Inhibiting microglia expansion prevents diet-induced hypothalamic and peripheral inflammation
Open accessAbstract
Cell proliferation and neuroinflammation in the adult hypothalamus may contribute to the pathogenesis of obesity. We tested whether the intertwining of these two processes plays a role in the metabolic changes caused by 3 weeks of a high-saturated fat diet (HFD) consumption. Compared with chow-fed mice, HFD-fed mice had a rapid increase in body weight and fat mass and specifically showed an increased number of microglia in the arcuate nucleus (ARC) of the hypothalamus. Microglia expansion required the adequate presence of fats and carbohydrates in the diet because feeding mice a very high-fat, very low-carbohydrate diet did not affect cell proliferation. Blocking HFD-induced cell proliferation by central delivery of the antimitotic drug arabinofuranosyl cytidine (AraC) blunted food intake, body weight gain, and adiposity. AraC treatment completely prevented the increase in number of activated microglia in the ARC, the expression of the proinflammatory cytokine tumor necrosis factor-α in microglia, and the recruitment of the nuclear factor-κB pathway while restoring hypothalamic leptin sensitivity. Central blockade of cell proliferation also normalized circulating levels of the cytokines leptin and interleukin 1β and decreased peritoneal proinflammatory CD86 immunoreactive macrophage number. These findings suggest that inhibition of diet-dependent microglia expansion hinders body weight gain while preventing central and peripheral inflammatory responses due to caloric overload.
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Reducing 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 Andre et al., 2017
Altered microglia function within the hypothalamus has been connected to the maintenance of body weight and obesity.
“Importantly, altered microglia function within the hypothalamus has been connected to the maintenance of body weight and obesity (Valdearcos et al., 2014, 2017; Andre et al., 2017; Dorfman et al., 2017; Gao et al., 2017; Rosin et al., 2018; De Luca et al., 2019; Kim et al., 2019; 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 Andre et al., 2017
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.”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [98]
A diet high in both lipids and carbohydrates is required to induce a significant increase in hypothalamic inflammation in rodents associated with an increase in body weight.
“In support of this, a diet high in both lipids and carbohydrates is required to induce a significant increase in hypothalamic inflammation in rodents associated with an increase in body weight.[1,150]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [150]
The high-fat and high-carbohydrate diet also caused an increase in CML immunoreactivity in both POMC and NPY neurons.
“The high-fat and high-carbohydrate diet also caused an increase in CML immunoreactivity in both POMC and NPY neurons.”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [150]
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- Authors
- André, C., Guzman-Quevedo, O., Rey, C., Rémus-Borel, J., Clark, S., Castellanos-Jankiewicz, A., Ladeveze, E., Leste-Lasserre, T., Nadjar, A., Abrous, D. N., Laye, S., & Cota, D.
- Affiliations
- Université de Bordeaux (FR)
- INSERM, Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, Bordeaux, France
- INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, Bordeaux, France
- Corresponding author
- Abrous, Djoher Nora
- Cota, Daniela
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2016-11-30
- Volume
- 66
- Issue
- 4
- Pages
- 908-919
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2558045643
- Cited by
- 182
- References
- 58
- Citations by year
- 2026: 6 · 2025: 12 · 2024: 21 · 2023: 17 · 2022: 18 · 2021: 27 · 2020: 22 · 2019: 27 · 2018: 18 · 2017: 13 · 2016: 1
- FWCI
- 10.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion)
- Funders
- Mexican Consejo Nacional de Ciencia y Tecnología (postdoctoral fellowship)
- Agence Nationale de la Recherche (ANR-10-LABX-43, ANR-2010-1414, ANR-13-BSV4-0006-01)
- Aquitaine Region
- Fondation Francophone pour la Recherche sur le Diabète
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- high saturated fat diet, obesity, arcuate nucleus, cell proliferation inhibition, TNF-α, NF-κB signaling, leptin sensitivity, IL-1β, peritoneal macrophages, CD86, dietary intake, weight gain, adiposity
- MeSH terms
- Animals, Arabinonucleosides, Arcuate Nucleus of Hypothalamus, Body Weight, Cytarabine, Cytidine, Eating, Hypothalamus, Inflammation, Male, Obesity, Tumor Necrosis Factor-alpha, Weight Gain, NF-kappa B, Microglia, Macrophages, Peritoneal, Leptin, Cell Proliferation, Adiposity, Antimitotic Agents, Mice, Interleukin-1beta, Diet, High-Fat
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