Astrocyte IKKβ/NF-κB signaling is required for diet-induced obesity and hypothalamic inflammation

Douglass, J.D.; Dorfman, M.D.; Fasnacht, R.; Shaffer, L.D.; Thaler, J.P.

doi:10.1016/j.molmet.2017.01.010

Cited by 252Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesNeuroinflammation and Neurodegeneration Mechanisms

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Astrocyte IKKβ/NF-κB signaling is required for diet-induced obesity and hypothalamic inflammation

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Douglass, J.D., Dorfman, M.D., Fasnacht, R., Shaffer, L.D., Thaler, J.P.·2017·Molecular Metabolism

DOI 10.1016/j.molmet.2017.01.010PMC PMC5369266

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Abstract

Objective Obesity and high fat diet (HFD) consumption in rodents is associated with hypothalamic inflammation and reactive gliosis. While neuronal inflammation promotes HFD-induced metabolic dysfunction, the role of astrocyte activation in susceptibility to hypothalamic inflammation and diet-induced obesity (DIO) remains uncertain. Methods Metabolic phenotyping, immunohistochemical analyses, and biochemical analyses were performed on HFD-fed mice with a tamoxifen-inducible astrocyte-specific knockout of IKKβ ( Gfap CreER Ikbkb fl/fl , IKKβ-AKO), an essential cofactor of NF-κB-mediated inflammation. Results IKKβ-AKO mice with tamoxifen-induced IKKβ deletion prior to HFD exposure showed equivalent HFD-induced weight gain and glucose intolerance as Ikbkb fl/fl littermate controls. In Gfap CreER TdTomato marker mice treated using the same protocol, minimal Cre-mediated recombination was observed in the mediobasal hypothalamus (MBH). By contrast, mice pretreated with 6 weeks of HFD exposure prior to tamoxifen administration showed substantially increased recombination throughout the MBH. Remarkably, this treatment approach protected IKKβ-AKO mice from further weight gain through an immediate reduction of food intake and increase of energy expenditure. Astrocyte IKKβ deletion after HFD exposure—but not before—also reduced glucose intolerance and insulin resistance, likely as a consequence of lower adiposity. Finally, both hypothalamic inflammation and astrocytosis were reduced in HFD-fed IKKβ-AKO mice. Conclusions These data support a requirement for astrocytic inflammatory signaling in HFD-induced hyperphagia and DIO susceptibility that may provide a novel target for obesity therapeutics.

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Reversing neuroinflammation via targeted genetic, pharmacological, or dietary approaches that rescue behavioral anomalies supports a causal role of neuroinflammation in obesity-induced neuropathophysiology.
“Reversing neuroinflammation via targeted genetic [96,97], pharmacological [98,99], or dietary [49,100] approaches that rescue behavioral anomalies offers convincing support for a causal role of neuroinflammation in obesity-induced neuropathophysiology.”
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Depletion of astrocyte inflammatory pathway in the arcuate nucleus of the hypothalamus is sufficient to prevent the diet-induced metabolic alterations of polygenically predisposed obese ratsPreprint
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Role of glial inflammation and cytokine production in regulating food intake and energy homeostasis in diet-resistant and diet-induced obese rats
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The involvement of 4‐1 BB /4‐1 BBL signaling in glial cell‐mediated hypothalamic inflammation in obesity
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Evidence for a novel functional role of astrocytes in the acute homeostatic response to high-fat diet intake in mice
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Authors: Douglass, J. D., Dorfman, M. D., Fasnacht, R., Shaffer, L. D., & Thaler, J. P.
Affiliations: University of Washington (US)
Corresponding author: Thaler, J.P.
ORCID: Douglass, J.D.
Dorfman, M.D.
Fasnacht, R.
Thaler, J.P.
Venue: Molecular Metabolism
Publisher: Elsevier BV
Published: 2017-04
Volume: 6
Issue: 4
Pages: 366-373
ISSN: 2212-8778 (ISSN-L)
DOI: 10.1016/j.molmet.2017.01.010
PMC: PMC5369266
OpenAlex: W2581154578
Cited by: 248
References: 37
Citations by year: 2026: 12 · 2025: 23 · 2024: 28 · 2023: 34 · 2022: 32 · 2021: 31 · 2020: 31 · 2019: 26 · 2018: 20 · 2017: 11
FWCI: 14.72
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor, 349 d)
Locations: Molecular Metabolism (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: American Diabetes Association (1-14-ACE-51)
NIDDK (K08 DK088872, T32 DK7247-37, F32 DK108473-01)
NIH (DK035816)
Diabetes Research Center (DK017047)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: diet-induced obesity, hypothalamic inflammation, astrocytes, IKKβ, NF-κB signaling, astrocyte-specific knockout, high-fat diet, impaired glucose tolerance, insulin resistance, hyperphagia, energy expenditure, reactive gliosis, astrocyte activation, mediobasal hypothalamus, obesity treatment
MeSH terms: Animals, Astrocytes, Cells, Cultured, Gliosis, Hypothalamus, Inflammation, Male, Mice, Inbred C57BL, Obesity, Signal Transduction, NF-kappa B, Mice, I-kappa B Kinase, Diet, High-Fat

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Astrocyte IKKβ/NF-κB signaling is required for diet-induced obesity and hypothalamic inflammation

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