ArticleThe Journal of clinical investigation2014
PPARγ ablation sensitizes proopiomelanocortin neurons to leptin during high-fat feeding.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Meta-analysis across Nellore cattle populations identifies common metabolic mechanisms that regulate feed efficiency-related traits.BMC genomics · 2022Pooled it
- Creation of true interspecies hybrids: Rescue of hybrid class with hybrid cytoplasm affecting growth and metabolism.Science advances · 2024Article
- Low Testosterone and High Leptin Activate PPAR Signaling to Induce Adipogenesis and Promote Fat Deposition in Caponized Ganders.International journal of molecular sciences · 2024Article
- Emerging roles of lipid and metabolic sensing in the neuroendocrine control of body weight and reproduction.Frontiers in endocrinology · 2024Review
- Article
- Biochemical Pathways Represented by Gene Ontology Causal Activity Models Identify Distinct Phenotypes Resulting from Mutations in Pathways.bioRxiv : the preprint server for biology · 2023Article
- Casein kinase 1α is required to maintain murine hypothalamic pro-opiomelanocortin expression.iScience · 2023Article
- Saturated Fatty Acids and Omega-3 Polyunsaturated Fatty Acids Improve Metabolic Parameters in Ovariectomized Female Mice.Endocrinology · 2023Article
- UCP2-dependent redox sensing in POMC neurons regulates feeding.Cell reports · 2022Article
- Deconstruction of a hypothalamic astrocyte-white adipocyte sympathetic axis that regulates lipolysis in mice.Nature communications · 2022Article
- Implications of peroxisome proliferator-activated receptor gamma (PPARY) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice.Journal of toxicology and environmental health. Part A · 2022Article
- Astrocytic lipid metabolism determines susceptibility to diet-induced obesity.Science advances · 2021Article
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- Maternal organophosphate flame-retardant exposure alters offspring feeding, locomotor and exploratory behaviors in a sexually-dimorphic manner in mice.Journal of applied toxicology : JAT · 2021Article
- The redox language in neurodegenerative diseases: oxidative post-translational modifications by hydrogen peroxide.Cell death & disease · 2021Review
- Lifestyle and Food Habits Impact on Chronic Diseases: Roles of PPARs.International journal of molecular sciences · 2019Review
- Mitochondrial Dynamics and Hypothalamic Regulation of Metabolism.Endocrinology · 2018Article
- Integrating Thyroid Hormone Signaling in Hypothalamic Control of Metabolism: Crosstalk Between Nuclear Receptors.International journal of molecular sciences · 2018Review
- Perinatal exposure to endocrine disrupting compounds and the control of feeding behavior-An overview.Hormones and behavior · 2018Review
- Organophosphate Flame-Retardants Alter Adult Mouse Homeostasis and Gene Expression in a Sex-Dependent Manner Potentially Through Interactions With ERα.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Activation of central PPARγ promotes food intake and body weight gain; however, the identity of the neurons that express PPARγ and mediate the effect of this nuclear receptor on energy homeostasis is unknown. Here, we determined that selective ablation of PPARγ in murine proopiomelanocortin (POMC) neurons decreases peroxisome density, elevates reactive oxygen species, and induces leptin sensitivity in these neurons. Furthermore, ablation of PPARγ in POMC neurons preserved the interaction between mitochondria and the endoplasmic reticulum, which is dysregulated by HFD. Compared with control animals, mice lacking PPARγ in POMC neurons had increased energy expenditure and locomotor activity; reduced body weight, fat mass, and food intake; and improved glucose metabolism when exposed to high-fat diet (HFD). Finally, peripheral administration of either a PPARγ activator or inhibitor failed to affect food intake of mice with POMC-specific PPARγ ablation. Taken together, our data indicate that PPARγ mediates cellular, biological, and functional adaptations of POMC neurons to HFD, thereby regulating whole-body energy balance.
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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.