The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Brain fatty acid synthase activates PPARα to maintain energy homeostasis
Open accessAbstract
Central nervous system control of energy balance affects susceptibility to obesity and diabetes, but how fatty acids, malonyl-CoA, and other metabolites act at this site to alter metabolism is poorly understood. Pharmacological inhibition of fatty acid synthase (FAS), rate limiting for de novo lipogenesis, decreases appetite independently of leptin but also promotes weight loss through activities unrelated to FAS inhibition. Here we report that the conditional genetic inactivation of FAS in pancreatic beta cells and hypothalamus produced lean, hypophagic mice with increased physical activity and impaired hypothalamic PPARalpha signaling. Administration of a PPARalpha agonist into the hypothalamus increased PPARalpha target genes and normalized food intake. Inactivation of beta cell FAS enzyme activity had no effect on islet function in culture or in vivo. These results suggest a critical role for brain FAS in the regulation of not only feeding, but also physical activity, effects that appear to be mediated through the provision of ligands generated by FAS to PPARalpha. Thus, 2 diametrically opposed proteins, FAS (induced by feeding) and PPARalpha (induced by starvation), unexpectedly form an integrative sensory module in the central nervous system to orchestrate energy balance.
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Cites
Central nervous system control of food intake and body weight
Morton, G. J., Cummings, D. E., Baskin, D. G., Barsh, G. S., & Schwartz, M. W. (2006) · Nature · doi:10.1038/nature05026 · Cited by 2,503
Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia
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Chronic intracerebroventricular infusion of insulin reduces food intake and body weight of baboons
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Central Administration of Oleic Acid Inhibits Glucose Production and Food Intake
Obici, S., Feng, Z., Morgan, K., Stein, D., Karkanias, G., & Rossetti, L. (2002) · Diabetes · doi:10.2337/diabetes.51.2.271 · Cited by 654
Obici, S., Feng, Z., Arduini, A., Conti, R., & Rossetti, L. (2003) · Nature Medicine · doi:10.1038/nm873 · Cited by 548
Dysregulation of insulin receptor substrate 2 in β cells and brain causes obesity and diabetes
Lin, X., Taguchi, A., Park, S., Kushner, J. A., Li, F., Li, Y., & White, M. F. (2004) · Journal of Clinical Investigation · doi:10.1172/jci22217 · Cited by 313
Restoration of hypothalamic lipid sensing normalizes energy and glucose homeostasis in overfed rats
Pocai, A. (2006) · Journal of Clinical Investigation · doi:10.1172/jci26640 · Cited by 211
PPARα is necessary for the lipopenic action of hyperleptinemia on white adipose and liver tissue
Lee, Y., Yu, X., Gonzales, F., Mangelsdorf, D. J., Wang, M.-Y., Richardson, C., Witters, L. A., & Unger, R. H. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.182420899 · Cited by 181
Cited by
Molecular Actions of PPARα in Lipid Metabolism and Inflammation
Bougarne, N., Weyers, B., Desmet, S. J., Deckers, J., Ray, D. W., Staels, B., & De Bosscher, K. (2018) · Endocrine Reviews · doi:10.1210/er.2018-00064 · Cited by 898
Identification of a Physiologically Relevant Endogenous Ligand for PPARα in Liver
Chakravarthy, M. V., Lodhi, I. J., Yin, L., Malapaka, R. R. V., Xu, H. E., Turk, J., & Semenkovich, C. F. (2009) · Cell · doi:10.1016/j.cell.2009.05.036 · Cited by 533
Self-citationThe Metabolic Serine Hydrolases and Their Functions in Mammalian Physiology and Disease
Long, J. Z., & Cravatt, B. F. (2011) · Chemical Reviews · doi:10.1021/cr200075y · Cited by 425
Fatty acid synthase and liver triglyceride metabolism: Housekeeper or messenger?
Jensen-Urstad, A. P. L., & Semenkovich, C. F. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2011.09.017 · Cited by 406
Self-citationPPARα: Energy Combustion, Hypolipidemia, Inflammation and Cancer
Pyper, S. R., Viswakarma, N., Yu, S., & Reddy, J. K. (2010) · Nuclear Receptor Signaling · doi:10.1621/nrs.08002 · Cited by 379
Metadata
- Authors
- Chakravarthy, M. V., Zhu, Y., López, M., Yin, L., Wozniak, D. F., Coleman, T., Hu, Z., Wolfgang, M., Vidal-Puig, A., Lane, M. D., & Semenkovich, C. F.
- Venue
- Journal of Clinical Investigation
- Published
- 2007-09-04
- Volume
- 117
- Issue
- 9
- Pages
- 2539-2552
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2131463221
- Cited by
- 207
- References
- 8
- FWCI
- 7.56
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Chakravarthy, M. V., Zhu, Y., López, M., Yin, L., Wozniak, D. F., Coleman, T., Hu, Z., Wolfgang, M., Vidal-Puig, A., Lane, M. D., & Semenkovich, C. F. (2007). Brain fatty acid synthase activates PPARα to maintain energy homeostasis. Journal of Clinical Investigation. https://doi.org/10.1172/jci31183
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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