ArticleMolecular metabolism2020
The transcriptional regulator PRDM12 is critical for Pomc expression in the mouse hypothalamus and controlling food intake, adiposity, and body weight.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Scalable hypothalamic neuron differentiation from human pluripotent stem cells suitable for modeling metabolic disorders.Stem cell reports · 2026Article
- Highly Conserved STAT3 Motifs Present in the Neuronal Pomc Enhancer nPE1 are Critical for Maximal Hypothalamic Pomc Expression.Molecular neurobiology · 2025Article
- Reduced Availability of Essential Amino Acids Disrupts Differentiation of Anorexigenic POMC Neurons in the Fetal Rat Hypothalamus.Molecular neurobiology · 2025Article
- Control of tuberal hypothalamic development and its implications in metabolic disorders.Nature reviews. Endocrinology · 2025Review
- The homeodomain transcription factor Six3 regulates hypothalamic Pomc expression and its absence from POMC neurons induces hyperphagia and mild obesity in male mice.Molecular metabolism · 2024Article
- AgRP neuron cis-regulatory analysis across hunger states reveals that IRF3 mediates leptin's acute effects.Nature communications · 2024Article
- A mammalian tripartite enhancer cluster controls hypothalamicProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Novel human pluripotent stem cell-derived hypothalamus organoids demonstrate cellular diversity.iScience · 2023Article
- Proopiomelanocortin (POMC) and psychodermatology.Skin health and disease · 2023Review
- Ontogenetic rules for the molecular diversification of hypothalamic neurons.Nature reviews. Neuroscience · 2022Review
- Article
- PRDM12 in Health and Diseases.International journal of molecular sciences · 2021Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
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Abstract
objectiveRegulation of food intake and energy balance depends on a group of hypothalamic neurons that release anorexigenic melanocortins encoded by the Pomc gene. Although the physiological importance of central melanocortins is well appreciated, the genetic program that defines the functional identity of melanocortin neurons and assures high levels of hypothalamic Pomc expression is only beginning to be understood. This study assessed whether the transcriptional regulator PRDM12, identified as a highly expressed gene in adult mouse POMC neurons, plays an important role in the identity and function of melanocortin neurons.
methodsWe first determined the cellular distribution of PRDM12 in the developing hypothalamus. Then we studied mutant mice with constitutively inactivated Prdm12 to evaluate possible changes in hypothalamic Pomc expression. In addition, we characterized conditional mutant mice specifically lacking Prdm12 in ISL1-positive or POMC neurons during development. Finally, we measured food intake, body weight progression up to 16 weeks of age, adiposity, and glucose tolerance in adult mice lacking Prdm12 selectively from POMC neurons.
resultsPRDM12 co-expressed with POMC in mouse hypothalamic neurons from early development to adulthood. Mice lacking Prdm12 displayed greatly reduced Pomc expression in the developing hypothalamus. Selective ablation of Prdm12 from ISL1 neurons prevented hypothalamic Pomc expression. The conditional ablation of Prdm12 limited to POMC neurons greatly reduced Pomc expression in the developing hypothalamus and in adult mice led to increased food intake, adiposity, and obesity.
conclusionsAltogether, our results demonstrate that PRDM12 plays an essential role in the early establishment of hypothalamic melanocortin neuron identity and the maintenance of high expression levels of Pomc. Its absence in adult mice greatly impairs Pomc expression and leads to increased food intake, adiposity, and obesity.
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