ArticleNature communications2024
Single cell tracing of Pomc neurons reveals recruitment of 'Ghost' subtypes with atypical identity in a mouse model of obesity.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Autophagy in hypothalamic POMC and AgRP neurons: mechanisms and therapeutic implications for obesity.International journal of obesity (2005) · 2026Review
- POMC AMPKα1 deletion drives male-specific BAT thermogenesis and obesity resistance.EMBO reports · 2026Article
- Narcolepsy is (not) an autoimmune disease.Nature reviews. Neurology · 2026Review
- Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026Review
- Early-life programming of hypothalamic circuits by maternal obesity: implications for neuroendocrine disorders.Reviews in endocrine & metabolic disorders · 2026Review
- Beyond satiety: unraveling the complex roles of POMC neurons in behavior and metabolism.Reviews in endocrine & metabolic disorders · 2026Review
- Hypothalamic regulation of sepsis-associated anorexia: cytokine and hormonal signalling through AgRP/POMC circuits.EMBO molecular medicine · 2026Review
- SF1-specific deletion of the energy sensor AMPKγ2 induces obesity.Molecular metabolism · 2025Article
- Anti-obesity compounds, Semaglutide and LiPR, and PrRP do not change the proportion of human and mouse POMC+ neurons.PloS one · 2025Article
- Molecular and functional mapping of the neuroendocrine hypothalamus: a new era begins.Journal of endocrinological investigation · 2024Review
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 2 countries.
Funding
Abstract
The hypothalamus contains a remarkable diversity of neurons that orchestrate behavioural and metabolic outputs in a highly plastic manner. Neuronal diversity is key to enabling hypothalamic functions and, according to the neuroscience dogma, it is predetermined during embryonic life. Here, by combining lineage tracing of hypothalamic pro-opiomelanocortin (Pomc) neurons with single-cell profiling approaches in adult male mice, we uncovered subpopulations of 'Ghost' neurons endowed with atypical molecular and functional identity. Compared to 'classical' Pomc neurons, Ghost neurons exhibit negligible Pomc expression and are 'invisible' to available neuroanatomical approaches and promoter-based reporter mice for studying Pomc biology. Ghost neuron numbers augment in diet-induced obese mice, independent of neurogenesis or cell death, but weight loss can reverse this shift. Our work challenges the notion of fixed, developmentally programmed neuronal identities in the mature hypothalamus and highlight the ability of specialised neurons to reversibly adapt their functional identity to adult-onset obesogenic stimuli.
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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.