The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
High-Fat-Diet-Induced Obesity and Heart Dysfunction Are Regulated by the TOR Pathway in Drosophila
Open accessAbstract
High Fat Diet (HFD)-induced obesity is a major contributor to diabetes and cardiovascular disease, but the underlying genetic mechanisms are poorly understood. Here, we use Drosophila to test the hypothesis that HFD-induced obesity and associated cardiac complications have early evolutionary origins involving nutrient-sensing signal transduction pathways. We find that HFD-fed flies exhibit increased triglyceride (TG) fat and alterations in insulin/glucose homeostasis, similar to mammalian responses. A HFD also causes cardiac lipid accumulation, reduced cardiac contractility, conduction blocks and severe structural pathologies, reminiscent of diabetic cardiomyopathies. Remarkably, these metabolic and cardiotoxic phenotypes elicited by HFD are blocked by inhibiting insulin-TOR signaling. Remarkably, reducing insulin-TOR activity by TSC1-2, 4EBP, FOXO) or increasing lipase expression in the myocardium suffices to efficiently alleviate cardiac fat accumulation and dysfunction induced by HFD. We conclude that deregulation of insulin-TOR signaling due to a HFD is responsible for mediating the detrimental effects on metabolism and heart function.
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Cites
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Mechanisms linking obesity with cardiovascular disease
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Influence of TOR kinase on lifespan in C. elegans
Vellai, T., Takacs-Vellai, K., Zhang, Y., Kovacs, A. L., Orosz, L., & Müller, F. (2003) · Nature · doi:10.1038/426620a · Cited by 1,057
Li, S., Brown, M. S., & Goldstein, J. L. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0914798107 · Cited by 733 · cited 6×
“In addition, this effect is also observed in mammalian hepatocytes where TOR function is required for SREBP activation (Li et al., 2010), and it has been proposed that TOR serves as an important fork in the road of diabetic insulin resistance separating gluconeogenesis from lipogenesis (Li et al.”
InfluentialBentzinger, C. F., Romanino, K., Cloëtta, D., Lin, S., Mascarenhas, J. B., Oliveri, F., Xia, J., Casanova, E., Costa, C. F., Brink, M., et al. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.10.002 · Cited by 640 · cited 2×
“Consistent with this idea, loss of SREBP and FAS function in mammalian models leads to low TG levels (Valet et al., 2002; Bentzinger et al., 2008), and loss of Drosophila easily shocked (eas), which encodes an ethanolamine kinase critical for PE synthesis, leads to increased levels of the active…”
BackgroundSestrin as a feedback inhibitor of TOR that prevents age-related pathologies
Lee, J. H., Budanov, A. V., Park, E. J., Birse, R., Kim, T. E., Perkins, G. A., Ocorr, K., Ellisman, M. H., Bodmer, R., Bier, E., et al. (2010) · Science · doi:10.1126/science.1182228 · Cited by 570
Self-citationLipid accumulation in non-adipose tissue and lipotoxicity
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The SREBP pathway — insights from insigs and insects
Rawson, R. B. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1174 · Cited by 323
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Cited by
Ageing as a Risk Factor for Disease
Niccoli, T., & Partridge, L. (2012) · Current Biology · doi:10.1016/j.cub.2012.07.024 · Cited by 1,831
Animal models of obesity and diabetes mellitus
Kleinert, M., Clemmensen, C., Hofmann, S. M., Moore, M. C., Renner, S., Woods, S. C., Huypens, P., Beckers, J., de Angelis, M. H., Schürmann, A., et al. (2018) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2017.161 · Cited by 832
Methods for studying metabolism in Drosophila
Tennessen, J. M., Barry, W. E., Cox, J., & Thummel, C. S. (2014) · Methods · doi:10.1016/j.ymeth.2014.02.034 · Cited by 445
Time-Restricted Eating to Prevent and Manage Chronic Metabolic Diseases
Chaix, A., Manoogian, E. N. C., Melkani, G. C., & Panda, S. (2019) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-082018-124320 · Cited by 398
Fat Body Biology in the Last Decade
Li, S., Yu, X., & Feng, Q. (2019) · Annual Review of Entomology · doi:10.1146/annurev-ento-011118-112007 · Cited by 331
Metadata
- Authors
- Birse, R. T., Choi, J., Reardon, K., Rodriguez, J., Graham, S., Diop, S., Ocorr, K., Bodmer, R., & Oldham, S.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-11
- Volume
- 12
- Issue
- 5
- Pages
- 533-544
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2005012161
- Cited by
- 385
- References
- 9
- FWCI
- 10.83
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Birse, R. T., Choi, J., Reardon, K., Rodriguez, J., Graham, S., Diop, S., Ocorr, K., Bodmer, R., & Oldham, S. (2010). High-Fat-Diet-Induced Obesity and Heart Dysfunction Are Regulated by the TOR Pathway in Drosophila. Cell Metabolism. https://doi.org/10.1016/j.cmet.2010.09.014
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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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