Influence of intensity of food restriction on skeletal muscle mitochondrial energy metabolism in rats

2006 ◽  
Vol 291 (3) ◽  
pp. E460-E467 ◽  
Author(s):  
Gyasi Johnson ◽  
Damien Roussel ◽  
Jean-François Dumas ◽  
Olivier Douay ◽  
Yves Malthièry ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Food Restriction ◽  
Metabolic Adaptation ◽  
Proton Leak ◽  
Mitochondrial Energy Metabolism ◽  
Respiration Rates ◽  
Mitochondrial Functions ◽  
Mitochondrial Adaptation ◽  
Putative Mechanism

Variable durations of food restriction (FR; lasting weeks to years) and variable FR intensities are applied to animals in life span-prolonging studies. A reduction in mitochondrial proton leak is suggested as a putative mechanism linking such diet interventions and aging retardation. Early mechanisms of mitochondrial metabolic adaptation induced by FR remain unclear. We investigated the influence of different degrees of FR over 3 days on mitochondrial proton leak and mitochondrial energy metabolism in rat hindlimb skeletal muscle. Animals underwent 25, 50, and 75% and total FR compared with control rats. Proton leak kinetics and mitochondrial functions were investigated in two mitochondrial subpopulations, intermyofibrillar (IMF) and subsarcolemmal (SSM) mitochondria. Regardless of the degree of restriction, skeletal muscle mass was not affected by 3 days of FR. Mitochondrial basal proton conductance was significantly decreased in 50% restricted rats in both mitochondrial subpopulations (46 and 40% for IMF and SSM, respectively) but was unaffected in other groups compared with controls. State 3 and uncoupled state 3 respiration rates were decreased in SSM mitochondria only for 50% restricted rats when pyruvate + malate was used as substrate (−34.5 and −38.9% compared with controls, P < 0.05). IMF mitochondria respiratory rates remained unchanged. Three days of FR, particularly at 50% FR, were sufficient to lower mitochondria energetic metabolism in both mitochondrial populations. Our study highlights an early step in mitochondrial adaptation to FR and the influence of the severity of restriction on this adaptation. This step may be involved in an aging-retardation process.

scholarly journals Mitochondrial energy metabolism in a model of undernutrition induced by dexamethasone

2003 ◽  
Vol 90 (5) ◽  
pp. 969-977 ◽  
Author(s):  
Jean-François Dumas ◽  
Gilles Simard ◽  
Damien Roussel ◽  
Olivier Douay ◽  
Françoise Foussard ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Treated Group ◽  
Liver Mitochondria ◽  
Proton Leak ◽  
Thermodynamic Efficiency ◽  
Liver Mass ◽  
Mitochondrial Energy Metabolism ◽  
Thermodynamic Coupling ◽  
And Control ◽  
Complex Activities

The present investigation was undertaken to evaluate whether mitochondrial energy metabolism is altered in a model of malnutrition induced by dexamethasone (DEX) treatment (1·5mg/kg per d for 5d). The gastrocnemius and liver mitochondria were isolated from DEX-treated, pair-fed (PF) and control (CON) rats. Body weight was reduced significantly more in the DEX-treated group (−16%) than in the PF group (−9%). DEX treatment increased liver mass (+59% v. PF, +23% v. CON) and decreased gastrocnemius mass. Moreover, in DEX-treated rats, liver mitochondria had an increased rate of non-phosphorylative O2 consumption with all substrates (approximately +42%). There was no difference in enzymatic complex activities in liver mitochondria between rat groups. Collectively, these results suggest an increased proton leak and/or redox slipping in the liver mitochondria of DEX-treated rats. In addition, DEX decreased the thermodynamic coupling and efficiency of oxidative phosphorylation. We therefore suggest that this increase in the proton leak and/or redox slip in the liver is responsible for the decrease in the thermodynamic efficiency of energy conversion. In contrast, none of the variables of energy metabolism determined in gastrocnemius mitochondria was altered by DEX treatment. Therefore, it appears that DEX specifically affects mitochondrial energy metabolism in the liver.

scholarly journals Mechanisms of Energy Metabolism in Skeletal Muscle Mitochondria Following Radiation Exposure

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 950 ◽  
Author(s):  
Kim ◽  
Lee ◽  
Kim ◽  
Kim ◽  
Yi
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Ionizing Radiation ◽  
Radiation Exposure ◽  
Biological Effects ◽  
Mitochondrial Protein ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
Mitochondrial Energy Metabolism ◽  
Effects Of Radiation

An understanding of cellular processes that determine the response to ionizing radiation exposure is essential for improving radiotherapy and assessing risks to human health after accidental radiation exposure. Radiation exposure leads to many biological effects, but the mechanisms underlying the metabolic effects of radiation are not well known. Here, we investigated the effects of radiation exposure on the metabolic rate and mitochondrial bioenergetics in skeletal muscle. We show that ionizing radiation increased mitochondrial protein and mass and enhanced proton leak and mitochondrial maximal respiratory capacity, causing an increase in the fraction of mitochondrial respiration devoted to uncoupling reactions. Thus, mice and cells treated with radiation became energetically efficient and displayed increased fatty acid and amino acid oxidation metabolism through the citric acid cycle. Finally, we demonstrate that radiation-induced alterations in mitochondrial energy metabolism involved adenosine monophosphate-activated kinase signaling in skeletal muscle. Together, these results demonstrate that alterations in mitochondrial mass and function are important adaptive responses of skeletal muscle to radiation.

