Mature-onset obesity and insulin resistance in mice deficient in the signaling adapter p62
Open accessAbstract
Signaling cascades that control adipogenesis are essential in the regulation of body weight and obesity. The adaptor p62 controls pathways that modulate cell differentiation. We report here that p62(-/-) mice develop mature-onset obesity, leptin resistance, as well as impaired glucose and insulin intolerance. The metabolic rate was significantly reduced in p62(-/-) nonobese mice, which displayed increased mRNA levels of PPAR-gamma and reduced levels of UCP-1 in adipose tissue. Basal activity of ERK was enhanced in fat from nonobese mutant mice. Embryo fibroblasts from p62(-/-) mice differentiated better than the wild-type controls into adipocytes, which was abrogated by pharmacological inhibition of the ERK pathway. p62 is induced during adipocyte differentiation and inhibits ERK activation by direct interaction. We propose that p62 normally antagonizes basal ERK activity and adipocyte differentiation and that its loss leads to the hyperactivation of ERK that favors adipogenesis and obesity.
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From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [136]
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Interaction Domains of p62: A Bridge Between p62 and Selective Autophagy
Lin, X., Li, S., Zhao, Y., Ma, X., Zhang, K., He, X., & Wang, Z. (2013) · DNA and Cell Biology · doi:10.1089/dna.2012.1915 · Cited by 161 · see citing works
“Moreover, targeted deletion of mice p62 have been found to lead to insulin resistance, type 2 diabetes, and leptin resistance (Rodriguez et al. , 2006; Moscat and Diaz-Meco, 2011).”
Kim, K., Kim, J.-H., Wang, Y., & Sul, H. S. (2007) · Molecular and Cellular Biology · doi:10.1128/mcb.02207-06 · Cited by 155 · see citing works
“In this regard, it has been shown genetically in mice that ERK is necessary for adipogenesis and adiposity in vivo (7, 15, 32) and that MEF and preadipocytes isolated from ERK1 knockout mice have impaired adipogenesis (7).”
BackgroundHypoxia-activated autophagy accelerates degradation of SQSTM1/p62
Pursiheimo, J.-P., Rantanen, K., Heikkinen, P., Johansen, T., & Jaakkola, P. (2009) · Oncogene · doi:10.1038/onc.2008.392 · Cited by 161 · see citing works
Therapeutic Targeting of Autophagy
Orogo, A. M., & Gustafsson, Å. B. (2015) · Circulation Research · doi:10.1161/circresaha.116.303791 · Cited by 153 · see citing works
p62/SQSTM1 at the interface of aging, autophagy, and disease
Bitto, A., Lerner, C. A., Nacarelli, T., Crowe, E. P., Torres, C. A., & Sell, C. (2014) · AGE · doi:10.1007/s11357-014-9626-3 · Cited by 144 · see citing works
“…a negative feedback on the insulin receptor substrate 1 (IRS-1), thereby impairing insulin signaling (Um et al. 2004). mTORC1 response to insulin is independent of p62/ SQSTM1 (Duran et al. 2011) and the insulin signaling pathway is not impaired in young Sqstm1 −/− mice (Rodriguez et al. 2006).”
Functional CRISPR screening identifies the ufmylation pathway as a regulator of SQSTM1/p62
DeJesus, R., Moretti, F., McAllister, G., Wang, Z., Bergman, P., Liu, S., Frias, E., Alford, J., Reece-Hoyes, J. S., Lindeman, A., et al. (2016) · eLife · doi:10.7554/elife.17290 · Cited by 145 · see citing works
“SQSTM1 is a multifunctional adaptor protein that is mutated and deregulated in several pathological conditions, including Paget disease, neurodegeneration, metabolic dysfunction or cancer (Laurin et al., 2002; Rodriguez et al., 2006; Rubino et al., 2012; Takamura et al., 2011).”
BackgroundMeenhuis, A., van Veelen, P. A., de Looper, H., van Boxtel, N., van den Berge, I. J., Sun, S. M., Taskesen, E., Stern, P., de Ru, A. H., van Adrichem, A. J., et al. (2011) · Blood · doi:10.1182/blood-2011-02-336487 · Cited by 142 · see citing works
Lu, X., Altshuler-Keylin, S., Wang, Q., Chen, Y., Henrique Sponton, C., Ikeda, K., Maretich, P., Yoneshiro, T., & Kajimura, S. (2018) · Science Signaling · doi:10.1126/scisignal.aap8526 · Cited by 143 · see citing works
Feedback on Fat: p62-mTORC1-Autophagy Connections
Moscat, J., & Díaz-Meco, M. T. (2011) · Cell · doi:10.1016/j.cell.2011.10.021 · Cited by 140 · see citing works
“Much evidence suggests that p62 represses adiposity in an ERK1-dependent cell-autonomous manner (Rodriguez et al., 2006).”
