The high-fat diet-fed mouse: a model for studying mechanisms and treatment of impaired glucose tolerance and type 2 diabetes.
(2004) In Diabetes 53(Suppl 3). p.215-219- Abstract
- This study characterizes the high-fat diet-fed mouse as a model for impaired glucose tolerance (IGT) and type 2 diabetes. Female C57BL/6J mice were fed a high-fat diet (58% energy by fat) or a normal diet (11% fat). Body weight was higher in mice fed the high-fat diet already after the first week, due to higher dietary intake in combination with lower metabolic efficiency. Circulating glucose increased after 1 week on high-fat diet and remained elevated at a level of approximately 1 mmol/l throughout the 12-month study period. In contrast, circulating insulin increased progressively by time. Intravenous glucose challenge revealed a severely compromised insulin response in association with marked glucose intolerance already after 1 week. To... (More)
- This study characterizes the high-fat diet-fed mouse as a model for impaired glucose tolerance (IGT) and type 2 diabetes. Female C57BL/6J mice were fed a high-fat diet (58% energy by fat) or a normal diet (11% fat). Body weight was higher in mice fed the high-fat diet already after the first week, due to higher dietary intake in combination with lower metabolic efficiency. Circulating glucose increased after 1 week on high-fat diet and remained elevated at a level of approximately 1 mmol/l throughout the 12-month study period. In contrast, circulating insulin increased progressively by time. Intravenous glucose challenge revealed a severely compromised insulin response in association with marked glucose intolerance already after 1 week. To illustrate the usefulness of this model for the development of new treatment, mice were fed an orally active inhibitor of dipeptidyl peptidase-IV (LAF237) in the drinking water (0.3 mg/ml) for 4 weeks. This normalized glucose tolerance, as judged by an oral glucose tolerance test, in association with augmented insulin secretion. We conclude that the high-fat diet-fed C57BL/6J mouse model is a robust model for IGT and early type 2 diabetes, which may be used for studies on pathophysiology and development of new treatment. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/130680
- author
- Sörhede Winzell, Maria LU and Ahrén, Bo LU
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Diabetes
- volume
- 53
- issue
- Suppl 3
- pages
- 215 - 219
- publisher
- American Diabetes Association Inc.
- external identifiers
-
- wos:000225460000032
- scopus:3543009434
- ISSN
- 1939-327X
- DOI
- 10.2337/diabetes.53.suppl_3.S215
- language
- English
- LU publication?
- yes
- id
- 28767fc6-bf7a-48e3-8bbc-55ebe760e557 (old id 130680)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15561913&dopt=Abstract
- date added to LUP
- 2016-04-01 16:48:22
- date last changed
- 2024-02-26 23:17:38
@article{28767fc6-bf7a-48e3-8bbc-55ebe760e557,
abstract = {{This study characterizes the high-fat diet-fed mouse as a model for impaired glucose tolerance (IGT) and type 2 diabetes. Female C57BL/6J mice were fed a high-fat diet (58% energy by fat) or a normal diet (11% fat). Body weight was higher in mice fed the high-fat diet already after the first week, due to higher dietary intake in combination with lower metabolic efficiency. Circulating glucose increased after 1 week on high-fat diet and remained elevated at a level of approximately 1 mmol/l throughout the 12-month study period. In contrast, circulating insulin increased progressively by time. Intravenous glucose challenge revealed a severely compromised insulin response in association with marked glucose intolerance already after 1 week. To illustrate the usefulness of this model for the development of new treatment, mice were fed an orally active inhibitor of dipeptidyl peptidase-IV (LAF237) in the drinking water (0.3 mg/ml) for 4 weeks. This normalized glucose tolerance, as judged by an oral glucose tolerance test, in association with augmented insulin secretion. We conclude that the high-fat diet-fed C57BL/6J mouse model is a robust model for IGT and early type 2 diabetes, which may be used for studies on pathophysiology and development of new treatment.}},
author = {{Sörhede Winzell, Maria and Ahrén, Bo}},
issn = {{1939-327X}},
language = {{eng}},
number = {{Suppl 3}},
pages = {{215--219}},
publisher = {{American Diabetes Association Inc.}},
series = {{Diabetes}},
title = {{The high-fat diet-fed mouse: a model for studying mechanisms and treatment of impaired glucose tolerance and type 2 diabetes.}},
url = {{http://dx.doi.org/10.2337/diabetes.53.suppl_3.S215}},
doi = {{10.2337/diabetes.53.suppl_3.S215}},
volume = {{53}},
year = {{2004}},
}