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Signals adapting the beta cells to changes in insulin sensitivity

Ahrén, Bo LU and Pacini, G (2003) 8th European Symposium on Metabolism In The metabolic syndrome: diabetes, obesity, hyperlipidemia and hypertension. Proceedings of the 8th European Symposium on Metabolism 1253. p.105-113
Abstract
Insulin sensitivity and secretion are related in a curvilinear inverse asymptotic function. However, the signaling factors mediating this relation are not known. In this study, we explored whether circulating glucose, lipids or two adipocyte-derived hormones, leptin and adiponectin, are related to the curvilinear function between insulin sensitivity and secretion in subjects with normal glucose tolerance. Thereby, insulin secretion (2-5-min insulin response to intravenous arginine) and insulin sensitivity (euglycemic, hyperinsulinemic clamp) were established in 68 healthy women, aged 61 years. We confirmed the curvilinear relation between insulin sensitivity and insulin secretion (r = -0.71, P < 0.001). To quantify the ability of the... (More)
Insulin sensitivity and secretion are related in a curvilinear inverse asymptotic function. However, the signaling factors mediating this relation are not known. In this study, we explored whether circulating glucose, lipids or two adipocyte-derived hormones, leptin and adiponectin, are related to the curvilinear function between insulin sensitivity and secretion in subjects with normal glucose tolerance. Thereby, insulin secretion (2-5-min insulin response to intravenous arginine) and insulin sensitivity (euglycemic, hyperinsulinemic clamp) were established in 68 healthy women, aged 61 years. We confirmed the curvilinear relation between insulin sensitivity and insulin secretion (r = -0.71, P < 0.001). To quantify the ability of the beta cells to secrete insulin for balancing a change in insulin sensitivity, we introduce the beta cell compensation index (BCI) by dividing insulin secretion by insulin sensitivity. This index correlated significantly with circulating triglycerides, leptin and adiponectin as well as BMI, but not fasting or 2-h glucose. A multivariate stepwise regression analysis using these variables as independent variables and lg BCI as the dependent variable revealed that leptin (r = 0.54, P < 0.001) and adiponectin (r = -0.33, P = 0.008) independently contributed to lg BCI (R-2 of the model = 0.19m, P = 0.038). The study, therefore, suggests that adipocyte-derived hormones contribute to the beta cell compensation to insulin resistance. (C) 2002 Elsevier Science B.V. All rights reserved. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
leptin, islet adaptation, insulin secretion, insulin sensitivity, adiponectin
in
The metabolic syndrome: diabetes, obesity, hyperlipidemia and hypertension. Proceedings of the 8th European Symposium on Metabolism
volume
1253
pages
105 - 113
publisher
Elsevier
conference name
8th European Symposium on Metabolism
external identifiers
  • wos:000186667300013
  • scopus:17644407937
ISSN
0531-5131
DOI
10.1016/S0531-5131(02)01281-5
language
English
LU publication?
yes
id
4ac5c57e-5692-44f4-be72-f9f751fed1bf (old id 1406881)
date added to LUP
2009-06-03 16:05:34
date last changed
2018-06-24 04:41:22
@inproceedings{4ac5c57e-5692-44f4-be72-f9f751fed1bf,
  abstract     = {Insulin sensitivity and secretion are related in a curvilinear inverse asymptotic function. However, the signaling factors mediating this relation are not known. In this study, we explored whether circulating glucose, lipids or two adipocyte-derived hormones, leptin and adiponectin, are related to the curvilinear function between insulin sensitivity and secretion in subjects with normal glucose tolerance. Thereby, insulin secretion (2-5-min insulin response to intravenous arginine) and insulin sensitivity (euglycemic, hyperinsulinemic clamp) were established in 68 healthy women, aged 61 years. We confirmed the curvilinear relation between insulin sensitivity and insulin secretion (r = -0.71, P &lt; 0.001). To quantify the ability of the beta cells to secrete insulin for balancing a change in insulin sensitivity, we introduce the beta cell compensation index (BCI) by dividing insulin secretion by insulin sensitivity. This index correlated significantly with circulating triglycerides, leptin and adiponectin as well as BMI, but not fasting or 2-h glucose. A multivariate stepwise regression analysis using these variables as independent variables and lg BCI as the dependent variable revealed that leptin (r = 0.54, P &lt; 0.001) and adiponectin (r = -0.33, P = 0.008) independently contributed to lg BCI (R-2 of the model = 0.19m, P = 0.038). The study, therefore, suggests that adipocyte-derived hormones contribute to the beta cell compensation to insulin resistance. (C) 2002 Elsevier Science B.V. All rights reserved.},
  author       = {Ahrén, Bo and Pacini, G},
  booktitle    = {The metabolic syndrome: diabetes, obesity, hyperlipidemia and hypertension. Proceedings of the 8th European Symposium on Metabolism},
  issn         = {0531-5131},
  keyword      = {leptin,islet adaptation,insulin secretion,insulin sensitivity,adiponectin},
  language     = {eng},
  pages        = {105--113},
  publisher    = {Elsevier},
  title        = {Signals adapting the beta cells to changes in insulin sensitivity},
  url          = {http://dx.doi.org/10.1016/S0531-5131(02)01281-5},
  volume       = {1253},
  year         = {2003},
}