The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
Hyperuricemia as a Mediator of the Proinflammatory Endocrine Imbalance in the Adipose Tissue in a Murine Model of the Metabolic Syndrome
Open accessAbstract
OBJECTIVE: Hyperuricemia is strongly associated with obesity and metabolic syndrome and can predict visceral obesity and insulin resistance. Previously, we showed that soluble uric acid directly stimulated the redox-dependent proinflammatory signaling in adipocytes. In this study we demonstrate the role of hyperuricemia in the production of key adipokines. RESEARCH DESIGN AND METHODS: We used mouse 3T3-L1 adipocytes, human primary adipocytes, and a mouse model of metabolic syndrome and hyperuricemia. RESULTS: Uric acid induced in vitro an increase in the production (mRNA and secreted protein) of monocyte chemotactic protein-1 (MCP-1), an adipokine playing an essential role in inducing the proinflammatory state in adipocytes in obesity. In addition, uric acid caused a decrease in the production of adiponectin, an adipocyte-specific insulin sensitizer and anti-inflammatory agent. Uric acid–induced increase in MCP-1 production was blocked by scavenging superoxide or by inhibiting NADPH oxidase and by stimulating peroxisome-proliferator–activated receptor-γ with rosiglitazone. Downregulation of the adiponectin production was prevented by rosiglitazone but not by antioxidants. In obese mice with metabolic syndrome, we observed hyperuricemia. Lowering uric acid in these mice by inhibiting xanthine oxidoreductase with allopurinol could improve the proinflammatory endocrine imbalance in the adipose tissue by reducing production of MCP-1 and increasing production of adiponectin. In addition, lowering uric acid in obese mice decreased macrophage infiltration in the adipose tissue and reduced insulin resistance. CONCLUSIONS: Hyperuricemia might be partially responsible for the proinflammatory endocrine imbalance in the adipose tissue, which is an underlying mechanism of the low-grade inflammation and insulin resistance in subjects with the metabolic syndrome.
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Cites
Obesity is associated with macrophage accumulation in adipose tissue
Weisberg, S. P., McCann, D., Desai, M., Rosenbaum, M., Leibel, R. L., & Ferrante, A. W. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319246 · Cited by 10,041
Adipose Expression of Tumor Necrosis Factor-α: Direct Role in Obesity-Linked Insulin Resistance
Hotamisligil, G. S., Shargill, N. S., & Spiegelman, B. M. (1993) · Science · doi:10.1126/science.7678183 · Cited by 7,518
Xu, H., Barnes, G. T., Yang, Q., Tan, G., Yang, D., Chou, C. J., Sole, J., Nichols, A., Ross, J. S., Tartaglia, L. A., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319451 · Cited by 6,760
Adipose Tissue as an Endocrine Organ
Kershaw, E. E., & Flier, J. S. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-0395 · Cited by 5,522
Increased oxidative stress in obesity and its impact on metabolic syndrome
Furukawa, S., Fujita, T., Shimabukuro, M., Iwaki, M., Yamada, Y., Nakajima, Y., Nakayama, O., Makishima, M., Matsuda, M., & Shimomura, I. (2004) · Journal of Clinical Investigation · doi:10.1172/jci21625 · Cited by 5,508
Inflammation, stress, and diabetes
Wellen, K. E., & Hotamisligil, G. S. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25102 · Cited by 4,143
Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome
Kadowaki, T. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29126 · Cited by 2,824
Kanda, H. (2006) · Journal of Clinical Investigation · doi:10.1172/jci26498 · Cited by 2,682
Adiponectin and Adiponectin Receptors
Kadowaki, T., & Yamauchi, T. (2005) · Endocrine Reviews · doi:10.1210/er.2005-0005 · Cited by 2,634
Uric Acid and Cardiovascular Risk
Feig, D. I., Kang, D.-H., & Johnson, R. J. (2008) · New England Journal of Medicine · doi:10.1056/nejmra0800885 · Cited by 2,440
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Sugar, Uric Acid, and the Etiology of Diabetes and Obesity
Johnson, R. J., Nakagawa, T., Sanchez-Lozada, L. G., Shafiu, M., Sundaram, S., Le, M., Ishimoto, T., Sautin, Y. Y., & Lanaspa, M. A. (2013) · Diabetes · doi:10.2337/db12-1814 · Cited by 760
Self-citationUric Acid Induces Hepatic Steatosis by Generation of Mitochondrial Oxidative Stress
Lanaspa, M. A., Sanchez-Lozada, L. G., Choi, Y.-J., Cicerchi, C., Kanbay, M., Roncal-Jimenez, C. A., Ishimoto, T., Li, N., Marek, G., Duranay, M., et al. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.399899 · Cited by 710
Self-citationThe pathophysiology of hypertension in patients with obesity
DeMarco, V. G., Aroor, A. R., & Sowers, J. R. (2014) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2014.44 · Cited by 545
Uric acid in metabolic syndrome: From an innocent bystander to a central player
Kanbay, M., Jensen, T., Solak, Y., Le, M., Roncal-Jimenez, C., Rivard, C., Lanaspa, M. A., Nakagawa, T., & Johnson, R. J. (2016) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2015.11.026 · Cited by 419
Self-citationJourdan, T., Godlewski, G., Cinar, R., Bertola, A., Szanda, G., Liu, J., Tam, J., Han, T., Mukhopadhyay, B., Skarulis, M. C., et al. (2013) · Nature Medicine · doi:10.1038/nm.3265 · Cited by 388
Metadata
- Authors
- Baldwin, W., McRae, S., Marek, G., Wymer, D., Pannu, V., Baylis, C., Johnson, R. J., & Sautin, Y. Y.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2011-03-22
- Volume
- 60
- Issue
- 4
- Pages
- 1258-1269
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2142436219
- Cited by
- 440
- References
- 49
- FWCI
- 17.94
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Baldwin, W., McRae, S., Marek, G., Wymer, D., Pannu, V., Baylis, C., Johnson, R. J., & Sautin, Y. Y. (2011). Hyperuricemia as a Mediator of the Proinflammatory Endocrine Imbalance in the Adipose Tissue in a Murine Model of the Metabolic Syndrome. Diabetes. https://doi.org/10.2337/db10-0916
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