Intermittent fasting effects on the central nervous system: how hunger modulates brain function (2017)
- Authors:
- Autor USP: KOWALTOWSKI, ALÍCIA JULIANA - IQ
- Unidade: IQ
- DOI: 10.1007/978-3-319-40007-5_29-1
- Subjects: SISTEMA NERVOSO CENTRAL; DOENÇAS NEURODEGENERATIVAS
- Language: Inglês
- Imprenta:
- ISBN: 978-33-19400-07-5
- Source:
- Título do periódico: Handbook of Famine, Starvation, and Nutrient Deprivation
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
-
ABNT
CERQUEIRA, Fernanda Menezes e CHAUSSE, Bruno e KOWALTOWSKI, Alicia Juliana. Intermittent fasting effects on the central nervous system: how hunger modulates brain function. Handbook of Famine, Starvation, and Nutrient Deprivation. Tradução . New York: Springer, 2017. . Disponível em: https://doi.org/10.1007/978-3-319-40007-5_29-1. Acesso em: 30 set. 2024. -
APA
Cerqueira, F. M., Chausse, B., & Kowaltowski, A. J. (2017). Intermittent fasting effects on the central nervous system: how hunger modulates brain function. In Handbook of Famine, Starvation, and Nutrient Deprivation. New York: Springer. doi:10.1007/978-3-319-40007-5_29-1 -
NLM
Cerqueira FM, Chausse B, Kowaltowski AJ. Intermittent fasting effects on the central nervous system: how hunger modulates brain function [Internet]. In: Handbook of Famine, Starvation, and Nutrient Deprivation. New York: Springer; 2017. [citado 2024 set. 30 ] Available from: https://doi.org/10.1007/978-3-319-40007-5_29-1 -
Vancouver
Cerqueira FM, Chausse B, Kowaltowski AJ. Intermittent fasting effects on the central nervous system: how hunger modulates brain function [Internet]. In: Handbook of Famine, Starvation, and Nutrient Deprivation. New York: Springer; 2017. [citado 2024 set. 30 ] Available from: https://doi.org/10.1007/978-3-319-40007-5_29-1 - Caloric restriction protects mice against isoproterenol-induced cardiac hypertrophy by mechanisms that involve mitochondrial ATP sensitive potassium channel and modulation of redox state
- Bioenergetic consequences of opening the ATP-sensitive `K POT. +´ channel of heart mitochondria
- Mechanisms by which opening the mitochondrial ATP- sensitive 'K POT. +' channel protects the ischemic heart
- Effect of Bcl-2 overexpression on mitochondrial structure and function
- Mitochondrial ATP-sensitive 'K POT. +' channel opening decreases reactive oxygen species generation
- Mitochondrial channels that regulate cell viability
- Mitochondrial permeability transition is delayed by ATP-sensitive 'K POT. +' channel ('Mitok IND. ATP') opening
- Protection against ischemic brain injury by inhibition of mitochondrial oxidative stress
- ATP-sensitive K+ channel (mitoKATP) opening protects against cellular damage preventing mitochondrial permeability transition
- Diet, mitochondria and energy metabolism
Informações sobre o DOI: 10.1007/978-3-319-40007-5_29-1 (Fonte: oaDOI API)
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