ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Deficiency of p62/Sequestosome 1 causes hyperphagia due to leptin resistance in the brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Secretion Patterns of Leptin: A Key Component in the Regulation of Energy Homeostasis and Its Therapeutic Applications.Biomolecules · 2026Review
- Mature-onset obesity in p62-deficient male mice maintains skeletal muscle mass despite metabolic dysfunction.Physiological reports · 2026Article
- Chchd10: A Novel Metabolic Sensor Modulating Adipose Tissue Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- 4-Hydroxy-2-nonenal causes nuclear accumulation of p62 by inhibiting Xpo1 and promoting the proteolytic pathway in the nucleus.PloS one · 2025Article
- P62 promotes FSH-induced antral follicle formation by directing degradation of ubiquitinated WT1.Cellular and molecular life sciences : CMLS · 2024Article
- Sequestosome 1 (p62) mitigates hypoxia-induced cardiac dysfunction by stabilizing hypoxia-inducible factor 1α and nuclear factor erythroid 2-related factor 2.Cardiovascular research · 2024Article
- Endothelium-specific deletion of p62 causes organ fibrosis and cardiac dysfunction.Journal of translational medicine · 2024Article
- Hypothalamic P62 (SQSTM1) regulates energy balance by modulating leptin signaling.Theranostics · 2024Article
- Muscle p62 stimulates the expression of antioxidant proteins alleviating cancer cachexia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Effects of invivo CXCR4 blockade and proteasome inhibition on bone marrow plasma cells in HLA-sensitized kidney transplant candidates.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Article
- Central role for p62/SQSTM1 in the elimination of toxic tau species in a mouse model of tauopathy.Aging cell · 2022Article
- p62/Sqstm1 rescue in muscle retards the progression of steatohepatitis inFrontiers in physiology · 2022Article
- Ciliary Type III Adenylyl Cyclase in the VMH Is Crucial for High-Fat Diet-Induced Obesity Mediated by Autophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Mitochondrial reactive oxygen species trigger metformin-dependent antitumor immunity via activation of Nrf2/mTORC1/p62 axis in tumor-infiltrating CD8T lymphocytes.Journal for immunotherapy of cancer · 2021Article
- Pituitary P62 deficiency leads to female infertility by impairing luteinizing hormone production.Experimental & molecular medicine · 2021Article
- Review
- Prevention of non-alcoholic steatohepatitis by long-term exercise via the induction of phenotypic changes in Kupffer cells of hyperphagic obese mice.Physiological reports · 2021Article
- Essential role of autophagy in protecting neonatal haematopoietic stem cells from oxidative stress in a p62-independent manner.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
The cytoplasmic regulatory protein p62 (Sequestosome 1/A170) is known to modulate various receptor-mediated intracellular signaling pathways. p62 deficiency was shown to result in mature-onset obesity in mice, but the mechanisms underlying this abnormality remained unclear. Here we report that hyperphagia due to central leptin resistance is the cause of obesity in p62(-/-) mice. We found that these mice show hyperphagia. Restriction of food to the amount eaten by wild-type mice prevented excess body weight gain and fat accumulation, suggesting that overfeeding is the primary cause of obesity in p62(-/-) mice. Brain-specific p62 deficiency caused mature-onset obesity to the same extent as in p62(-/-) mice, further supporting a neuronal mechanism as the major cause of obesity in these mice. Immunohistochemical analysis revealed that p62 is highly expressed in hypothalamic neurons, including POMC neurons in the arcuate nucleus. Central leptin resistance was observed even in young preobese p62(-/-) mice. We found a defect in intracellular distribution of the transcription factor Stat3, which is essential for the action of leptin, in p62(-/-) mice. These results indicate that brain p62 plays an important role in bodyweight control by modulating the central leptin-signaling pathway and that lack of p62 in the brain causes leptin resistance, leading to hyperphagia. Thus, p62 could be a clinical target for treating obesity and metabolic syndrome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.