ArticleNature communications2021
Histone H4 lysine 16 acetylation controls central carbon metabolism and diet-induced obesity in mice.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- The Genetic Basis of Childhood Obesity: A Systematic Review.Nutrients · 2023Pooled it
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- Rapid Histone Post-Translational Modification Analysis Using Alternative Proteases and Tandem Mass Tags.Analytical chemistry · 2026Article
- Rapid Histone Post-Translational Modification Analysis Using Alternative Proteases and Tandem Mass Tags.bioRxiv : the preprint server for biology · 2026Article
- Histone H4K5 deacetylation by enhanced HDAC1 expression drives endothelial inflammation in diabetes through repression of the KLF2-eNOS axis.Human cell · 2026Article
- Ep300-mediated acetylation plasticity in the acetyl-CoA metabolic network drives the protective role of intensive lifestyle intervention in visceral white adipose tissue.Cell communication and signaling : CCS · 2026Article
- Targeting KAT8 alleviates self-RNA-driven skin inflammation by modulating histone H4 lysine 16 acetylation in psoriasis.Cell death and differentiation · 2026Article
- H4K16 acylations destabilize chromatin architecture and facilitate transcriptional response during metabolic perturbations.Molecular cell · 2026Article
- KANSL3 directs transcriptional programs essential for hepatic metabolism and differentiation.Life science alliance · 2025Article
- Dynamic Rendition of Adipose Genes Under Epigenetic Regulation: Revealing New Mechanisms of Obesity Occurrence.Current issues in molecular biology · 2025Review
- Epigenetic regulation of nuclear receptors: Implications for endocrine-related diseases and therapeutic strategies.Genes & diseases · 2025Review
- Lysine Acetyltransferase 8: A Target for Natural Compounds in Cancer Therapy.International journal of molecular sciences · 2025Review
- Oncogenic IDH1Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The research progress and future directions in the pathophysiological mechanisms of type 2 diabetes mellitus from the perspective of precision medicine.Frontiers in medicine · 2025Article
- Protein posttranslational modifications in metabolic diseases: basic concepts and targeted therapies.MedComm · 2024Review
- A novel peptide encoded by circ-SLC9A6 promotes lipid dyshomeostasis through the regulation of H4K16ac-mediated CD36 transcription in NAFLD.Clinical and translational medicine · 2024Article
- KAT8-mediated H4K16ac is essential for sustaining trophoblast self-renewal and proliferation via regulating CDX2.Nature communications · 2024Article
- Article
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- KAT8-catalyzed lactylation promotes eEF1A2-mediated protein synthesis and colorectal carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Noncommunicable diseases (NCDs) account for over 70% of deaths world-wide. Previous work has linked NCDs such as type 2 diabetes (T2D) to disruption of chromatin regulators. However, the exact molecular origins of these chronic conditions remain elusive. Here, we identify the H4 lysine 16 acetyltransferase MOF as a critical regulator of central carbon metabolism. High-throughput metabolomics unveil a systemic amino acid and carbohydrate imbalance in Mof deficient mice, manifesting in T2D predisposition. Oral glucose tolerance testing (OGTT) reveals defects in glucose assimilation and insulin secretion in these animals. Furthermore, Mof deficient mice are resistant to diet-induced fat gain due to defects in glucose uptake in adipose tissue. MOF-mediated H4K16ac deposition controls expression of the master regulator of glucose metabolism, Pparg and the entire downstream transcriptional network. Glucose uptake and lipid storage can be reconstituted in MOF-depleted adipocytes in vitro by ectopic Glut4 expression, PPARγ agonist thiazolidinedione (TZD) treatment or SIRT1 inhibition. Hence, chronic imbalance in H4K16ac promotes a destabilisation of metabolism triggering the development of a metabolic disorder, and its maintenance provides an unprecedented regulatory epigenetic mechanism controlling diet-induced obesity.
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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.