Intermittent fasting results in tissue-specific changes in bioenergetics and redox state

PLoS One. 2015 Mar 6;10(3):e0120413. doi: 10.1371/journal.pone.0120413. eCollection 2015.

Abstract

Intermittent fasting (IF) is a dietary intervention often used as an alternative to caloric restriction (CR) and characterized by 24 hour cycles alternating ad libitum feeding and fasting. Although the consequences of CR are well studied, the effects of IF on redox status are not. Here, we address the effects of IF on redox state markers in different tissues in order to uncover how changes in feeding frequency alter redox balance in rats. IF rats displayed lower body mass due to decreased energy conversion efficiency. Livers in IF rats presented increased mitochondrial respiratory capacity and enhanced levels of protein carbonyls. Surprisingly, IF animals also presented an increase in oxidative damage in the brain that was not related to changes in mitochondrial bioenergetics. Conversely, IF promoted a substantial protection against oxidative damage in the heart. No difference in mitochondrial bioenergetics or redox homeostasis was observed in skeletal muscles of IF animals. Overall, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain and protection against oxidative damage in the heart.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Injuries* / metabolism
  • Brain Injuries* / pathology
  • Brain* / metabolism
  • Brain* / pathology
  • Energy Metabolism*
  • Fasting / metabolism*
  • Liver* / injuries
  • Liver* / metabolism
  • Liver* / pathology
  • Male
  • Mitochondria, Liver* / metabolism
  • Mitochondria, Liver* / pathology
  • Oxidation-Reduction
  • Oxygen Consumption
  • Rats
  • Rats, Sprague-Dawley

Grants and funding

This work was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), grant 10/51906, Instituto Nacional de Ciência e Tecnologia de Processos Redox em Biomedicina (INCT Redoxoma), Núcleo de Apoio à Pesquisa Redoxoma (NAP Redoxoma), Centro de Pesquisa, Inovação e Difusão de Processos Redox em Biomedicina (CEPID Redoxoma) grant 13/07937-8, and the John Simon Guggenheim Memorial Foundation. MAVL (grant 13/14203-0) is supported by an undergraduate fellowship from FAPESP. BC is supported by a CNPq fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.