BackgroundInfluentialSelf-citationAssurance of mitochondrial integrity and mammalian longevity by the p62–Keap1–Nrf2–Nqo1 cascade
Kwon, J., Han, E., Bui, C., Shin, W., Lee, J. H., Lee, S., Choi, Y., Lee, A., Lee, K., Park, C., et al. (2012) · EMBO Reports · doi:10.1038/embor.2011.246 · Cited by 139 · see citing works
“Thus, mature-onset obesity and features of neurodegeneration observed previously in p62 (cid:2) / (cid:2) mice (Rodriguez et al , 2006; Ramesh Babu et al , 2008) seem to have an inseparable relationship with the rapid ageing phenotype described in the present study.”
Role of p62/SQSTM1 in liver physiology and pathogenesis
Manley, S., Williams, J. A., & Ding, W.-X. (2013) · Experimental Biology and Medicine · doi:10.1177/1535370213489446 · Cited by 135 · see citing works
“Conversely, tyrosine phosphorylation of both IRS-1 and its downstream target Akt in response to insulin injection was severely decreased in both muscle and fat tissues of p62 KO mice.(94) These results suggest that p62 may play a positive role in insulin sensitivity by enhancing the insulin signalling pathway, and p62…”
BackgroundInfluentialEmerging role of p62/sequestosome-1 in the pathogenesis of Alzheimer's disease
Salminen, A., Kaarniranta, K., Haapasalo, A., Hiltunen, M., Soininen, H., & Alafuzoff, I. (2012) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2011.11.005 · Cited by 153 · see citing works
Rivera, J. F., Gurlo, T., Daval, M., Huang, C. J., Matveyenko, A. V., Butler, P. C., & Costes, S. (2010) · Cell Death and Differentiation · doi:10.1038/cdd.2010.111 · Cited by 136 · see citing works
“J Moscat (Cincinnati, OH, USA).(40) For plasmid amplification, 50ml of DH5a competent cells (Invitrogen) were transformed with either LC3-RFP or p62-GFP plasmid.”
MethodAdipose tissue macrophage in obesity-associated metabolic diseases
Yao, J., Wu, D., & Qiu, Y. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.977485 · Cited by 143 · see citing works
Tightrope act: autophagy in stem cell renewal, differentiation, proliferation, and aging
Phadwal, K., Watson, A., & Simon, A. K. (2012) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-012-1032-3 · Cited by 124 · see citing works
“targeting of poly-ubiquitinated proteins destined for degradation by autophagy and proteasomal pathways [54–56].”
BackgroundPB1 Domain Interaction of p62/Sequestosome 1 and MEKK3 Regulates NF-κB Activation
Nakamura, K., Kimple, A. J., Siderovski, D. P., & Johnson, G. L. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.065102 · Cited by 125 · see citing works
p62 Links β-adrenergic input to mitochondrial function and thermogenesis
Müller, T. D., Lee, S. J., Jastroch, M., Kabra, D. G., Stemmer, K., Aichler, M., Abplanalp, B., Ananthakrishnan, G., Bhardwaj, N. J., Collins, S., et al. (2012) · Journal of Clinical Investigation · doi:10.1172/jci64209 · Cited by 122 · see citing works
“We have previously shown that global ablation of p62 in mice results in obesity and systemic glucose intolerance and insulin resistance (18, 19).”
Self-citationHaack, T. B., Ignatius, E., Calvo‐Garrido, J., Iuso, A., Isohanni, P., Maffezzini, C., Lönnqvist, T. R. I., Suomalainen, A., Gorza, M., Kremer, L. S., et al. (2016) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2016.06.026 · Cited by 122 · see citing works
“In mice, the knock out of Sqstm1 leads to matureonset obesity, leptine resistance, and impaired glucose tolerance and insulin resistance potentially mediated by disturbed regulation of adipocyte differentiation due to enhanced basal ERK activity.(22) Furthermore, the chronic absence of Sqstm1/p62 promotes mature-onset…”
BackgroundApoptosis and autophagy: Targeting autophagy signalling in cancer cells –‘trick or treats’?
