ArticleScientific reports2019
High Fat Diet Triggers a Reduction in Body Fat Mass in Female Mice Deficient for Utx demethylase.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Deficiencies in methionine, tryptophan, and niacin remodels intestinal transcriptome and gut microbiota in female mice.Scientific reports · 2025Article
- Diet-Induced Obesity Alters Granulosa Cell Transcriptome and Ovarian Immune Environment in Mice.Life (Basel, Switzerland) · 2025Article
- Osteopontin Exacerbates High-Fat Diet-Induced Metabolic Disorders in a Microbiome-Dependent Manner.mBio · 2022Article
- AdipocyteCells · 2022Article
- Epigenetic interaction between UTX and DNMT1 regulates diet-induced myogenic remodeling in brown fat.Nature communications · 2021Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Obesity increases the risk of metabolic disorders like diabetes mellitus and dyslipidemia. However, how metabolic status is sensed and regulates cellular behavior is unclear. Utx is an H3K27 demethylase that influences adipocyte function in vitro. To examine its role in vivo, we generated mice lacking Utx in adipocytes (UtxAKO). Although all UtxAKO mice grew normally on a normal chow diet (NCD), female UtxAKO mice on a high fat diet (HFD) showed striking reductions in body fat compared to control mice (Ctrl). Gene expression profiling of adipose tissues of HFD-fed UtxAKO female mice revealed decreased expression of rate-limiting enzymes of triacylglycerol synthesis but increased expression of those of cholesterol/steroid hormone synthesis. Moreover, these animals resisted adiposity induced by ovariectomy and exhibited increased estrogen in visceral adipose tissues. Thus, upon HFD feeding, Utx regulates lipid metabolism in adipose tissues by influencing the local hormonal microenvironment. Conversely, Utx deficiency skews lipid catabolism to enhance cholesterol/steroid hormone production and repress obesity.
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