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Insulin resistance is accompanied by increased fasting glucagon and delayed glucagon suppression in individuals with normal and impaired glucose regulation

Færch, Kristine ; Vistisen, Dorte ; Pacini, Giovanni ; Torekov, Signe S. ; Johansen, Nanna B. ; Witte, Daniel R. ; Jonsson, Anna LU ; Pedersen, Oluf ; Hansen, Torben and Lauritzen, Torsten , et al. (2016) In Diabetes 65(11). p.3473-3481
Abstract

Hyperinsulinemia is an adaptive mechanism that enables the maintenance of normoglycemia in the presence of insulin resistance. We assessed whether glucagon is also involved in the adaptation to insulin resistance. A total of 1,437 individuals underwent an oral glucose tolerance test with measurements of circulating glucose, insulin, and glucagon concentrations at 0, 30 and 120 min. Early glucagon suppression was defined as suppression in the period from 0 to 30 min, and late glucagon suppression as 30 to 120 min after glucose intake. Insulin sensitivity was estimated by the validated insulin sensitivity index. Individuals with screen-detected diabetes had 30% higher fasting glucagon levels and diminished early glucagon suppression, but... (More)

Hyperinsulinemia is an adaptive mechanism that enables the maintenance of normoglycemia in the presence of insulin resistance. We assessed whether glucagon is also involved in the adaptation to insulin resistance. A total of 1,437 individuals underwent an oral glucose tolerance test with measurements of circulating glucose, insulin, and glucagon concentrations at 0, 30 and 120 min. Early glucagon suppression was defined as suppression in the period from 0 to 30 min, and late glucagon suppression as 30 to 120 min after glucose intake. Insulin sensitivity was estimated by the validated insulin sensitivity index. Individuals with screen-detected diabetes had 30% higher fasting glucagon levels and diminished early glucagon suppression, but greater late glucagon suppression when compared with individuals with normal glucose tolerance (P 0.014). Higher insulin resistance was associated with higher fasting glucagon levels, less early glucagon suppression, and greater late glucagon suppression (P < 0.001). The relationship between insulin sensitivity and fasting glucagon concentrations was nonlinear (P < 0.001). In conclusion, increased fasting glucagon levels and delayed glucagon suppression, together with increased circulating insulin levels, develop in parallel with insulin resistance. Therefore, glucose maintenance during insulin resistance may depend not only on hyperinsulinemia but also on the ability to suppress glucagon early after glucose intake.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Diabetes
volume
65
issue
11
pages
9 pages
publisher
American Diabetes Association Inc.
external identifiers
  • pmid:27504013
  • wos:000386538500025
  • scopus:84994259654
ISSN
0012-1797
DOI
10.2337/db16-0240
language
English
LU publication?
yes
id
0d31b04c-388d-4cb1-9e51-85911d9ca785
date added to LUP
2016-12-06 09:54:34
date last changed
2024-09-08 02:35:42
@article{0d31b04c-388d-4cb1-9e51-85911d9ca785,
  abstract     = {{<p>Hyperinsulinemia is an adaptive mechanism that enables the maintenance of normoglycemia in the presence of insulin resistance. We assessed whether glucagon is also involved in the adaptation to insulin resistance. A total of 1,437 individuals underwent an oral glucose tolerance test with measurements of circulating glucose, insulin, and glucagon concentrations at 0, 30 and 120 min. Early glucagon suppression was defined as suppression in the period from 0 to 30 min, and late glucagon suppression as 30 to 120 min after glucose intake. Insulin sensitivity was estimated by the validated insulin sensitivity index. Individuals with screen-detected diabetes had 30% higher fasting glucagon levels and diminished early glucagon suppression, but greater late glucagon suppression when compared with individuals with normal glucose tolerance (P 0.014). Higher insulin resistance was associated with higher fasting glucagon levels, less early glucagon suppression, and greater late glucagon suppression (P &lt; 0.001). The relationship between insulin sensitivity and fasting glucagon concentrations was nonlinear (P &lt; 0.001). In conclusion, increased fasting glucagon levels and delayed glucagon suppression, together with increased circulating insulin levels, develop in parallel with insulin resistance. Therefore, glucose maintenance during insulin resistance may depend not only on hyperinsulinemia but also on the ability to suppress glucagon early after glucose intake.</p>}},
  author       = {{Færch, Kristine and Vistisen, Dorte and Pacini, Giovanni and Torekov, Signe S. and Johansen, Nanna B. and Witte, Daniel R. and Jonsson, Anna and Pedersen, Oluf and Hansen, Torben and Lauritzen, Torsten and Jørgensen, Marit E. and Ahrén, Bo and Holst, Jens Juul}},
  issn         = {{0012-1797}},
  language     = {{eng}},
  month        = {{11}},
  number       = {{11}},
  pages        = {{3473--3481}},
  publisher    = {{American Diabetes Association Inc.}},
  series       = {{Diabetes}},
  title        = {{Insulin resistance is accompanied by increased fasting glucagon and delayed glucagon suppression in individuals with normal and impaired glucose regulation}},
  url          = {{http://dx.doi.org/10.2337/db16-0240}},
  doi          = {{10.2337/db16-0240}},
  volume       = {{65}},
  year         = {{2016}},
}