ArticleScientific reports2016
Defective regulation of POMC precedes hypothalamic inflammation in diet-induced obesity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 82 citations in OpenAlex.
- POMC AMPKα1 deletion drives male-specific BAT thermogenesis and obesity resistance.EMBO reports · 2026Article
- Increase of astrocyte apposition on GnRH neurons in early puberty onset induced by high fat diet.Journal of neuroendocrinology · 2025Article
- Obesity: pathophysiology and therapeutic interventions.Molecular biomedicine · 2025Review
- Comparative Hypothalamic Proteomic Analysis Between Diet-Induced Obesity and Diet-Resistant Rats.International journal of molecular sciences · 2025Article
- Smoking, Obesity, and Post-Cessation Weight Gain: Neurobiological Intersection and Treatment Recommendations.Journal of multidisciplinary healthcare · 2025Review
- Regulation of leptin signaling and diet-induced obesity by SEL1L-HRD1 ER-associated degradation in POMC expressing neurons.Nature communications · 2024Article
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- Determinants of obesity in Latin America.Nature metabolism · 2024 · on this mapReview
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- SEL1L-HRD1 ER-associated degradation regulates leptin receptor maturation and signaling in POMC neurons in diet-induced obesity.Research square · 2024Article
- Microglia in physiological conditions and the importance of understanding their homeostatic functions in the arcuate nucleus.Frontiers in immunology · 2024Review
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- Strength training alters the tissue fatty acids profile and slightly improves the thermogenic pathway in the adipose tissue of obese mice.Scientific reports · 2022Article
- Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington's disease.Scientific reports · 2022Article
- Hypothalamic inflammation in metabolic disorders and aging.Cellular and molecular life sciences : CMLS · 2021Review
- A Single Dose ofBrain sciences · 2021Article
- 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
- Interleukin-6 actions in the hypothalamus protects against obesity and is involved in the regulation of neurogenesis.Journal of neuroinflammation · 2021Article
- AMPK in the gut-liver-brain axis and its influence on OP rats in an HSHF intake and WTD rat model.Pflugers Archiv : European journal of physiology · 2021Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is the result of a long-term positive energy balance in which caloric intake overrides energy expenditure. This anabolic state results from the defective activity of hypothalamic neurons involved in the sensing and response to adiposity. However, it is currently unknown what the earliest obesity-linked hypothalamic defect is and how it orchestrates the energy imbalance present in obesity. Using an outbred model of diet-induced obesity we show that defective regulation of hypothalamic POMC is the earliest marker distinguishing obesity-prone from obesity-resistant mice. The early inhibition of hypothalamic POMC was sufficient to transform obesity-resistant in obesity-prone mice. In addition, the post-prandial change in the blood level of β-endorphin, a POMC-derived peptide, correlates with body mass gain in rodents and humans. Taken together, these results suggest that defective regulation of POMC expression, which leads to a change of β-endorphin levels, is the earliest hypothalamic defect leading to obesity.
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