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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Genetic or pharmacologic treatments that increase microgliosis within the mediobasal hypothalamus are capable of inducing obesity even in the absence of dietary challenge.
“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
The Abstract (page not provided) reports that genetic activation of microglia caused MBH microgliosis and weight gain in mice without a dietary challenge. It does not support the pharmacologic part: the pharmacologic treatment described in the Abstract and Results depleted microglia and reduced weight gain rather than inducing obesity. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBoth increased and decreased microglial inflammatory activity within the mediobasal hypothalamus can disrupt leptin/melanocortin related neuronal signaling, a pathway central to the regulation of energy balance.
“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
The Results section (‘Microglial A20 Deletion Induces Diet-Independent Metabolic Dysfunction’; page not provided) reports that increased microglial inflammatory activation reduced leptin-induced signaling in mediobasal hypothalamic neurons. The Introduction (page not provided) says that restraining microglial inflammatory activity protected mice from diet-induced hyperphagia and obesity. The paper does not show that decreased activity disrupts leptin or melanocortin neuronal signaling. (LLM, conf=0.88)
Experimental — accuracy not yet measuredReducing dietary induced microgliosis can mitigate weight gain.
“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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- 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 › Epidemiology › 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
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