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Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice.
J. Clin. Invest. 117, 2877-2888 (2007)
Obesity is associated with a state of chronic, low-grade inflammation characterized by abnormal cytokine production and macrophage infiltration into adipose tissue, which may contribute to the development of insulin resistance. During immune responses, tissue infiltration by macrophages is dependent on the expression of osteopontin, an extracellular matrix protein and proinflammatory cytokine that promotes monocyte chemotaxis and cell motility. In the present study, we used a murine model of diet-induced obesity to examine the role of osteopontin in the accumulation of adipose tissue macrophages and the development of insulin resistance during obesity. Mice exposed to a high-fat diet exhibited increased plasma osteopontin levels, with elevated expression in macrophages recruited into adipose tissue. Obese mice lacking osteopontin displayed improved insulin sensitivity in the absence of an effect on diet-induced obesity, body composition, or energy expenditure. These mice further demonstrated decreased macrophage infiltration into adipose tissue, which may reflect both impaired macrophage motility and attenuated monocyte recruitment by stromal vascular cells. Finally, obese osteopontin-deficient mice exhibited decreased markers of inflammation, both in adipose tissue and systemically. Taken together, these results suggest that osteopontin may play a key role in linking obesity to the development of insulin resistance by promoting inflammation and the accumulation of macrophages in adipose tissue.
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Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
2007
HGF-reported in Year
2007
ISSN (print) / ISBN
0021-9738
e-ISSN
1558-8238
Quellenangaben
Volume: 117,
Issue: 10,
Pages: 2877-2888
Publisher
American Society of Clinical Investigation
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
DOI
10.1172/JCI31986
PubMed ID
17823662
Erfassungsdatum
2020-02-24