Oxidative stress and neuroinflammation in a rat model of co-morbid obesity and psychogenic stress

•Predatory odor stress heightens footshock reactivity and anxiety-like behaviors in Lewis rats.•WD intake increases glutathione reductase activity in plasma.•WD intake increases the brain protein levels of catalase and the glial fibrillary acidic protein.•Redox/neuroinflammatory biomarkers are close...

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Published in:Behavioural brain research 2021-02, Vol.400, p.112995-112995, Article 112995
Main Authors: Santiago Santana, Jose M., Vega-Torres, Julio D., Ontiveros-Angel, Perla, Bin Lee, Jeong, Arroyo Torres, Yaria, Cruz Gonzalez, Alondra Y., Aponte Boria, Esther, Zabala Ortiz, Deisha, Alvarez Carmona, Carolina, Figueroa, Johnny D.
Format: Article
Language:English
Subjects:
Animals
Anxiety - metabolism
Anxiety - physiopathology
Behavior, Animal - physiology
Biomarkers - metabolism
Catalase - metabolism
Diet, High-Fat - adverse effects
Diet-induced obesity rat
Disease Models, Animal
Fear - physiology
Glial Fibrillary Acidic Protein - metabolism
Glutathione Peroxidase - blood
Glutathione Reductase - blood
Inflammation - metabolism
Male
Neuroinflammation
Obesity - metabolism
Oxidative Stress - physiology
PTSD
Rats
Rats, Inbred Lew
Reactive oxygen species
Reactive Oxygen Species - metabolism
Stress, Psychological - metabolism
Stress, Psychological - physiopathology
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Summary:•Predatory odor stress heightens footshock reactivity and anxiety-like behaviors in Lewis rats.•WD intake increases glutathione reductase activity in plasma.•WD intake increases the brain protein levels of catalase and the glial fibrillary acidic protein.•Redox/neuroinflammatory biomarkers are closely associated with behavioral proxies related to fear and anxiety in rats. There is growing recognition for a reciprocal, bidirectional link between anxiety disorders and obesity. Although the mechanisms linking obesity and anxiety remain speculative, this bidirectionality suggests shared pathophysiological processes. Neuroinflammation and oxidative damage are implicated in both pathological anxiety and obesity. This study investigates the relative contribution of comorbid diet-induced obesity and stress-induced anxiety to neuroinflammation and oxidative stress. Thirty-six (36) male Lewis rats were divided into four groups based on diet type and stress exposure: 1) control diet unexposed (CDU) and 2) exposed (CDE), 3) Western-like high-saturated fat diet unexposed (WDU) and 4) exposed (WDE). Neurobehavioral tests were performed to assess anxiety-like behaviors. The catalytic concentrations of glutathione peroxidase and reductase were measured from plasma samples, and neuroinflammatory/oxidative stress biomarkers were measured from brain samples using Western blot. Correlations between behavioral phenotypes and biomarkers were assessed with Pearson's correlation procedures. We found that WDE rats exhibited markedly increased levels of glial fibrillary acidic protein (185 %), catalase protein (215 %), and glutathione reductase (GSHR) enzymatic activity (418 %) relative to CDU rats. Interestingly, the brain protein levels of glutathione peroxidase (GPx) and catalase were positively associated with body weight and behavioral indices of anxiety. Together, our results support a role for neuroinflammation and oxidative stress in heightened emotional reactivity to obesogenic environments and psychogenic stress. Uncovering adaptive responses to obesogenic environments characterized by high access to high-saturated fat/high-sugar diets and toxic stress has the potential to strongly impact how we treat psychiatric disorders in at-risk populations.
ISSN:0166-4328
1872-7549
DOI:10.1016/j.bbr.2020.112995