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Increased 4E-BP1 Expression Protects against Diet-Induced Obesity and Insulin Resistance in Male Mice
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Genetic depletion of mTORC1 subunits, deletion of S6K1 or downstream substrates, or expression of dominant negative 4E-BP1 in specific tissues extends lifespan and healthspan of mice.
“Studies in mice have likewise shown that genetic depletion of mTORC1 subunits, deletion of S6K1 or downstream substrates, or expression of dominant negative 4E-BP1 in specific tissues extends the lifespan and healthspan of mice 13–16.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [16]
The Results section reports lifespan extension in female S6K1-knockout mice and protection from aging-related metabolic decline in mice overexpressing wild-type 4E-BP1. The Discussion reports metabolic benefits from tissue-specific expression of activated 4E-BP1, but the paper does not report lifespan extension from that intervention or from depletion of mTORC1 subunits. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredWhole body overexpression of 4E-BP1 has positive effects on healthspan, protecting male mice from diet-induced obesity.
“Interestingly, whole body overexpression of 4E-BP1 also has positive effects on healthspan, protecting male mice from diet-induced obesity 16.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [16]
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Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity
Um, S. H., Frigerio, F., Watanabe, M., Picard, F., Joaquin, M., Sticker, M., Fumagalli, S., Allegrini, P. R., Kozma, S. C., Auwerx, J., et al. (2004) · Nature · doi:10.1038/nature02866 · Cited by 1,677
Ribosomal Protein S6 Kinase 1 Signaling Regulates Mammalian Life Span
Selman, C., Tullet, J. M. A., Wieser, D., Irvine, E., Lingard, S. J., Choudhury, A. I., Claret, M., Al-Qassab, H., Carmignac, D., Ramadani, F., et al. (2009) · Science · doi:10.1126/science.1177221 · Cited by 1,120 · cited 1×
“The distinct expression pattern of 4E-BP1 and S6K1 in aging mouse tissues could be the reason why only female s6k1 knockout mice have lifespan extension (Selman et al., 2009) and male 4EBP1wt-OE mice are protected from aging-induced metabolic decline.”
BackgroundCopps, K. D., & White, M. F. (2012) · Diabetologia · doi:10.1007/s00125-012-2644-8 · Cited by 1,017 · cited 1×
“The protein stability of IRS1, insulin receptor substrate 1, is affected through serine phosphorylation by either S6K1 at Ser-307 or mTORC1 at Ser-636/639, and has been proposed to lead to insulin resistance (Copps and White, 2012; Um et al., 2006).”
BackgroundAdaptive thermogenesis in adipocytes: Is beige the new brown?
Wu, J., Cohen, P., & Spiegelman, B. M. (2013) · Genes & Development · doi:10.1101/gad.211649.112 · Cited by 828 · cited 2×
“White adipose is the major tissue that stores excess energy and regulates thermogenesis (Tseng et al., 2010; Wu et al., 2013).”
BackgroundCowie, C. C., Rust, K. F., Byrd-Holt, D. D., Gregg, E. W., Ford, E. S., Geiss, L. S., Bainbridge, K. E., & Fradkin, J. E. (2010) · Diabetes Care · doi:10.2337/dc09-1524 · Cited by 689
Cellular bioenergetics as a target for obesity therapy
Tseng, Y.-H., Cypess, A. M., & Kahn, C. R. (2010) · Nature Reviews Drug Discovery · doi:10.1038/nrd3138 · Cited by 591
Association of Weight Status With Mortality in Adults With Incident Diabetes
Carnethon, M. R., De Chavez, P. J. D., Biggs, M. L., Lewis, C. E., Pankow, J. S., Bertoni, A. G., Golden, S. H., Liu, K., Mukamal, K. J., Campbell-Jenkins, B., et al. (2012) · JAMA · doi:10.1001/jama.2012.9282 · Cited by 567
Role of mTOR in podocyte function and diabetic nephropathy in humans and mice
Gödel, M., Hartleben, B., Herbach, N., Liu, S., Zschiedrich, S., Lu, S., Debreczeni-Mór, A., Lindenmeyer, M. T., Rastaldi, M.-P., Hartleben, G., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci44774 · Cited by 547
mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy in mice
Inoki, K., Mori, H., Wang, J., Suzuki, T., Hong, S., Yoshida, S., Blattner, S. M., Ikenoue, T., Rüegg, M. A., Hall, M. N., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci44771 · Cited by 538
Adipose-Specific Knockout of raptor Results in Lean Mice with Enhanced Mitochondrial Respiration
Polak, P., Cybulski, N., Feige, J. N., Auwerx, J., Rüegg, M. A., & Hall, M. N. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.09.003 · Cited by 480 · cited 2×
“Reduced mTORC1 activity has been reported to prevent development of T2D and protect against diabetic nephropathy in both type I and type II diabetic mouse models (Godel et al., 2011; Inoki et al., 2011; Polak et al., 2008; Um et al., 2004; Yang et al., 2007).”
