Obesity induces neuroinflammation mediated by altered expression of the renin-angiotensin system in mouse forebrain nuclei.
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Obesity is a widespread health concern that is associated with an increased prevalence of hypertension and cardiovascular disease. Both obesity and hypertension have independently been associated with increased levels of inflammatory cytokines and immune cells within specific brain regions, as well as increased activity of the renin-angiotensin system (RAS). To test the hypothesis that high-fat diet (HFD) induced obesity leads to an angiotensin-II (Ang-II)-dependent increase in inflammatory cells within specific forebrain regions that are important for cardiovascular regulation, we first assessed microglial activation, astrocyte activation, inflammation and RAS component gene expression within selected metabolic and cardiovascular control centers of the forebrain in adult male C57BL/6 mice given either a HFD or a low-fat diet (LFD) for 8weeks. Subsequently, we assessed the necessity of the paraventricular nucleus of the hypothalamus (PVN) angiotensin type-1a (AT1a) receptor for these responses by using the Cre/lox system in mice to selectively delete the AT1a receptor from the PVN. These studies reveal that in addition to the arcuate nucleus of the hypothalamus (ARC), the PVN and the subfornical organ (SFO), two brain regions that are known to regulate blood pressure and energy balance, also initiate proinflammatory responses after the consumption of a diet high in fat. They further indicate that some, but not all, of these responses are reversed upon deletion of AT1a specifically within the PVN.
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Multiple studies have demonstrated that microglia number increases within the mediobasal hypothalamus during diet induced obesity.
“Multiple studies have demonstrated that microglia number increases within the mediobasal hypothalamus during diet induced obesity (Thaler et al., 2012; de Kloet et al., 2014; Valdearcos et al., 2014; Schur et al., 2015; Waise et al., 2015; Baufeld et al., 2016; Guillemot-Legris et al., 2016).”
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 de Kloet et al., 2014
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- Authors
- de Kloet, A. D., Pioquinto, D. J., Nguyen, D., Wang, L., Smith, J. A., Hiller, H., & Sumners, C.
- Affiliations
- University of Florida (US)
- Venue
- Physiology & Behavior
- Publisher
- Elsevier BV
- Published
- 2014-09
- Volume
- 136
- Pages
- 31-38
- ISSN
- 0031-9384 (ISSN-L)
- PMC
- PMC4125551
- OpenAlex
- W2065660454
- Cited by
- 66
- References
- 62
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 2 · 2023: 5 · 2022: 10 · 2021: 6 · 2020: 4 · 2019: 6 · 2018: 7 · 2017: 3 · 2016: 9 · 2015: 5 · 2014: 4
- FWCI
- 4.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Physiology & Behavior (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association Postdoctoral Fellowship (12POST11550013)
- NIH T32 Training Grant (HL-083810)
- NIH postdoctoral fellowship (F32-HL-116074)
- NIH (HL-076803)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- obesity, neuroinflammation, renin-angiotensin system, angiotensin II, angiotensin type 1a receptor, paraventricular nucleus, arcuate nucleus, subfornical organ, microglial activation, astrocyte activation, high-fat diet, blood pressure regulation, energy balance, forebrain
- MeSH terms
- Angiotensin II, Animals, Calcium-Binding Proteins, Disease Models, Animal, Encephalitis, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Male, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Microfilament Proteins, Neuroglia, Obesity, Renin-Angiotensin System, Repressor Proteins, Body Mass Index, Cytokines, Prosencephalon, Adiposity, Apoptosis Regulatory Proteins, Mice, Basic Helix-Loop-Helix Proteins, Basic Helix-Loop-Helix Transcription Factors, Diet, High-Fat
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