Corcelle–Termeau, E., Puustinen, P., & Jäättelä, M. (2009) · FEBS Journal · doi:10.1111/j.1742-4658.2009.07332.x · Cited by 121 · see citing works
Cancer and the Nuclear Pore Complex
Simon, D. N., & Rout, M. P. (2014) · Advances in experimental medicine and biology · doi:10.1007/978-1-4899-8032-8_13 · Cited by 121 · see citing works
Livingston, M. J., Zhang, M., Kwon, S., Chen, J., Li, H., Manicassamy, S., & Dong, Z. (2023) · Autophagy · doi:10.1080/15548627.2023.2281156 · Cited by 120 · see citing works
“Previous studies suggest that during adipogenesis SQSTM1/p62 may sequester MAPK/ERK into cytoplasmic aggregates to prevent the access of MAPK/ERK to its upstream kinase for phosphorylation and activation [32].”
BackgroundResultp62/SQSTM1 synergizes with autophagy for tumor growth in vivoPreprint
Wei, H., Wang, C., Croce, C. M., & Guan, J. (2014) · Genes & Development · doi:10.1101/gad.237354.113 · Cited by 115 · see citing works
“2006), p62-null mice can survive for more than 1 year but with defects in adult mice such as adult-onset obesity and diabetes (Rodriguez et al. 2006).”
BackgroundUse of p62/SQSTM1 antibodies for neuropathological diagnosis
Kuusisto, E., Kauppinen, T., & Alafuzoff, I. I. (2007) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2007.00884.x · Cited by 113 · see citing works
The Pathways Underlying the Multiple Roles of p62 in Inflammation and Cancer
Hennig, P., Fenini, G., Filippo, M. D., Karakaya, T., & Beer, H. (2021) · Biomedicines · doi:10.3390/biomedicines9070707 · Cited by 117 · see citing works
Milan, E., Perini, T., Resnati, M., Orfanelli, U., Oliva, L., Raimondi, A., Cascio, P., Bachi, A., Marcatti, M., Ciceri, F., et al. (2015) · Autophagy · doi:10.1080/15548627.2015.1052928 · Cited by 112 · see citing works
p62/ SQSTM 1—Dr. Jekyll and Mr. Hyde that prevents oxidative stress but promotes liver cancer
Taniguchi, K., Yamachika, S., He, F., & Karin, M. (2016) · FEBS Letters · doi:10.1002/1873-3468.12301 · Cited by 112 · see citing works
“adipogenesis [16, 288] although it was also reported that absence of p62 in the brain causes”
BackgroundHepatic ERK activity plays a role in energy metabolism
Jiao, P., Feng, B., Li, Y., He, Q., & Xu, H. (2013) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2013.05.021 · Cited by 112 · see citing works
“Deficiency of the signaling adaptor p62, a protein that antagonizes basal ERK activity, promotes adipogenesis in vitro and mature-onset obesity and insulin resistance in vivo (Rodriguez et al., 2006).”
BackgroundHuang, J., Durán, Á., Reina‐Campos, M., Valencia, T., Castilla, E. A., Müller, T. D., Tschöp, M. H., Moscat, J., & Díaz-Meco, M. T. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.03.001 · Cited by 111 · see citing works
“…tissue from non-tumor-bearing p62Adipo mice showed a significant increase in crown-like structure (CLS) compared with WT mice (Figures 6A and 6B), consistent with the enhanced inflammation previously reported in the adipose tissue of these mutant mice (Muller et al., 2013; Rodriguez et al., 2006).”
InfluentialSelf-citationKao, C., Chao, A., Tsai, C.-L., Chuang, W.-C., Huang, W.-P., Chen, G., Lin, C.-Y., Th, W., Wang, H., & Lai, C. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.468 · Cited by 109 · see citing works
“P62/ SQSTM1 was also shown to inhibit ERK phosphorylation, and the knockout of p62 was shown to enhance ERK activation in vivo.(47) On the other hand, ERK knockdown has been shown to induce autophagy,(48) and sustained ERK activation may inhibit the autophagic flux.”
BackgroundAutophagy as an emerging target in cardiorenal metabolic disease: From pathophysiology to management
Zhang, Y., Whaley‐Connell, A. T., Sowers, J. R., & Ren, J. T. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2018.06.004 · Cited by 109 · see citing works
“Global deletion of p62 promotes insulin resistance along with increased body fat mass (Rodriguez et al., 2006).”
A functional role for the p62–ERK1 axis in the control of energy homeostasis and adipogenesis
Lee, S. J., Pfluger, P. T., Kim, J. Y., Nogueiras, R., Durán, Á., Pagès, G., Pouysségur, J., Tschöp, M. H., Díaz-Meco, M. T., & Moscat, J. (2010) · EMBO Reports · doi:10.1038/embor.2010.7 · Cited by 108 · see citing works
“Interestingly, activation of ERK during in vitro adipogenesis has been reported to be biphasic (Sale et al, 1995).”
