The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Deficiency of the Leukotriene B4 Receptor, BLT-1, Protects against Systemic Insulin Resistance in Diet-Induced Obesity
Open accessAbstract
Chronic inflammation is an underlying factor linking obesity with insulin resistance. Diet-induced obesity promotes an increase in circulating levels of inflammatory monocytes and their infiltration into expanding adipose tissue. Nevertheless, the endogenous pathways that trigger and sustain chronic low-grade inflammation in obesity are incompletely understood. In this study, we report that a high-fat diet selectively increases the circulating levels of CD11b+ monocytes in wild-type mice that express leukotriene B4 receptor, BLT-1, and that this increase is abolished in BLT-1–null mice. The accumulation of classically activated (M1) adipose tissue macrophages (ATMs) and the expression of proinflammatory cytokines and chemokines (i.e., IL-6 and Ccl2) was largely blunted in adipose tissue of obese BLT-1−/− mice, whereas the ratio of alternatively activated (M2) ATMs to M1 ATMs was increased. Obese BLT-1−/− mice were protected from systemic glucose and insulin intolerance and this was associated with a decrease in inflammation in adipose tissue and liver and a decrease in hepatic triglyceride accumulation. Deletion of BLT-1 prevented high fat-induced loss of insulin signaling in liver and skeletal muscle. These observations elucidate a novel role of chemoattractant receptor, BLT-1, in promoting monocyte trafficking to adipose tissue and promoting chronic inflammation in obesity and could lead to the identification of new therapeutic targets for treating insulin resistance in obesity.
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Citations
Cites
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“In particular, insulin resistance in the liver can be driven by fatty acid release from adipose tissue, resulting in hepatic triglyceride accumulation, and it can also arise from increased production of inflammatory cytokines from the adipose tissue (31, 32).”
BackgroundMacrophage-specific PPARγ controls alternative activation and improves insulin resistance
Odegaard, J. I., Ricardo-Gonzalez, R. R., Goforth, M. H., Morel, C. R., Subramanian, V., Mukundan, L., Eagle, A. R., Vats, D., Brombacher, F., Ferrante, A. W., et al. (2007) · Nature · doi:10.1038/nature05894 · Cited by 2,107 · cited 1×
“nuclear receptor is associated with increased insulin sensitivity (43), it is likely that PPARg may be in part responsible for the higher proportion of M2 macrophages in adipose tissue of BLT-1 mice.”
Background
Cited by
Inflammation in obesity, diabetes, and related disorders
Rohm, T. V., Meier, D. T., Olefsky, J. M., & Donath, M. Y. (2022) · Immunity · doi:10.1016/j.immuni.2021.12.013 · Cited by 2,066
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Inflammation and Lipid Signaling in the Etiology of Insulin Resistance
Glass, C. K., & Olefsky, J. M. (2012) · Cell Metabolism · doi:10.1016/j.cmet.2012.04.001 · Cited by 935
Metadata
- Authors
- Spite, M., Hellmann, J., Tang, Y., Mathis, S. P., Kosuri, M., Bhatnagar, A., Jala, V. R., & Haribabu, B.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-08
- Volume
- 187
- Issue
- 4
- Pages
- 1942-1949
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2158768487
- Cited by
- 175
- References
- 18
- FWCI
- 8.21
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Deficiency of the Leukotriene B4 Receptor, BLT-1, Protects against Systemic Insulin Resistance in Diet-Induced Obesity. https://app.cochat.ai/papers/10.4049/jimmunol.1100196
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- Spite, M., Hellmann, J., Tang, Y., Mathis, S. P., Kosuri, M., Bhatnagar, A., Jala, V. R., & Haribabu, B. (2011). Deficiency of the Leukotriene B4 Receptor, BLT-1, Protects against Systemic Insulin Resistance in Diet-Induced Obesity. The Journal of Immunology. https://doi.org/10.4049/jimmunol.1100196
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