Advanced

Temporal and dietary fat content-dependent islet adaptation to high-fat feeding-induced glucose intolerance in mice.

Sörhede Winzell, Maria LU ; Magnusson, Caroline LU and Ahrén, Bo LU (2007) In Metabolism, Clinical and Experimental 56(1). p.122-128
Abstract
The high fat-fed mouse is an experimental model for studies of islet dysfunction as a mechanism for glucose intolerance and for evaluation of therapeutic targets. This model is, however, dynamic with a temporal and dietary fat content-dependent impact on islet function and glucose tolerance, the details of which are unknown. This study therefore examined the time course of changes in the insulin response to intravenous glucose (1 g/kg) in relation to glucose tolerance in female mice after 1, 3, 8, or 16 weeks of feeding with diets containing 11% fat (normal diet [ND]), 30% fat (medium-fat diet [MFD]), or 58% fat (high-fat diet [HFD]:, by energy). High-fat diet increased body weight and body fat content, whereas MFD did not. The insulin... (More)
The high fat-fed mouse is an experimental model for studies of islet dysfunction as a mechanism for glucose intolerance and for evaluation of therapeutic targets. This model is, however, dynamic with a temporal and dietary fat content-dependent impact on islet function and glucose tolerance, the details of which are unknown. This study therefore examined the time course of changes in the insulin response to intravenous glucose (1 g/kg) in relation to glucose tolerance in female mice after 1, 3, 8, or 16 weeks of feeding with diets containing 11% fat (normal diet [ND]), 30% fat (medium-fat diet [MFD]), or 58% fat (high-fat diet [HFD]:, by energy). High-fat diet increased body weight and body fat content, whereas MFD did not. The insulin response (postglucose suprabasal mean 1- and 5-minute insulin) was impaired after 1 week on NIFD (481 +/- 33 pmol/L) or HFD (223 +/- 31 pmol/L) compared with ND (713 +/- 46 pmol/L, both P <.001). This was accompanied by impaired glucose elimination compared with ND (both P <.001). Over the 16-week study period, the insulin response adaptively increased in the groups fed with HFD and MFD, to be not significantly different from ND after 16 weeks. This compensation normalized glucose tolerance in MFD, whereas the glucose tolerance was still below normal in HFD. Insulin clearance, as judged by elimination of intravenous human insulin, was not altered in HFD, suggesting that the observed changes in insulin responses to glucose are due to changes in insulin secretion rather than to changes in insulin clearance. We conclude that time- and dietary fat dependent dynamic adaptive islet compensation evolves after introducing HFD in mice and that MFD-fed mice is a novel nonobese model of glucose intolerance. (c) 2007 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Metabolism, Clinical and Experimental
volume
56
issue
1
pages
122 - 128
publisher
Elsevier
external identifiers
  • wos:000243029600017
  • scopus:33845189881
ISSN
1532-8600
DOI
10.1016/j.metabol.2006.09.008
language
English
LU publication?
yes
id
b8b053f1-ba6f-418f-8d5f-daaa18436edc (old id 164071)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17161234&dopt=Abstract
date added to LUP
2007-07-10 14:16:37
date last changed
2017-07-23 04:30:56
@article{b8b053f1-ba6f-418f-8d5f-daaa18436edc,
  abstract     = {The high fat-fed mouse is an experimental model for studies of islet dysfunction as a mechanism for glucose intolerance and for evaluation of therapeutic targets. This model is, however, dynamic with a temporal and dietary fat content-dependent impact on islet function and glucose tolerance, the details of which are unknown. This study therefore examined the time course of changes in the insulin response to intravenous glucose (1 g/kg) in relation to glucose tolerance in female mice after 1, 3, 8, or 16 weeks of feeding with diets containing 11% fat (normal diet [ND]), 30% fat (medium-fat diet [MFD]), or 58% fat (high-fat diet [HFD]:, by energy). High-fat diet increased body weight and body fat content, whereas MFD did not. The insulin response (postglucose suprabasal mean 1- and 5-minute insulin) was impaired after 1 week on NIFD (481 +/- 33 pmol/L) or HFD (223 +/- 31 pmol/L) compared with ND (713 +/- 46 pmol/L, both P &lt;.001). This was accompanied by impaired glucose elimination compared with ND (both P &lt;.001). Over the 16-week study period, the insulin response adaptively increased in the groups fed with HFD and MFD, to be not significantly different from ND after 16 weeks. This compensation normalized glucose tolerance in MFD, whereas the glucose tolerance was still below normal in HFD. Insulin clearance, as judged by elimination of intravenous human insulin, was not altered in HFD, suggesting that the observed changes in insulin responses to glucose are due to changes in insulin secretion rather than to changes in insulin clearance. We conclude that time- and dietary fat dependent dynamic adaptive islet compensation evolves after introducing HFD in mice and that MFD-fed mice is a novel nonobese model of glucose intolerance. (c) 2007 Elsevier Inc. All rights reserved.},
  author       = {Sörhede Winzell, Maria and Magnusson, Caroline and Ahrén, Bo},
  issn         = {1532-8600},
  language     = {eng},
  number       = {1},
  pages        = {122--128},
  publisher    = {Elsevier},
  series       = {Metabolism, Clinical and Experimental},
  title        = {Temporal and dietary fat content-dependent islet adaptation to high-fat feeding-induced glucose intolerance in mice.},
  url          = {http://dx.doi.org/10.1016/j.metabol.2006.09.008},
  volume       = {56},
  year         = {2007},
}