BackgroundSelf-citationSergin, I., Bhattacharya, S., Emanuel, R., Esen, E., Stokes, C. J., Evans, T. D., Arif, B., Curci, J. A., & Razani, B. (2016) · Science Signaling · doi:10.1126/scisignal.aad5614 · Cited by 108 · see citing works
Nucleophagy: from homeostasis to disease
Papandreou, M., & Tavernarakis, N. (2019) · Cell Death and Differentiation · doi:10.1038/s41418-018-0266-5 · Cited by 104 · see citing works
Age-associated oxidative damage to the p62 promoter: implications for Alzheimer disease
Du, Y., Wooten, M. C., Gearing, M., & Wooten, M. W. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2008.11.003 · Cited by 104 · see citing works
“Knockout mice (p62) were generated as described previously [25].”
Wu, Z., Jiao, P., Huang, X., Feng, B., Feng, Y., Yang, S., Hwang, P. W., Du, J., Nie, Y., Xiao, G., et al. (2010) · Journal of Clinical Investigation · doi:10.1172/jci43250 · Cited by 99 · see citing works
Transactivation of Atg4b by C/EBPβ Promotes Autophagy To Facilitate Adipogenesis
Guo, L., Huang, J.-X., Liu, Y., Li, X., Zhou, S.-R., Qian, S.-W., Liu, Y., Zhu, H., Huang, H.-Y., Dang, Y., et al. (2013) · Molecular and Cellular Biology · doi:10.1128/mcb.00193-13 · Cited by 100 · see citing works
Inside the β Cell: Molecular Stress Response Pathways in Diabetes Pathogenesis
Kulkarni, A., Muralidharan, C., May, S. C., Tersey, S. A., & Mirmira, R. G. (2022) · Endocrinology · doi:10.1210/endocr/bqac184 · Cited by 95 · see citing works
Cardioprotection requires taking out the trash
Gottlieb, R. A., Finley, K. D., & Mentzer, R. M. (2009) · Basic Research in Cardiology · doi:10.1007/s00395-009-0011-9 · Cited by 96 · see citing works
“Interestingly, genetic deletion of murine p62 results in viable adult mice that develop insulin resistance and obesity as early as 4 months of age [83].”
Shen, Y., Yang, J., Zhao, J., Xiao, C., Xu, C., & Xiang, Y. (2015) · Experimental Cell Research · doi:10.1016/j.yexcr.2015.04.010 · Cited by 92 · see citing works
Lattante, S., de Calbiac, H., Le Ber, I., Brice, A., Ciura, S., & Kabashi, E. (2015) · Human Molecular Genetics · doi:10.1093/hmg/ddu580 · Cited by 90 · see citing works
Mitochondrial homeostasis in adipose tissue remodeling
Altshuler-Keylin, S., & Kajimura, S. (2017) · Science Signaling · doi:10.1126/scisignal.aai9248 · Cited by 89 · see citing works
Linares, J. F., Amanchy, R., Díaz-Meco, M. T., & Moscat, J. (2010) · Molecular and Cellular Biology · doi:10.1128/mcb.00620-10 · Cited by 85 · see citing works
“The protein scaffold and signaling regulator p62 has been implicated in critical cellular functions such as bone homeostasis (2), obesity (20), and cancer (1) through the regulation of important signaling intermediaries like TRAF6/NF- B (23), the atypical protein kinase C isoforms (23), caspase-8 (4), ERK1 (10), and t…”
BackgroundSelf-citationSequestosome-1/p62 Is the Key Intracellular Target of Innate Defense Regulator Peptide
Yu, H. B., Kielczewska, A., Rozek, A., Takenaka, S., Li, Y., Thorson, L., Hancock, R. E. W., Guarna, M. M., North, J. R., Foster, L. J., et al. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.c109.073627 · Cited by 81 · see citing works
Huang, H., Zhu, J., Li, Y., Zhang, L., Gu, J., Xie, Q., Jin, H., Che, X., Li, J., Huang, C., et al. (2016) · Autophagy · doi:10.1080/15548627.2016.1196313 · Cited by 82 · see citing works
A role for sequestosome 1/p62 in mitochondrial dynamics, import and genome integrity
Seibenhener, M. L., Du, Y., Díaz-Meco, M. T., Moscat, J., Wooten, M. C., & Wooten, M. W. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2012.11.004 · Cited by 82 · see citing works
“Glucose tolerance tests in aged p62−/− mice have also shown to be defective in glucose uptake and insulin tolerance [4] indicative of glycolytic defects.”
