mean +/- SD] years) and body mass index (BMI; 26.0 +/- 4.0 kg/m(2)) did not differ between the groups. Subjects with IGT displayed lower TIS during the initial 30 minutes after oral glucose (0.97 +/- 0.17 [mean +/- SEM] v 1.75 +/- 0.23 nmol/L in NGT; P = .018) and lower OGIS (397 21 v 463 12 mL/min/m(2); P = .005). The incremental 30-minute TIS times OGIS (reflecting insulin secretion in relation to insulin sensitivity) was significantly reduced in IGT (359 51 v 774 91 nmol/min/m(2), p = .001). This measure correlated inversely to the 2-hour glucose level (r = -0.71; P &lt; .001). In contrast, TIS over the whole 180-minute period was higher in IGT (26.2 +/- 2.4 v 20.0 +/- 2.0 nmol/L; P = .035). Hepatic insulin extraction correlated linearly with OGIS (r = 0.71; P &lt; .001), but was not significantly different between the groups although there was a trend with lower extraction in IGT (P = .055). Plasma levels of GLP-1 and GIP increased after oral glucose. Total secretion of these incretin hormones during the 3-hour test did not differ between the 2 groups. However, the 30-minute increase in GLP-1 concentrations was lower in IGT than in NGT (P = .036). We conclude that also in non-obese subjects with IGT, when adiposity is controlled for in relation to NGT, defective early insulin secretion after oral glucose is a key factor. This defective beta-cell function is associated with, and may be caused by, a reduced early GLP-1 response. (C) 2004 Elsevier Inc. All rights reserved.},
  author       = {Rask, E and Olsson, T and Soderberg, S and Holst, JJ and Tura, A and Pacini, G and Ahrén, Bo},
  issn         = {1532-8600},
  language     = {eng},
  number       = {5},
  pages        = {624--631},
  publisher    = {Elsevier},
  series       = {Metabolism, Clinical and Experimental},
  title        = {Insulin secretion and incretin hormones after oral glucose in non-obese subjects with impaired glucose tolerance},
  url          = {http://dx.doi.org/10.1016/j.metabol.2003.11.011},
  volume       = {53},
  year         = {2004},
}