Advanced

Mature-onset obesity in interleukin-1 receptor I knockout mice

Garcia, MC; Wernstedt, I; Berndtsson, A; Enge, M; Bell, M; Hultgren, O; Horn, M; Ahrén, Bo LU ; Enerback, S and Ohlsson, C, et al. (2006) In Diabetes 55(5). p.1205-1213
Abstract
Interleukin-1 (IL-1) is a major mediator of inflammation that exerts its biological activities through the IL-1 type I receptor (IL-1RI). The body weights of IL-1RI(-/-) mice of both sexes started to deviate from those of wild-type mice at 5-6 months of age and were 20% higher at 9 months of age. Visceral and subcutaneous fat mass, measured by dual-energy X-ray absorptiometry and magnetic resonance imaging, was markedly (1.5- to 2.5-fold) increased. Lean body mass and crown-rump length were also slightly (11 and 5%, respectively) increased, as was serum IGF-I Obese IL-1RI(-/-) mice were insulin resistant, as evidenced by hyperinsulinemia, decreased glucose tolerance, and insulin sensitivity. To elucidate the mechanisms for the development... (More)
Interleukin-1 (IL-1) is a major mediator of inflammation that exerts its biological activities through the IL-1 type I receptor (IL-1RI). The body weights of IL-1RI(-/-) mice of both sexes started to deviate from those of wild-type mice at 5-6 months of age and were 20% higher at 9 months of age. Visceral and subcutaneous fat mass, measured by dual-energy X-ray absorptiometry and magnetic resonance imaging, was markedly (1.5- to 2.5-fold) increased. Lean body mass and crown-rump length were also slightly (11 and 5%, respectively) increased, as was serum IGF-I Obese IL-1RI(-/-) mice were insulin resistant, as evidenced by hyperinsulinemia, decreased glucose tolerance, and insulin sensitivity. To elucidate the mechanisms for the development of obesity, young preobese IL-IRI-/- mice were investigated. They showed decreased suppression of body weight and food intake in response to systemic leptin treatment. The decreased leptin responsiveness was even more pronounced in older obese animals. Moreover, spontaneous locomotor activity and fat utilization, as measured by respiratory quotient, were decreased in preobese IL-1RI(-/-) mice. In conclusion, lack of 11-1RI-mediated biological activity causes mature-onset obesity. This obese phenotype is preceded by decreased leptin sensitivity, fat utilization, and locomotor activity. (Less)
Please use this url to cite or link to this publication:
author
, et al. (More)
(Less)
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Diabetes
volume
55
issue
5
pages
1205 - 1213
publisher
American Diabetes Association Inc.
external identifiers
  • wos:000237303800004
  • pmid:16644674
  • scopus:33745302882
ISSN
1939-327X
DOI
10.2337/db05-1304
language
English
LU publication?
yes
id
6181f60e-b4e2-4f31-84bb-a581e541d2c4 (old id 410493)
date added to LUP
2007-10-03 08:21:58
date last changed
2019-09-11 02:33:54
@article{6181f60e-b4e2-4f31-84bb-a581e541d2c4,
  abstract     = {Interleukin-1 (IL-1) is a major mediator of inflammation that exerts its biological activities through the IL-1 type I receptor (IL-1RI). The body weights of IL-1RI(-/-) mice of both sexes started to deviate from those of wild-type mice at 5-6 months of age and were 20% higher at 9 months of age. Visceral and subcutaneous fat mass, measured by dual-energy X-ray absorptiometry and magnetic resonance imaging, was markedly (1.5- to 2.5-fold) increased. Lean body mass and crown-rump length were also slightly (11 and 5%, respectively) increased, as was serum IGF-I Obese IL-1RI(-/-) mice were insulin resistant, as evidenced by hyperinsulinemia, decreased glucose tolerance, and insulin sensitivity. To elucidate the mechanisms for the development of obesity, young preobese IL-IRI-/- mice were investigated. They showed decreased suppression of body weight and food intake in response to systemic leptin treatment. The decreased leptin responsiveness was even more pronounced in older obese animals. Moreover, spontaneous locomotor activity and fat utilization, as measured by respiratory quotient, were decreased in preobese IL-1RI(-/-) mice. In conclusion, lack of 11-1RI-mediated biological activity causes mature-onset obesity. This obese phenotype is preceded by decreased leptin sensitivity, fat utilization, and locomotor activity.},
  author       = {Garcia, MC and Wernstedt, I and Berndtsson, A and Enge, M and Bell, M and Hultgren, O and Horn, M and Ahrén, Bo and Enerback, S and Ohlsson, C and Wallenius, V and Jansson, JO},
  issn         = {1939-327X},
  language     = {eng},
  number       = {5},
  pages        = {1205--1213},
  publisher    = {American Diabetes Association Inc.},
  series       = {Diabetes},
  title        = {Mature-onset obesity in interleukin-1 receptor I knockout mice},
  url          = {http://dx.doi.org/10.2337/db05-1304},
  volume       = {55},
  year         = {2006},
}