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Microglial inflammatory signaling orchestrates the hypothalamic immune response to dietary excess and mediates obesity susceptibility.
Open accessAbstract
Dietary excess triggers accumulation of pro-inflammatory microglia in the mediobasal hypothalamus (MBH), but the components of this microgliosis and its metabolic consequences remain uncertain. Here, we show that microglial inflammatory signaling determines the immunologic response of the MBH to dietary excess and regulates hypothalamic control of energy homeostasis in mice. Either pharmacologically depleting microglia or selectively restraining microglial NF-κB-dependent signaling sharply reduced microgliosis, an effect that includes prevention of MBH entry by bone-marrow-derived myeloid cells, and greatly limited diet-induced hyperphagia and weight gain. Conversely, forcing microglial activation through cell-specific deletion of the negative NF-κB regulator A20 induced spontaneous MBH microgliosis and cellular infiltration, reduced energy expenditure, and increased both food intake and weight gain even in absence of a dietary challenge. Thus, microglial inflammatory activation, stimulated by dietary excess, orchestrates a multicellular hypothalamic response that mediates obesity susceptibility, providing a mechanistic rationale for non-neuronal approaches to treat metabolic diseases.
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“It has also been reported that genetic or pharmacologic treatments that increase microgliosis within the mediobasal hypothalamus are capable of inducing obesity even in the absence of dietary challenge (Valdearcos et al., 2017; Campolim et al., 2020).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Valdearcos et al., 2017
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“Recent studies have shown that both increased and decreased microglial inflammatory activity within the mediobasal hypothalamus can disrupt leptin/melanocortin related neuronal signaling, a pathway that is central to the regulation of energy balance (Gao et al., 2017; Valdearcos et al., 2017; Kim et al., 2019).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Valdearcos et al., 2017
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“Further, it has been demonstrated that reducing this dietary induced microgliosis can mitigate weight gain (Andre et al., 2017; Valdearcos et al., 2017; Kim et al., 2019).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Valdearcos et al., 2017
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Metadata
- Authors
- Valdearcos, M., Douglass, J. D., Robblee, M. M., Dorfman, M. D., Stifler, D. R., Bennett, M. L., Gerritse, I., Fasnacht, R., Barres, B. A., Thaler, J. P., & Koliwad, S. K.
- Affiliations
- University of Washington (US)
- University of California, San Francisco (US)
- Stanford Medicine (US)
- Corresponding author
- Thaler, Joshua P.
- Koliwad, Suneil K.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2017-07
- Volume
- 26
- Issue
- 1
- Pages
- 185-197.e3
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC5569901
- OpenAlex
- W2727793071
- Cited by
- 477
- References
- 58
- Citations by year
- 2026: 38 · 2025: 50 · 2024: 69 · 2023: 49 · 2022: 49 · 2021: 59 · 2020: 53 · 2019: 65 · 2018: 39 · 2017: 6
- FWCI
- 22.20
- Type
- journal article
- Language
- en
- Update notices
- erratum (2018-06-05)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- American Diabetes Association (1-14-ACE-51)
- NIDDK (K08 DK088872, T32 DK7247-37, F32 DK108473-01, R01 DK103175-02)
- UCSF Diabetes Family Fund
- Nutrition Obesity Research Centers (DK098722)
- University of Washington (DK035816)
- Diabetes Research Center (DK017047)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- microglia, microglial activation, mediobasal hypothalamus, dietary excess, obesity susceptibility, NF-κB signaling, A20, energy homeostasis, hyperphagia, weight gain, myeloid cell infiltration, energy expenditure, diet-induced obesity
- MeSH terms
- Animals, Appetite Regulation, Energy Metabolism, Hyperphagia, Hypothalamus, Inflammation, Male, Mice, Inbred C57BL, Obesity, Signal Transduction, NF-kappa B, Microglia, Myeloid Cells, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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