ArticleMolecular metabolism2020
Pro-opiomelanocortin (POMC) neuron translatome signatures underlying obesogenic gestational malprogramming in mice.
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 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Beyond satiety: unraveling the complex roles of POMC neurons in behavior and metabolism.Reviews in endocrine & metabolic disorders · 2026Review
- Maternal Nutrition and Hypothalamic Programming of Offspring Metabolic Health.The Journal of nutrition · 2026Review
- The long-term impact of obesity in pregnancy on offspring hypothalamic feeding pathways.Royal Society open science · 2025Review
- Pregnancy Protects against Abnormal Gut Permeability Promoted via the Consumption of a High-Fat Diet in Mice.Nutrients · 2023Article
- Maternal emulsifier consumption programs offspring metabolic and neuropsychological health in mice.PLoS biology · 2023Article
- Emerging role of hypothalamus in the metabolic regulation in the offspring of maternal obesity.Frontiers in nutrition · 2023Review
- Developmental programming of hypothalamic melanocortin circuits.Experimental & molecular medicine · 2022Review
- Mechanisms mediating the impact of maternal obesity on offspring hypothalamic development and later function.Frontiers in endocrinology · 2022Review
- Arcuate Nucleus Overexpression of NHLH2 Reduces Body Mass and Attenuates Obesity-Associated Anxiety/Depression-like Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Mitochondrial cristae-remodeling protein OPA1 in POMC neurons couples CaCell metabolism · 2021Article
- POMC neuronal heterogeneity in energy balance and beyond: an integrated view.Nature metabolism · 2021Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMaternal unbalanced nutritional habits during embryonic development and perinatal stages perturb hypothalamic neuronal programming of the offspring, thus increasing obesity-associated diabetes risk. However, the underlying molecular mechanisms remain largely unknown. In this study we sought to determine the translatomic signatures associated with pro-opiomelanocortin (POMC) neuron malprogramming in maternal obesogenic conditions.
methodsWe used the RiboTag mouse model to specifically profile the translatome of POMC neurons during neonatal (P0) and perinatal (P21) life and its neuroanatomical, functional, and physiological consequences.
resultsMaternal high-fat diet (HFD) exposure did not interfere with offspring's hypothalamic POMC neuron specification, but significantly impaired their spatial distribution and axonal extension to target areas. Importantly, we established POMC neuron-specific translatome signatures accounting for aberrant neuronal development and axonal growth. These anatomical and molecular alterations caused metabolic dysfunction in early life and adulthood.
conclusionsOur study provides fundamental insights on the molecular mechanisms underlying POMC neuron malprogramming in obesogenic contexts.
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