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Abnormal release of incretins and cortisol after oral glucose in subjects with insulin-resistant myotonic dystrophy

Johansson, A; Olsson, T; Cederquist, K; Forsberg, H; Holst, JJ; Seckl, JR and Ahrén, Bo LU (2002) In European Journal of Endocrinology1994-01-01+01:00 146(3). p.397-405
Abstract
Objective: Although the incretins, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), as well as glucagon and cortisol, are known to influence islet function, the role of these hormones in conditions of insulin resistance and development of type 2 diabetes is unknown. An interesting model for the study of hormonal perturbations accompanying marked insulin resistance without concomitant diabetes is myotonic dystrophy (DM1). Design: The work was carried out in an out-patient setting. Methods: An oral glucose tolerance test was performed in 18 males with DM1 and 18 controls to examine the release of incretins and counter-regulatory hormones. Genetic analyses were also performed in patients. Results: We found that the... (More)
Objective: Although the incretins, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), as well as glucagon and cortisol, are known to influence islet function, the role of these hormones in conditions of insulin resistance and development of type 2 diabetes is unknown. An interesting model for the study of hormonal perturbations accompanying marked insulin resistance without concomitant diabetes is myotonic dystrophy (DM1). Design: The work was carried out in an out-patient setting. Methods: An oral glucose tolerance test was performed in 18 males with DM1 and 18 controls to examine the release of incretins and counter-regulatory hormones. Genetic analyses were also performed in patients. Results: We found that the increment in GLP-1 after oral glucose was significantly greater in patients, while there was no significant difference in GIP or glucagon responses between patients and controls, although long CTG repeat expansions were associated with a more pronounced GIP response. Interestingly, the GLP-1 response to oral glucose correlated with the insulin response in patients but not in controls whereas, in controls, the insulin response closely correlated with the GIP response. Furthermore, cortisol and ACTH levels increased paradoxically in patients after glucose; this was more pronounced in patients with long CTG repeat expansions. Conclusions: This study showed that the GLP-1 and ACTH/cortisol responses to oral glucose are abnormal in insulin-resistant DM1. patients and that CTG triplet repeats are linked to GIP release. These abnormalities may contribute both to the severe insulin resistance and hyperinsulinemia in DM1 and to the preservation of adequate islet function, enabling glucose tolerance to be normal in spite of this marked insulin resistance in DM1. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
European Journal of Endocrinology1994-01-01+01:00
volume
146
issue
3
pages
397 - 405
publisher
Society of the European Journal of Endocrinology
external identifiers
  • wos:000178742900017
  • pmid:11888847
  • scopus:0036204546
ISSN
1479-683X
DOI
10.1530/eje.0.1460397
language
English
LU publication?
yes
id
8e068223-e39d-43bb-996a-ac6ad8d101ed (old id 892560)
date added to LUP
2008-01-23 16:09:12
date last changed
2017-01-01 04:39:55
@article{8e068223-e39d-43bb-996a-ac6ad8d101ed,
  abstract     = {Objective: Although the incretins, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), as well as glucagon and cortisol, are known to influence islet function, the role of these hormones in conditions of insulin resistance and development of type 2 diabetes is unknown. An interesting model for the study of hormonal perturbations accompanying marked insulin resistance without concomitant diabetes is myotonic dystrophy (DM1). Design: The work was carried out in an out-patient setting. Methods: An oral glucose tolerance test was performed in 18 males with DM1 and 18 controls to examine the release of incretins and counter-regulatory hormones. Genetic analyses were also performed in patients. Results: We found that the increment in GLP-1 after oral glucose was significantly greater in patients, while there was no significant difference in GIP or glucagon responses between patients and controls, although long CTG repeat expansions were associated with a more pronounced GIP response. Interestingly, the GLP-1 response to oral glucose correlated with the insulin response in patients but not in controls whereas, in controls, the insulin response closely correlated with the GIP response. Furthermore, cortisol and ACTH levels increased paradoxically in patients after glucose; this was more pronounced in patients with long CTG repeat expansions. Conclusions: This study showed that the GLP-1 and ACTH/cortisol responses to oral glucose are abnormal in insulin-resistant DM1. patients and that CTG triplet repeats are linked to GIP release. These abnormalities may contribute both to the severe insulin resistance and hyperinsulinemia in DM1 and to the preservation of adequate islet function, enabling glucose tolerance to be normal in spite of this marked insulin resistance in DM1.},
  author       = {Johansson, A and Olsson, T and Cederquist, K and Forsberg, H and Holst, JJ and Seckl, JR and Ahrén, Bo},
  issn         = {1479-683X},
  language     = {eng},
  number       = {3},
  pages        = {397--405},
  publisher    = {Society of the European Journal of Endocrinology},
  series       = {European Journal of Endocrinology1994-01-01+01:00},
  title        = {Abnormal release of incretins and cortisol after oral glucose in subjects with insulin-resistant myotonic dystrophy},
  url          = {http://dx.doi.org/10.1530/eje.0.1460397},
  volume       = {146},
  year         = {2002},
}