Increased mitochondrial proton leak in skeletal muscle mitochondria of UCP1-deficient mice

2000 ◽  
Vol 279 (4) ◽  
pp. E941-E946 ◽  
Author(s):  
Shadi Monemdjou ◽  
Wolfgang E. Hofmann ◽  
Leslie P. Kozak ◽  
Mary-Ellen Harper
Keyword(s):  
Skeletal Muscle ◽  
Proton Leak ◽  
Deficient Mouse ◽  
Muscle Mitochondria ◽  
Respiration Rates ◽  
Skeletal Muscle Mitochondria ◽  
Brown Adipose ◽  
Kinetics Of ◽  
Overall Kinetics ◽  
Deficient Mice

Mice having targeted inactivation of uncoupling protein 1 (UCP1) are cold sensitive but not obese (Enerbäck S, Jacobsson A, Simpson EM, Guerra C, Yamashita H, Harper M-E, and Kozak LP. Nature 387: 90–94, 1997). Recently, we have shown that proton leak in brown adipose tissue (BAT) mitochondria from UCP1-deficient mice is insensitive to guanosine diphosphate (GDP), a well known inhibitor of UCP1 activity (Monemdjou S, Kozak LP, and Harper M-E. Am J Physiol Endocrinol Metab 276: E1073-E1082, 1999). Moreover, despite a fivefold increase of UCP2 mRNA in BAT of UCP1-deficient mice, we found no differences in the overall kinetics of this GDP-insensitive proton leak between UCP1 -deficient mice and controls. Based on these findings, which show no adaptive increase in UCP1-independent leak in BAT, we hypothesized that adaptive thermogenesis may be occurring in other tissues of the UCP1-deficient mouse (e.g. , skeletal muscle), thus allowing them to maintain their normal resting metabolic rate, feed efficiency, and adiposity. Here, we report on the overall kinetics of the mitochondrial proton leak, respiratory chain, and ATP turnover in skeletal muscle mitochondria from UCP1-deficient and heterozygous control mice. Over a range of mitochondrial protonmotive force (Δp) values, leak-dependent oxygen consumption is higher in UCP1-deficient mice compared with controls. State 4 (maximal leak-dependent) respiration rates are also significantly higher in the mitochondria of mice deficient in UCP1, whereas state 4 Δp is significantly lower. No significant differences in state 3 respiration rates or Δp values were detected between the two groups. Thus the altered kinetics of the mitochondrial proton leak in skeletal muscle of UCP1 -deficient mice indicate a thermogenic mechanism favoring the lean phenotype of the UCP1 -deficient mouse.

scholarly journals The role and mechanism of mitochondrial functions and energy metabolism in the function regulation of the mesenchymal stem cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wanhao Yan ◽  
Shu Diao ◽  
Zhipeng Fan
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Energy Metabolism ◽  
Self Renewal ◽  
Mitochondrial Energy Metabolism ◽  
Functional Reconstruction ◽  
Multipotent Cells ◽  
Mitochondrial Functions ◽  
Adenosine Triphosphate Production ◽  
Control Direction

AbstractMesenchymal stem cells (MSCs) are multipotent cells that show self-renewal, multi-directional differentiation, and paracrine and immune regulation. As a result of these properties, the MSCs have great clinical application prospects, especially in the regeneration of injured tissues, functional reconstruction, and cell therapy. However, the transplanted MSCs are prone to ageing and apoptosis and have a difficult to control direction differentiation. Therefore, it is necessary to effectively regulate the functions of the MSCs to promote their desired effects. In recent years, it has been found that mitochondria, the main organelles responsible for energy metabolism and adenosine triphosphate production in cells, play a key role in regulating different functions of the MSCs through various mechanisms. Thus, mitochondria could act as effective targets for regulating and promoting the functions of the MSCs. In this review, we discuss the research status and current understanding of the role and mechanism of mitochondrial energy metabolism, morphology, transfer modes, and dynamics on MSC functions.

scholarly journals Astaxanthin as a Novel Mitochondrial Regulator: A New Aspect of Carotenoids, beyond Antioxidants

Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 107
Author(s):  
Yasuhiro Nishida ◽  
Allah Nawaz ◽  
Karen Hecht ◽  
Kazuyuki Tobe
Keyword(s):  
Antioxidant Activity ◽  
Free Radical ◽  
Energy Metabolism ◽  
Molecular Targets ◽  
Marine Organisms ◽  
Mitochondrial Energy Metabolism ◽  
Mitochondrial Functions ◽  
Antioxidant Function

Astaxanthin is a member of the carotenoid family that is found abundantly in marine organisms, and has been gaining attention in recent years due to its varied biological/physiological activities. It has been reported that astaxanthin functions both as a pigment, and as an antioxidant with superior free radical quenching capacity. We recently reported that astaxanthin modulated mitochondrial functions by a novel mechanism independent of its antioxidant function. In this paper, we review astaxanthin’s well-known antioxidant activity, and expand on astaxanthin’s lesser-known molecular targets, and its role in mitochondrial energy metabolism.

scholarly journals Mitigation of Glucolipotoxicity-Induced Apoptosis, Mitochondrial Dysfunction, and Metabolic Stress by N-Acetyl Cysteine in Pancreatic β-Cells

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 239 ◽  
Author(s):  
Arwa Alnahdi ◽  
Annie John ◽  
Haider Raza
Keyword(s):  
Energy Metabolism ◽  
Palmitic Acid ◽  
Mitochondrial Dysfunction ◽  
High Glucose ◽  
High Energy ◽  
Metabolic Adaptation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Mitochondrial Energy Metabolism ◽  
Acetyl Cysteine

Glucolipotoxicity caused by hyperglycemia and hyperlipidemia are the common features of diabetes-induced complications. Metabolic adaptation, particularly in energy metabolism; mitochondrial dysfunction; and increased inflammatory and oxidative stress responses are considered to be the main characteristics of diabetes and metabolic syndrome. However, due to various fluctuating endogenous and exogenous stimuli, the precise role of these factors under in vivo conditions is not clearly understood. In the present study, we used pancreatic β-cells, Rin-5F, to elucidate the molecular and metabolic changes in glucolipotoxicity. Cells treated with high glucose (25 mM) and high palmitic acid (up to 0.3 mM) for 24 h exhibited increased caspase/poly-ADP ribose polymerase (PARP)-dependent apoptosis followed by DNA fragmentation, alterations in mitochondrial membrane permeability, and bioenergetics, accompanied by alterations in glycolytic and mitochondrial energy metabolism. Our results also demonstrated alterations in the expression of mammalian target of rapamycin (mTOR)/5′ adenosine monophosphate-activated protein kinase (AMPK)-dependent apoptotic and autophagy markers. Furthermore, pre-treatment of cells with 10 mM N-acetyl cysteine attenuated the deleterious effects of high glucose and high palmitic acid with improved cellular functions and survival. These results suggest that the presence of high energy metabolites enhance mitochondrial dysfunction and apoptosis by suppressing autophagy and adapting energy metabolism, mediated, at least in part, via enhanced oxidative DNA damage and mTOR/AMPK-dependent cell signaling.

scholarly journals Reduced mitochondrial fission and impaired energy metabolism in human primary skeletal muscle cells of Megaconial Congenital Muscular Dystrophy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Evrim Aksu-Menges ◽  
Cemil Can Eylem ◽  
Emirhan Nemutlu ◽  
Merve Gizer ◽  
Petek Korkusuz ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscular Dystrophy ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Congenital Muscular Dystrophy ◽  
Autosomal Recessive Disorder ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Mitochondrial Energy Metabolism

AbstractMegaconial Congenital Muscular Dystrophy (CMD) is a rare autosomal recessive disorder characterized by enlarged mitochondria located mainly at the periphery of muscle fibers and caused by mutations in the Choline Kinase Beta (CHKB) gene. Although the pathogenesis of this disease is not well understood, there is accumulating evidence for the presence of mitochondrial dysfunction. In this study, we aimed to investigate whether imbalanced mitochondrial dynamics affects mitochondrial function and bioenergetic efficiency in skeletal muscle cells of Megaconial CMD. Immunofluorescence, confocal and transmission electron microscopy studies revealed impaired mitochondrial network, morphology, and localization in primary skeletal muscle cells of Megaconial CMD. The organelle disruption was specific only to skeletal muscle cells grown in culture. The expression levels of mitochondrial fission proteins (DRP1, MFF, FIS1) were found to be decreased significantly in both primary skeletal muscle cells and tissue sections of Megaconial CMD by Western blotting and/or immunofluorescence analysis. The metabolomic and fluxomic analysis, which were performed in Megaconial CMD for the first time, revealed decreased levels of phosphonucleotides, Krebs cycle intermediates, ATP, and altered energy metabolism pathways. Our results indicate that reduced mitochondrial fission and altered mitochondrial energy metabolism contribute to mitochondrial dysmorphology and dysfunction in the pathogenesis of Megaconial CMD.

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