High-fructose diet during adolescent development increases neuroinflammation and depressive-like behavior without exacerbating outcomes after stroke

• Type of Material: Article
• Authors: CS Harrell, Emory University; C Zainaldin, Emory University; D McFarlane, Emory University; MM Hyer, Virginia Commonwealth University; D Stein, Emory University; Iqbal Sayeed, Emory University; Gretchen Neigh, Emory University
• Language: English
• Date: 2018-10-01
• Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2018 Elsevier Inc. All rights reserved.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.bbi.2018.05.018
• Title of Journal or Parent Work: BRAIN BEHAVIOR AND IMMUNITY
• Volume: 73
• Start Page: 340
• End Page: 351
• Keywords: COMPLEMENT CASCADE; Neurosciences; ANXIETY-LIKE; FUNCTIONAL RECOVERY; Affective-like behavior; FEMALE CALIFORNIA MICE; Fructose; Immunology; Adolescence; Psychiatry; Stroke; Complement; Neurosciences & Neurology; Life Sciences & Biomedicine; METABOLIC SYNDROME; AGED RATS; Science & Technology; INSULIN-RESISTANCE; ISCHEMIC-STROKE; OXIDATIVE STRESS; ENDURING CONSEQUENCES

Abstract

Diseases, disorders, and insults of aging are frequently studied in otherwise healthy animal models despite rampant co-morbidities and exposures among the human population. Stressor exposures can increase neuroinflammation and augment the inflammatory response following a challenge. The impact of dietary exposure on baseline neural function and behavior has gained attention; in particular, a diet high in fructose can increase activation of the hypothalamic-pituitary-adrenal axis and alter behavior. The current study considers the implications of a diet high in fructose for neuroinflammation and outcomes following the cerebrovascular challenge of stroke. Ischemic injury may come as a “second hit” to pre-existing metabolic pathology, exacerbating inflammatory and behavioral sequelae. This study assesses the neuroinflammatory consequences of a peri-adolescent high-fructose diet model and assesses the impact of diet-induced metabolic dysfunction on behavioral and neuropathological outcomes after middle cerebral artery occlusion. We demonstrate that consumption of a high-fructose diet initiated during adolescent development increases brain complement expression, elevates plasma TNFα and serum corticosterone, and promotes depressive-like behavior. Despite these adverse effects of diet exposure, peri-adolescent fructose consumption did not exacerbate neurological behaviors or lesion volume after middle cerebral artery occlusion.