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Glucagon secretion in relation to insulin sensitivity in healthy subjects.

Ahrén, Bo LU (2006) In Diabetologia 49(1). p.117-122
Abstract
Aims/hypothesis: The study evaluated whether glucagon secretion is regulated by changes in insulin sensitivity under normal conditions. Materials and methods: A total of 155 healthy women with NGT (aged 53-70 years) underwent a glucose-dependent arginine-stimulation test for evaluation of glucagon secretion. Arginine (5 g) was injected i.v. under fasting conditions (plasma glucose 4.8 +/- 0.1 mmol/l) and after raising blood glucose concentrations to 14.8 +/- 0.1 and 29.8 +/- 0.2 mmol/l. The acute glucagon response (AGR) to arginine during the three glucose levels (AGR(1), AGR(2), AGR(3)) was estimated, as was the suppression of baseline glucagon by the increased glucose. All women also underwent a 2-h euglycaemic-hyperinsulinaemic clamp... (More)
Aims/hypothesis: The study evaluated whether glucagon secretion is regulated by changes in insulin sensitivity under normal conditions. Materials and methods: A total of 155 healthy women with NGT (aged 53-70 years) underwent a glucose-dependent arginine-stimulation test for evaluation of glucagon secretion. Arginine (5 g) was injected i.v. under fasting conditions (plasma glucose 4.8 +/- 0.1 mmol/l) and after raising blood glucose concentrations to 14.8 +/- 0.1 and 29.8 +/- 0.2 mmol/l. The acute glucagon response (AGR) to arginine during the three glucose levels (AGR(1), AGR(2), AGR(3)) was estimated, as was the suppression of baseline glucagon by the increased glucose. All women also underwent a 2-h euglycaemic-hyperinsulinaemic clamp study for estimation of insulin sensitivity. Results: Insulin sensitivity was normally distributed, with a mean of 73.2 +/- 29.3 (SD) nmol glucose kg(-1) min(-1)/pmol insulin l(-1). When relating the variables obtained from the arginine test to insulin sensitivity, insulin resistance was associated with increased AGR and with increased suppression of glucagon levels by glucose. For example, the regression between insulin sensitivity and AGR(2) was r=-0.38 (p < 0.001) and between insulin sensitivity and suppression of glucagon levels by 14.8 mmol/l glucose r=0.36 (p < 0.001). Insulin sensitivity also correlated negatively with insulin secretion; multivariate analysis revealed that changes in insulin sensitivity and insulin secretion were independently related to changes in glucagon secretion. Conclusions/interpretation: The body adapts to insulin resistance by increasing the glucagon response to arginine and by increasing the suppression of glucagon levels by glucose. Hence, not only the islet beta cells but also the alpha cells seem to undergo compensatory changes during the development of insulin resistance. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
glucagon, insulin sensitivity, glucose tolerance, arginine
in
Diabetologia
volume
49
issue
1
pages
117 - 122
publisher
Springer
external identifiers
  • wos:000234923700018
  • scopus:31444433502
ISSN
1432-0428
DOI
10.1007/s00125-005-0056-8
language
English
LU publication?
yes
id
1184cff8-3e26-43f0-9e3a-d31ee26ef448 (old id 148603)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16362283&dopt=Abstract
date added to LUP
2016-04-01 12:20:37
date last changed
2024-01-08 17:12:03
@article{1184cff8-3e26-43f0-9e3a-d31ee26ef448,
  abstract     = {{Aims/hypothesis: The study evaluated whether glucagon secretion is regulated by changes in insulin sensitivity under normal conditions. Materials and methods: A total of 155 healthy women with NGT (aged 53-70 years) underwent a glucose-dependent arginine-stimulation test for evaluation of glucagon secretion. Arginine (5 g) was injected i.v. under fasting conditions (plasma glucose 4.8 +/- 0.1 mmol/l) and after raising blood glucose concentrations to 14.8 +/- 0.1 and 29.8 +/- 0.2 mmol/l. The acute glucagon response (AGR) to arginine during the three glucose levels (AGR(1), AGR(2), AGR(3)) was estimated, as was the suppression of baseline glucagon by the increased glucose. All women also underwent a 2-h euglycaemic-hyperinsulinaemic clamp study for estimation of insulin sensitivity. Results: Insulin sensitivity was normally distributed, with a mean of 73.2 +/- 29.3 (SD) nmol glucose kg(-1) min(-1)/pmol insulin l(-1). When relating the variables obtained from the arginine test to insulin sensitivity, insulin resistance was associated with increased AGR and with increased suppression of glucagon levels by glucose. For example, the regression between insulin sensitivity and AGR(2) was r=-0.38 (p &lt; 0.001) and between insulin sensitivity and suppression of glucagon levels by 14.8 mmol/l glucose r=0.36 (p &lt; 0.001). Insulin sensitivity also correlated negatively with insulin secretion; multivariate analysis revealed that changes in insulin sensitivity and insulin secretion were independently related to changes in glucagon secretion. Conclusions/interpretation: The body adapts to insulin resistance by increasing the glucagon response to arginine and by increasing the suppression of glucagon levels by glucose. Hence, not only the islet beta cells but also the alpha cells seem to undergo compensatory changes during the development of insulin resistance.}},
  author       = {{Ahrén, Bo}},
  issn         = {{1432-0428}},
  keywords     = {{glucagon; insulin sensitivity; glucose tolerance; arginine}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{117--122}},
  publisher    = {{Springer}},
  series       = {{Diabetologia}},
  title        = {{Glucagon secretion in relation to insulin sensitivity in healthy subjects.}},
  url          = {{https://lup.lub.lu.se/search/files/2884820/625184.pdf}},
  doi          = {{10.1007/s00125-005-0056-8}},
  volume       = {{49}},
  year         = {{2006}},
}