ArticleCell metabolism2023
Obesity-associated microglial inflammatory activation paradoxically improves glucose tolerance.
Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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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.
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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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Microglia Mediate Metabolic Dysfunction From Common Air Pollutants Through NF-κB Signaling.Diabetes · 2024Pooled it
- Ablation of microglial estrogen receptor alpha predisposes male mice to diet-induced obesity.Metabolism: clinical and experimental · 2026Article
- Effects of obesity on brain health and cognition.Nature reviews. Neurology · 2026Review
- ALKBH5-mediated microglia-neuron crosstalk inhibits sympathetic innervation and adipocyte browning in male mice.Nature communications · 2026Article
- Weight loss aggravates obesity-induced hypothalamic inflammation in mid-aged mice.GeroScience · 2026Article
- PLX3397 Reshapes Hepatic Lipid Metabolism Independent of Microglial Depletion.Neuroscience bulletin · 2026Article
- Sex-specific dynamics of MASLD reveal early hepatic and extrahepatic metabolic deterioration in females despite long-term protection.Biology of sex differences · 2026Article
- Central Irisin Administration Attenuates Hypothalamic TLR4/MyD88-Mediated Neuroinflammatory Signaling in Diet-Induced Obese Mice.Molecular neurobiology · 2026Article
- ApoE-Dependent Lipid Handling by Median Eminence Microglia Preserves Myelin Integrity and Metabolic Function.bioRxiv : the preprint server for biology · 2026Article
- THIK-1 channel mediates microglial glucose sensing and modulates AgRP neurons.bioRxiv : the preprint server for biology · 2026Article
- PANoptosis in diabetes: immunometabolic insights and treatments.Apoptosis : an international journal on programmed cell death · 2026Review
- Artery Tertiary Lymphoid Organs Form Neuroimmune Cardiovascular Interfaces in Atherosclerosis.Immunological reviews · 2026Review
- Border-associated macrophages: an emerging perspective from physiological basis and multi-disease roles to the mechanism of vascular cognitive impairment and dementia.Journal of neuroinflammation · 2025Review
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- Review
- Microglia/macrophage-specific deletion of TLR-4 protects against neural effects of diet-induced obesity in a sexually dimorphic manner.Journal of neuroinflammation · 2025Article
- Hypothalamic gliosis as a potential mediator of improved glucose tolerance induced by time-restricted feeding in obese mice.American journal of physiology. Cell physiology · 2025Article
- Circadian rhythms in metabolism and mental health: a reciprocal regulatory network with implications for metabolic and neuropsychiatric disorders.Current opinion in physiology · 2025Review
- Neuro-immune Interactions in Metabolic Regulation: Brain and Adipose Tissue Crosstalk.Journal of obesity & metabolic syndrome · 2025Review
- An adeno-associated virus gene therapy strategy for anti-obesity treatment by nanocarrier-based delivery systems.Journal of nanobiotechnology · 2025Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Hypothalamic gliosis associated with high-fat diet (HFD) feeding increases susceptibility to hyperphagia and weight gain. However, the body-weight-independent contribution of microglia to glucose regulation has not been determined. Here, we show that reducing microglial nuclear factor κB (NF-κB) signaling via cell-specific IKKβ deletion exacerbates HFD-induced glucose intolerance despite reducing body weight and adiposity. Conversely, two genetic approaches to increase microglial pro-inflammatory signaling (deletion of an NF-κB pathway inhibitor and chemogenetic activation through a modified Gq-coupled muscarinic receptor) improved glucose tolerance independently of diet in both lean and obese rodents. Microglial regulation of glucose homeostasis involves a tumor necrosis factor alpha (TNF-α)-dependent mechanism that increases activation of pro-opiomelanocortin (POMC) and other hypothalamic glucose-sensing neurons, ultimately leading to a marked amplification of first-phase insulin secretion via a parasympathetic pathway. Overall, these data indicate that microglia regulate glucose homeostasis in a body-weight-independent manner, an unexpected mechanism that limits the deterioration of glucose tolerance associated with 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 Socratic graph.