Self-citationWhitehouse, C. A., Waters, S., Marchbank, K., Horner, A. A., McGowan, N. W. A., Jovanovic, J. V., Xavier, G. M., Kashima, T. G., Cobourne, M. T., Richards, G. O., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0913058107 · Cited by 83 · see citing works
“p62 null mice show defects in osteoclastogenesis in vitro because of reduced receptor activator for nuclear factorκ B ligand (RANKL)–stimulated NF-κB signaling and develop mature-onset obesity and insulin resistance through hyperactivation of ERK and adipogenesis (4).”
BackgroundForced lipophagy reveals that lipid droplets are required for early embryonic development in mouse
Tatsumi, T., Takayama, K., Ishii, S., Yamamoto, A., Hara, T., Minami, N., Miyasaka, N., Kubota, T., Matsuura, A., Itakura, E., et al. (2018) · Development · doi:10.1242/dev.161893 · Cited by 82 · see citing works
“Although we used the p62T352A mutant to prevent secondary effects of p62, we were still concerned that p62 overexpression alone might induce lipophagy, largely because p62 plays multiple roles in cell signaling, including lipid metabolism (Rodriguez et al., 2006).”
MethodEmerging role of epigenetics and miRNA in diabetic cardiomyopathy
Asrih, M., & Steffens, S. (2012) · Cardiovascular Pathology · doi:10.1016/j.carpath.2012.07.004 · Cited by 81 · see citing works
“On the other hand, reduced availability of FFA also disturbs myocardial bioenergetics and contraction/relaxation coupling [40].”
BackgroundMoscat, J., Díaz-Meco, M. T., & Wooten, M. W. (2009) · Cell Death and Differentiation · doi:10.1038/cdd.2009.119 · Cited by 81 · see citing works
“data showing the negative regulation of ERK by p62 and its role in obesity in p62-deficient mice.(137) Consistent with the notion that p62 is a ‘signaling organizer’ rather than ‘garbage disposal’ are the very recent data from the Ashkenazi laboratory.”
BackgroundSelf-citationChoe, J., Jung, H., Park, K.-Y., & Kim, S.-K. (2014) · Lara D. Veeken · doi:10.1093/rheumatology/ket474 · Cited by 80 · see citing works
Accumulation of p62 is associated with poor prognosis in patients with triple-negative breast cancer
Yuan, Z.-Y., Luo, Li, M., Xi, S., Fu, J., & He (2013) · OncoTargets and Therapy · doi:10.2147/ott.s46222 · Cited by 79 · see citing works
Target acquired: Selective autophagy in cardiometabolic disease
Evans, T. D., Sergin, I., Zhang, X., & Razani, B. (2017) · Science Signaling · doi:10.1126/scisignal.aag2298 · Cited by 73 · see citing works
Cundy, T. (2018) · Metabolism · doi:10.1016/j.metabol.2017.06.010 · Cited by 76 · see citing works
- Authors
- Rodriguez, A., Durán, A., Selloum, M., Champy, M.-F., Diez-Guerra, F. J., Flores, J. M., Serrano, M., Auwerx, J., Diaz-Meco, M. T., & Moscat, J.
- Affiliations
- Phénotypage et ingénierie précliniques des systèmes d’organismes modèles (FR)
- Universidad Complutense de Madrid (ES)
- Spanish National Cancer Research Centre (ES)
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Moscat, Jorge
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2006-03
- Volume
- 3
- Issue
- 3
- Pages
- 211-222
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2096738869
- Cited by
- 290
- References
- 34
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 8 · 2023: 3 · 2022: 14 · 2021: 19 · 2020: 14 · 2019: 14 · 2018: 24 · 2017: 17 · 2016: 19 · 2015: 14 · 2014: 22 · 2013: 26 · 2012: 21
- FWCI
- 9.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- p62, insulin resistance, leptin resistance, adipogenesis, ERK signaling, PPARγ, UCP1, metabolic rate, adipose tissue, impaired glucose tolerance
- MeSH terms
- Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Embryo, Mammalian, Fibroblasts, HeLa Cells, Humans, Insulin Resistance, RNA, Messenger, Transcription Factors, Signal Transduction, Adipocytes, Mice, Knockout, 3T3-L1 Cells, Extracellular Signal-Regulated MAP Kinases, Adipogenesis, Mice, Transcription Factor TFIIH
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