The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Interleukin-33 Induces Protective Effects in Adipose Tissue Inflammation During Obesity in Mice
Open accessAbstract
Rationale: Chronic low-grade inflammation involving adipose tissue likely contributes to the metabolic consequences of obesity. The cytokine interleukin (IL)-33 and its receptor ST2 are expressed in adipose tissue, but their role in adipose tissue inflammation during obesity is unclear. Objective: To examine the functional role of IL-33 in adipose tissues and investigate the effects on adipose tissue inflammation and obesity in vivo. Methods and Results: We demonstrate that treatment of adipose tissue cultures in vitro with IL-33 induced production of Th2 cytokines (IL-5, IL-13, IL-10) and reduced expression of adipogenic and metabolic genes. Administration of recombinant IL-33 to genetically obese diabetic ( ob/ob ) mice led to reduced adiposity, reduced fasting glucose and improved glucose and insulin tolerance. IL-33 also induced accumulation of Th2 cells in adipose tissue and polarization of adipose tissue macrophages toward an M2 alternatively activated phenotype (CD206 + ), a lineage associated with protection against obesity-related metabolic events. Furthermore, mice lacking endogenous ST2 fed high-fat diet had increased body weight and fat mass and impaired insulin secretion and glucose regulation compared to WT controls fed high-fat diet. Conclusions: In conclusion, IL-33 may play a protective role in the development of adipose tissue inflammation during obesity.
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Cites
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Cited by
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Metadata
- Authors
- Miller, A. M., Asquith, D. L., Hueber, A. J., Anderson, L. A., Holmes, W. M., McKenzie, A. N., Xu, D., Sattar, N., McInnes, I. B., & Liew, F. Y.
- Venue
- Circulation Research
- Published
- 2010-09-03
- Volume
- 107
- Issue
- 5
- Pages
- 650-658
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2163863824
- Cited by
- 324
- References
- 16
- FWCI
- 10.06
- Type
- journal article
- Language
- en
- Open access
- bronze
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