Next Article in Journal
Ocrelizumab Depletes CD20+ T Cells in Multiple Sclerosis Patients
Next Article in Special Issue
Mitochondrial DNA Integrity: Role in Health and Disease
Previous Article in Journal
SpermQ–A Simple Analysis Software to Comprehensively Study Flagellar Beating and Sperm Steering
Previous Article in Special Issue
The Role of Mitochondria in Reactive Oxygen Species Generation and Its Implications for Neurodegenerative Diseases
Open AccessEditor’s ChoiceArticle

A Rise in ATP, ROS, and Mitochondrial Content upon Glucose Withdrawal Correlates with a Dysregulated Mitochondria Turnover Mediated by the Activation of the Protein Deacetylase SIRT1

Department of Life Science, University of Seoul, Dongdaemun-Gu, Seoul 02504, Korea
*
Author to whom correspondence should be addressed.
Cells 2019, 8(1), 11; https://doi.org/10.3390/cells8010011
Received: 8 November 2018 / Revised: 17 December 2018 / Accepted: 20 December 2018 / Published: 27 December 2018
(This article belongs to the Special Issue Mitochondrial Biology in Health and Disease)
Glucose withdrawal has been used as a model for the study of homeostatic defense mechanisms, especially for how cells cope with a shortage of nutrient supply by enhancing catabolism. However, detailed cellular responses to glucose withdrawal have been poorly studied, and are controversial. In this study, we determined how glucose withdrawal affects mitochondrial activity, and the quantity and the role of SIRT1 in these changes. The results of our study indicate a substantial increase in ATP production from mitochondria, through an elevation of mitochondrial biogenesis, mediated by SIRT1 activation that is driven by increased NAD+/NADH ratio. Moreover, mitochondria persisted in the cells as elongated forms, and apparently evaded mitophagic removal. This led to a steady increase in mitochondria content and the reactive oxygen species (ROS) generated from them, indicating failure in ATP and ROS homeostasis, due to a misbalance in SIRT1-mediated mitochondria turnover in conditions of glucose withdrawal. Our results suggest that SIRT1 activation alone cannot properly manage energy homeostasis under certain metabolic crisis conditions. View Full-Text
Keywords: ATP; mitochondria; glycolysis; glucose withdrawal; SIRT1; autophagy ATP; mitochondria; glycolysis; glucose withdrawal; SIRT1; autophagy
Show Figures

Graphical abstract

MDPI and ACS Style

Song, S.B.; Hwang, E.S. A Rise in ATP, ROS, and Mitochondrial Content upon Glucose Withdrawal Correlates with a Dysregulated Mitochondria Turnover Mediated by the Activation of the Protein Deacetylase SIRT1. Cells 2019, 8, 11. https://doi.org/10.3390/cells8010011

AMA Style

Song SB, Hwang ES. A Rise in ATP, ROS, and Mitochondrial Content upon Glucose Withdrawal Correlates with a Dysregulated Mitochondria Turnover Mediated by the Activation of the Protein Deacetylase SIRT1. Cells. 2019; 8(1):11. https://doi.org/10.3390/cells8010011

Chicago/Turabian Style

Song, Seon B.; Hwang, Eun S. 2019. "A Rise in ATP, ROS, and Mitochondrial Content upon Glucose Withdrawal Correlates with a Dysregulated Mitochondria Turnover Mediated by the Activation of the Protein Deacetylase SIRT1" Cells 8, no. 1: 11. https://doi.org/10.3390/cells8010011

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop