ArticleMolecular metabolism2014
The histone acetyltransferase MOF activates hypothalamic polysialylation to prevent diet-induced obesity in mice.
Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The Genetic Basis of Childhood Obesity: A Systematic Review.Nutrients · 2023Pooled it
- Histone H4 lysine 16 acetylation controls central carbon metabolism and diet-induced obesity in mice.Nature communications · 2021Article
- Lack of Hypothalamus Polysialylation Inducibility Correlates With Maladaptive Eating Behaviors and Predisposition to Obesity.Frontiers in nutrition · 2018Article
- Perinatal Western Diet Consumption Leads to Profound Plasticity and GABAergic Phenotype Changes within Hypothalamus and Reward Pathway from Birth to Sexual Maturity in Rat.Frontiers in endocrinology · 2017Article
- Brain Control of Plasma Cholesterol Involves Polysialic Acid Molecules in the Hypothalamus.Frontiers in neuroscience · 2017Article
- An assessment of molecular pathways of obesity susceptible to nutrient, toxicant and genetically induced epigenetic perturbation.The Journal of nutritional biochemistry · 2016Review
- The Functional Analysis of Histone Acetyltransferase MOF in Tumorigenesis.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overfeeding causes rapid synaptic remodeling in hypothalamus feeding circuits. Polysialylation of cell surface molecules is a key step in this neuronal rewiring and allows normalization of food intake. Here we examined the role of hypothalamic polysialylation in the long-term maintenance of body weight, and deciphered the molecular sequence underlying its nutritional regulation. We found that upon high fat diet (HFD), reduced hypothalamic polysialylation exacerbated the diet-induced obese phenotype in mice. Upon HFD, the histone acetyltransferase MOF was rapidly recruited on the St8sia4 polysialyltransferase-encoding gene. Mof silencing in the mediobasal hypothalamus of adult mice prevented activation of the St8sia4 gene transcription, reduced polysialylation, altered the acute homeostatic feeding response to HFD and increased the body weight gain. These findings indicate that impaired hypothalamic polysialylation contribute to the development of obesity, and establish a role for MOF in the brain control of energy balance.
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Registered trials
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