The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Reversal of Hypertriglyceridemia, Fatty Liver Disease, and Insulin Resistance by a Liver-Targeted Mitochondrial Uncoupler
Open accessAbstract
Summary Non-alcoholic fatty liver disease (NAFLD) affects one in three Americans and is a major predisposing condition for type 2 diabetes (T2D), however there are currently no drugs available to treat this disease. We examined whether a functionally liver-targeted derivative of 2,4-dinitrophenol (DNP), DNP-methyl ether (DNPME), could safely decrease hypertriglyceridemia, NAFLD and insulin resistance without systemic toxicities. Treatment with DNPME reversed hypertriglyceridemia, fatty liver and whole-body insulin resistance in high-fat fed rats and decreased hyperglycemia in a rat model of T2D with a wide therapeutic index. The reversal of liver and muscle insulin resistance was associated with reductions in tissue diacylglycerol content and reductions in PKCε and PKCθ activity in liver and muscle respectively. These results demonstrate that the beneficial effects of DNP on hypertriglyceridemia, fatty liver and insulin resistance can be dissociated from systemic toxicities and suggest the potential utility of liver-targeted mitochondrial uncoupling agents for the treatment of the related epidemics of NAFLD, metabolic syndrome and type 2 diabetes.
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Cites
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“The COBAS Mira Plus (Roche Diagnostics) was used to measure plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), and blood urea nitrogen (BUN), and creatinine was measured by LC-MS/MS. Daily creatinine clearance was measured by housing rats treated with DNPME or vehicle in metabolic cages for 24 hr…”
BackgroundMethodInfluentialSelf-citationMechanism of hepatic insulin resistance in non-alcoholic fatty liver disease
Samuel, V. T., Liu, Z.-X., Qu, X., Elder, B. D., Bilz, S., Befroy, D., Romanelli, A. J., & Shulman, G. I. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m313478200 · Cited by 1,322
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UCP2 mediates ghrelin’s action on NPY/AgRP neurons by lowering free radicals
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MethodSelf-citation
Cited by
Mechanisms of Insulin Action and Insulin Resistance
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Metadata
- Authors
- Perry, R. J., Kim, T., Zhang, X.-M., Lee, H.-Y., Pesta, D., Popov, V. B., Zhang, D., Rahimi, Y., Jurczak, M. J., Cline, G. W., Spiegel, D. A., & Shulman, G. I.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 18
- Issue
- 5
- Pages
- 740-748
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2017004251
- Cited by
- 230
- References
- 11
- FWCI
- 9.73
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Perry, R. J., Kim, T., Zhang, X.-M., Lee, H.-Y., Pesta, D., Popov, V. B., Zhang, D., Rahimi, Y., Jurczak, M. J., Cline, G. W., Spiegel, D. A., & Shulman, G. I. (2013). Reversal of Hypertriglyceridemia, Fatty Liver Disease, and Insulin Resistance by a Liver-Targeted Mitochondrial Uncoupler. Cell Metabolism. https://doi.org/10.1016/j.cmet.2013.10.004
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
