The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
PPARδ regulates glucose metabolism and insulin sensitivity
Abstract
The metabolic syndrome is a collection of obesity-related disorders. The peroxisome proliferator-activated receptors (PPARs) regulate transcription in response to fatty acids and, as such, are potential therapeutic targets for these diseases. We show that PPARδ (NR1C2) knockout mice are metabolically less active and glucose-intolerant, whereas receptor activation in db/db mice improves insulin sensitivity. Euglycemic–hyperinsulinemic-clamp experiments further demonstrate that a PPARδ-specific agonist suppresses hepatic glucose output, increases glucose disposal, and inhibits free fatty acid release from adipocytes. Unexpectedly, gene array and functional analyses suggest that PPARδ ameliorates hyperglycemia by increasing glucose flux through the pentose phosphate pathway and enhancing fatty acid synthesis. Coupling increased hepatic carbohydrate catabolism with its ability to promote β-oxidation in muscle allows PPARδ to regulate metabolic homeostasis and enhance insulin action by complementary effects in distinct tissues. The combined hepatic and peripheral actions of PPARδ suggest new therapeutic approaches to treat type II diabetes.
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Self-citationPeroxisome-Proliferator-Activated Receptor δ Activates Fat Metabolism to Prevent Obesity
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Self-citationKamei, Y., Ohizumi, H., Fujitani, Y., Nemoto, T., Tanaka, T., Takahashi, N., Kawada, T., Miyoshi, M., Ezaki, O., & Kakizuka, A. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2135217100 · Cited by 357
Activation of PPARδ alters lipid metabolism in db/db mice
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Cited by
Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver
Friedman, S. L. (2008) · Physiological Reviews · doi:10.1152/physrev.00013.2007 · Cited by 2,842
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Mechanisms underlying the resistance to diet-induced obesity in germ-free mice
Bäckhed, F., Manchester, J. K., Semenkovich, C. F., & Gordon, J. I. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605374104 · Cited by 2,615
PPARs in Obesity-Induced T2DM, Dyslipidaemia and NAFLD
Gross, B., Pawlak, M., Lefebvre, P., & Staels, B. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.135 · Cited by 778
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Metadata
- Authors
- Lee, C.-H., Olson, P., Hevener, A., Mehl, I., Chong, L.-W., Olefsky, J. M., Gonzalez, F. J., Ham, J., Kang, H., Peters, J. M., & Evans, R. M.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2006-02-21
- Volume
- 103
- Issue
- 9
- Pages
- 3444-3449
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2128557965
- Cited by
- 497
- References
- 9
- FWCI
- 15.72
- Type
- journal article
- Language
- en
- Open access
- closed
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- Lee, C.-H., Olson, P., Hevener, A., Mehl, I., Chong, L.-W., Olefsky, J. M., Gonzalez, F. J., Ham, J., Kang, H., Peters, J. M., & Evans, R. M. (2006). PPARδ regulates glucose metabolism and insulin sensitivity. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0511253103
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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