BackgroundDazert, E., & Hall, M. N. (2011) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2011.09.003 · Cited by 460
Sex and depot differences in adipocyte insulin sensitivity and glucose metabolism
Macotela, Y., Boucher, J., Tran, T. T., & Kahn, C. R. (2009) · Diabetes · doi:10.2337/db08-1054 · Cited by 401
A microarray analysis of sexual dimorphism of adipose tissues in high-fat-diet-induced obese mice
Grove, K. L., Fried, S. K., Greenberg, A. S., Xiao, X. Q., & Clegg, D. J. (2010) · International Journal of Obesity · doi:10.1038/ijo.2010.12 · Cited by 208
Stubbins, R. E., Najjar, K., Holcomb, V. B., Hong, J., & Núñez, N. P. (2012) · Diabetes, Obesity and Metabolism · doi:10.1111/j.1463-1326.2011.01488.x · Cited by 204
Flagged first, then by citations
Research works printed but not linked: 28
- Baar, 2016, Sex- and tissue-specific changes in mTOR signaling with age in C57BL/6J mice, Aging Cell, 15, 155, 10.1111/acel.12425 · DOI · Paper page
- Bloor, 2014, Sexual dimorphism in white and brown adipose tissue with obesity and inflammation, Horm. Behav., 66, 95, 10.1016/j.yhbeh.2014.02.007 · DOI
- Blüher, 2003, Extended longevity in mice lacking the insulin receptor in adipose tissue, Science, 299, 572, 10.1126/science.1078223 · DOI · Paper page
- Brown, 2010, Metabolic impact of sex hormones on obesity, Brain Res., 1350, 77, 10.1016/j.brainres.2010.04.056 · DOI
- Cornu, 2013, mTOR in aging, metabolism, and cancer, Curr. Opin. Genet. Dev., 23, 53, 10.1016/j.gde.2012.12.005 · DOI
- Elbein, 2012, Genetic risk factors for type 2 diabetes: a trans-regulatory genetic architecture?, Am. J. Hum. Genet., 91, 466, 10.1016/j.ajhg.2012.08.002 · DOI
- Laplante, 2012, mTOR signaling in growth control and disease, Cell, 149, 274, 10.1016/j.cell.2012.03.017 · DOI · Paper page
- Laplante, 2012, DEPTOR cell-autonomously promotes adipogenesis, and its expression is associated with obesity, Cell Metab., 16, 202, 10.1016/j.cmet.2012.07.008 · DOI
- Le Bacquer, 2007, Elevated sensitivity to diet-induced obesity and insulin resistance in mice lacking 4E-BP1 and 4E-BP2, J. Clin. Invest., 117, 387, 10.1172/JCI29528 · DOI
- Lyssenko, 2013, Genetic screening for the risk of type 2 diabetes: worthless or valuable?, Diabetes Care, 36, S120, 10.2337/dcS13-2009 · DOI
- Mauvais-Jarvis, 2013, The role of estrogens in control of energy balance and glucose homeostasis, Endocr. Rev., 34, 309, 10.1210/er.2012-1055 · DOI · Paper page
- Morris, 2012, Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes, Nat. Genet., 44, 981, 10.1038/ng.2383 · DOI · Paper page
- Oshiro, 2007, The proline-rich Akt substrate of 40 kDa (PRAS40) is a physiological substrate of mammalian target of rapamycin complex 1, J Biol Chem., 282, 20329, 10.1074/jbc.M702636200 · DOI
- Nickelson, 2012, A comparison of inflammatory and oxidative stress markers in adipose tissue from weight-matched obese male and female mice, Exp. Diabetes Res., 2012, 859395, 10.1155/2012/859395 · DOI
