Jose M Santiago Santana1, Julio D Vega-Torres2, Perla Ontiveros-Angel2, Jeong Bin Lee2, Yaria Arroyo Torres3, Alondra Y Cruz Gonzalez1, Esther Aponte Boria1, Deisha Zabala Ortiz1, Carolina Alvarez Carmona1, Johnny D Figueroa4. 1. Neuroregeneration Division, Neuroscience Research Laboratory, Natural Sciences Department, University of Puerto Rico Carolina Campus, Puerto Rico. 2. Center for Health Disparities and Molecular Medicine and Department of Basic Sciences, Physiology Division, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA, United States. 3. Neuroregeneration Division, Neuroscience Research Laboratory, Natural Sciences Department, University of Puerto Rico Carolina Campus, Puerto Rico; Universidad Metropolitana de Cupey Sciences and Technology School, Puerto Rico. 4. Center for Health Disparities and Molecular Medicine and Department of Basic Sciences, Physiology Division, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA, United States. Electronic address: jfigueroa@llu.edu.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: Julio David Vega-Torres; Elizabeth Haddad; Jeong Bin Lee; Priya Kalyan-Masih; Wanda I Maldonado George; Leonardo López Pérez; Darla M Piñero Vázquez; Yaría Arroyo Torres; José M Santiago Santana; Andre Obenaus; Johnny D Figueroa Journal: Brain Behav Immun Date: 2018-02-08 Impact factor: 7.217
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