Publication

Initial Assessment of Lactate as Mediator of Exercise-Induced Retinal Protection

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Last modified
  • 05/21/2025
Type of Material
Authors
    Jana T. Sellers, Emory UniversityMicah A. Chrenek, Emory UniversityPreston E. Girardot, Emory UniversityJohn Nickerson, Emory UniversityMachelle Pardue, Emory UniversityJeffrey Boatright, Emory University
Language
  • English
Date
  • 2019-01-01
Publisher
  • Springer International Publishing A.G.
Publication Version
Copyright Statement
  • © Springer Nature Switzerland AG 2019, Corrected Publication 2020.
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 1185
Start Page
  • 451
End Page
  • 455
Grant/Funding Information
  • NIH R01EY028859, R01EY028450, R01EY021592, T32EY07092, and P30EY006360; and an unrestricted grant from Research to Prevent Blindness, Inc.
  • The Abraham J. & Phyllis Katz Foundation; VA RR&D Center Grant C9246C,
  • Research Career Scientist Award C9257, Merit Award I01RX002806, and SPiRE Award Number I21RX001924;
Abstract
  • Physical exercise is protective in rodent models of retinal injury and disease. Data suggest that this is in part mediated by brain-derived neurotrophic factor (BDNF) signal transduction. It has been hypothesized that exercised-induced neuroprotection may be mediated by increases in circulating lactate that in turn alter BDNF secretion. We therefore tested whether mice undergoing a treadmill running regimen previously shown to be protective in a mouse model of retinal degeneration (RD) have increased serum levels of lactate. Lactate levels in exercised and non-exercised mice were statistically indistinguishable. A role for circulating lactate in exercise-induced retinal protection is unsupported.
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