- Pettersson, 2012, Female mice are protected against high-fat diet induced metabolic syndrome and increase the regulatory T cell population in adipose tissue, PLoS ONE, 7, e46057, 10.1371/journal.pone.0046057 · DOI
- Rolli-Derkinderen, 2003, ERK and p38 inhibit the expression of 4E-BP1 repressor of translation through induction of Egr-1, J. Biol. Chem., 278, 18859, 10.1074/jbc.M211696200 · DOI
- Samuel, 2012, Mechanisms for insulin resistance: common threads and missing links, Cell, 148, 852, 10.1016/j.cell.2012.02.017 · DOI · Paper page
- Sonenberg, 2009, Regulation of translation initiation in eukaryotes: mechanisms and biological targets, Cell, 136, 731, 10.1016/j.cell.2009.01.042 · DOI · Paper page
- Tominaga, 2010, The JNK pathway modulates expression and phosphorylation of 4E-BP1 in MIN6 pancreatic beta-cells under oxidative stress conditions, Cell Biochem. Funct., 28, 387, 10.1002/cbf.1667 · DOI
- Tsai, 2015, Muscle-specific 4E-BP1 signaling activation improves metabolic parameters during aging and obesity, J. Clin. Invest., 125, 2952, 10.1172/JCI77361 · DOI · Paper page
- Tsukiyama-Kohara, 2001, Adipose tissue reduction in mice lacking the translational inhibitor 4E-BP1, Nat. Med., 7, 1128, 10.1038/nm1001-1128 · DOI
- Um, 2006, Nutrient overload, insulin resistance, and ribosomal protein S6 kinase 1, S6K1, Cell Metab., 3, 393, 10.1016/j.cmet.2006.05.003 · DOI · Paper page
- Walsh, 2008, Eukaryotic translation initiation factor 4F architectural alterations accompany translation initiation factor redistribution in poxvirus-infected cells, Mol. Cell. Biol., 28, 2648, 10.1128/MCB.01631-07 · DOI
- Wang, 2008, Regulation of proline-rich Akt substrate of 40 kDa (PRAS40) function by mammalian target of rapamycin complex 1 (mTORC1)-mediated phosphorylation, J Biol Chem., 283, 15619, 10.1074/jbc.M800723200 · DOI
- Weichhart, 2008, The TSC-mTOR signaling pathway regulates the innate inflammatory response, Immunity, 29, 565, 10.1016/j.immuni.2008.08.012 · DOI · Paper page
- Williams, 2014, Sequence variants in SLC16A11 are a common risk factor for type 2 diabetes in Mexico, Nature, 506, 97, 10.1038/nature12828 · DOI
- Yang, 2007, Rapamycin prevents early steps of the development of diabetic nephropathy in rats, Am. J. Nephrol., 27, 495, 10.1159/000106782 · DOI
- Zeyda, 2007, Adipose tissue macrophages, Immunol. Lett., 112, 61, 10.1016/j.imlet.2007.07.003 · DOI
Cited by
Sorted by citations
Targeting the biology of aging with mTOR inhibitors
Mannick, J. B., & Lamming, D. W. (2023) · Nature Aging · doi:10.1038/s43587-023-00416-y · Cited by 372
Metadata
- Authors
- Tsai, S.-Y., Rodriguez, A. A., Dastidar, S. G., Del Greco, E., Carr, K. L., Sitzmann, J. M., Academia, E. C., Viray, C. M., Martinez, L. L., Kaplowitz, B. S., Ashe, T. D., La Spada, A. R., & Kennedy, B. K.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 16
- Issue
- 7
- Pages
- 1903-1914
- ISSN
- 2211-1247
- PMC
- PMC4988876
- Cited by
- 63
- References
- 14
- Language
- en
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