ArticleDiabetes2023
Prostaglandin PGE2 Receptor EP4 Regulates Microglial Phagocytosis and Increases Susceptibility to Diet-Induced Obesity.
Article in Diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 19 citations in OpenAlex.
- Ablation of microglial estrogen receptor alpha predisposes male mice to diet-induced obesity.Metabolism: clinical and experimental · 2026Article
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
- Prostaglandin signaling drives peripheral inflammation-induced reduction of hypothalamic oxytocin-positive neurons.Cellular and molecular life sciences : CMLS · 2026Article
- The role of prostanoids in the retina and optic nerve in health and disease.Progress in retinal and eye research · 2026Review
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- Dysfunction of lipid metabolism and lysosomal capacity: at the core of microglial aging?Frontiers in aging neuroscience · 2026Review
- Article
- Metabolic inflammation at the adipose-brain axis.Frontiers in physiology · 2026Review
- Review
- Deletion of EP3 prostaglandin receptor in murine macrophages aggravates diet-induced obesity by suppressing SPARC.The EMBO journal · 2025Article
- Review
- Hypothalamic neuronal-glial crosstalk in metabolic disease.npj metabolic health and disease · 2024Review
- Emerging mechanisms of obesity-associated immune dysfunction.Nature reviews. Endocrinology · 2024Review
- Microglia heterogeneity in health and disease.FEBS open bio · 2024Review
- Microglia in Central Control of Metabolism.Physiology (Bethesda, Md.) · 2024Review
- Obesity-associated microglial inflammatory activation paradoxically improves glucose tolerance.Cell metabolism · 2023Article
- Palmitic Acid Modulates Microglial Cell Response to Metabolic Endotoxemia in an In Vitro Study.Nutrients · 2023Article
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
- Lipopolysaccharide-induced immune stress negatively regulates broiler chicken growthFrontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
In rodents, susceptibility to diet-induced obesity requires microglial activation, but the molecular components of this pathway remain incompletely defined. Prostaglandin PGE2 levels increase in the mediobasal hypothalamus during high-fat-diet (HFD) feeding, and the PGE2 receptor EP4 regulates microglial activation state and phagocytic activity, suggesting a potential role for microglial EP4 signaling in obesity pathogenesis. To test the role of microglial EP4 in energy balance regulation, we analyzed the metabolic phenotype in a microglia-specific EP4 knockout (MG-EP4 KO) mouse model. Microglial EP4 deletion markedly reduced weight gain and food intake in response to HFD feeding. Corresponding with this lean phenotype, insulin sensitivity was also improved in HFD-fed MG-EP4 KO mice, though glucose tolerance remained surprisingly unaffected. Mechanistically, EP4-deficient microglia showed an attenuated phagocytic state marked by reduced CD68 expression and fewer contacts with pro-opiomelanocortin (POMC) neuron processes. These cellular changes observed in the MG-EP4 KO mice corresponded with an increased density of POMC neurites extending into the paraventricular nucleus (PVN). These findings reveal that microglial EP4 signaling promotes body weight gain and insulin resistance during HFD feeding. Furthermore, the data suggest that curbing microglial phagocytic function may preserve POMC cytoarchitecture and PVN input to limit overconsumption during diet-induced obesity.
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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.