Functional changes induced by caloric restriction in cardiac and skeletal muscle mitochondria

Serna, Julian David C.; Silva, Camille C. Caldeira da; Kowaltowski, Alicia J.

doi:10.1007/s10863-020-09838-4

Cited by 23 publications

(16 citation statements)

References 43 publications

(47 reference statements)

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“…In the heart (but not in skeletal muscle), lower maximal respiratory rates and a reduced rate of hydrogen peroxide release were reported. In this model, no changes in the respiratory control ratios were found (Serna et al, 2020 ).…”

Section: Mitochondrial Metabolismmentioning

confidence: 81%

Impact of Dietary Restriction Regimens on Mitochondria, Heart, and Endothelial Function: A Brief Overview

et al. 2021

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Caloric restriction (CR) and intermittent fasting (IF) are strategies aimed to promote health beneficial effects by interfering with several mechanisms responsible for cardiovascular diseases. Both dietary approaches decrease body weight, insulin resistance, blood pressure, lipids, and inflammatory status. All these favorable effects are the result of several metabolic adjustments, which have been addressed in this review, i.e., the improvement of mitochondrial biogenesis, the reduction of reactive oxygen species (ROS) production, and the improvement of cardiac and vascular function. CR and IF are able to modulate mitochondrial function via interference with dynamics (i.e., fusion and fission), respiration, and related oxidative stress. In the cardiovascular system, both dietary interventions are able to improve endothelium-dependent relaxation, reduce cardiac hypertrophy, and activate antiapoptotic signaling cascades. Further clinical studies are required to assess the long-term safety in the clinical setting.

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Section: Mitochondrial Metabolismmentioning

confidence: 81%

Impact of Dietary Restriction Regimens on Mitochondria, Heart, and Endothelial Function: A Brief Overview

et al. 2021

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“…To avoid malnutrition, CR rats were fed with an AIM93G diet supplemented with vitamins and minerals to the same levels as AL animals consumed (34). Details regarding the CR protocol and its effects can be consulted in our previous publications (29–31). Prior to the experiments, animals were fasted for 10-12 h, beginning at 19:00.…”

Section: Methodsmentioning

confidence: 99%

“…The effects of CR on mitochondrial Ca 2+ transport are, however, organ-specific (31), and have not been explored in kidneys to date. Kidneys are known to be protected from damage induced by ischemia/reperfusion in animals submitted to dietary restriction or fasting (32,33).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Kidney Mitochondrial Function by Caloric Restriction

Serna

Amaral

Silva

et al. 2021

Preprint

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Caloric restriction (CR) prevents obesity, promotes healthy aging, and increases resilience against several pathological stimuli in laboratory rodents. At the mitochondrial level, protection promoted by CR in the brain and liver is related to higher calcium uptake rates and capacities, avoiding Ca2+-induced mitochondrial permeability transition. Dietary restriction has also been shown to increase kidney resistance against damaging stimuli such as ischemia/reperfusion, but if these effects are related to similar mitochondrial adaptations had not yet been uncovered. Here, we characterized changes in mitochondrial function in response to six months of CR in rats, measuring bioenergetic parameters, redox balance and calcium homeostasis. CR promoted an increase in mitochondrial oxygen consumption rates under non-phosphorylating and uncoupled conditions. While CR prevents mitochondrial reactive oxygen species production in many tissues, in kidney we found that mitochondrial H2O2 release was enhanced, although levels of carbonylated proteins and methionine sulfoxide were unchanged. Surprisingly, and opposite to the effects observed in brain and liver, mitochondria from CR animals are more prone to Ca2+-induced mitochondrial permeability transition. CR mitochondria also displayed higher calcium uptake rates, which were not accompanied by changes in calcium efflux rates, nor related to altered inner mitochondrial membrane potentials or the amounts of the mitochondrial calcium uniporter (MCU). Instead, increased mitochondrial calcium uptake rates in CR kidneys correlate with a loss of MICU2, an MCU modulator. Interestingly, MICU2 is also modulated by CR in liver, suggesting it has a broader diet-sensitive regulatory role controlling mitochondrial calcium homeostasis. Together, our results highlight the organ-specific bioenergetic, redox, and ionic transport effects of CR. Specifically, we describe the regulation of the expression of MICU2 and its effects on mitochondrial calcium transport as a novel and interesting aspect of the metabolic responses to dietary interventions.

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“…These may be a result of less ROS production or increased antioxidant levels. Indeed, evidence shows that calorie restriction decreases mitochondrial ROS released [19][20][21]. Even though that idea is somehow controversial [22] animal studies have shown that calorie restriction lowers the levels of oxidatively modified lipids [23,24], proteins [25], and DNA [26].…”

Section: Introductionmentioning

confidence: 99%

“…Even though that idea is somehow controversial [22] animal studies have shown that calorie restriction lowers the levels of oxidatively modified lipids [23,24], proteins [25], and DNA [26]. Strikingly, calorie restriction seems to protect cardiac mitochondrial components from ROSinduced oxidative damage [20], in parallel with lower mitochondrial ROS production by this organ [19,21].…”

Section: Introductionmentioning

confidence: 99%

Calorie Restriction Maintains Mitochondrial Function and Redox Balance Avoiding Lipidomic Reprogramming during Isoproterenol-Induced Cardiac Hypertrophy

Ceb

Amb

Plo

et al. 2021

Preprint

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Cardiac hypertrophy induces a metabolic shift, leading to a preferential consumption of glucose (over fatty acids) to support the high energetic demand. Typically, health cardiac tissue utilizes more fat than any other organ. Calorie restriction is a dietary procedure that induces health benefits and lifespan extension in many organisms. Given the beneficial effects of calorie restriction and the metabolic dysregulation seen during cardiac hypertrophy, we hypothesized that calorie restriction prevents cardiac hypertrophy, lipid, mitochondrial, and redox dysregulations. Strikingly, calorie restriction reversed isoproterenol-induced cardiac hypertrophy, lowered succinate driven mitochondrial H2O2 production, improved mitochondrial function (indicated as a higher Respiratory Control Ratio – RCR) and avoided mitochondrial superoxide dismutase (MnSOD) and glutathione peroxidase (GPX) repression. To gain insight into how calorie restriction could interfere with the metabolic changes induced by cardiac hypertrophy, we performed lipidomic profiling. Calorie restriction protected against the consumption of several triglycerides (TG) linked to unsaturated fatty acids, and the accumulation of TGs containing saturated fatty acids observed in hypertrophic samples. Cardiac hypertrophy induced an increase in ceramides, phosphoethanolamines and acylcarnitines (12:0, 14:0, 16:0 and 18:0) that were also reversed by calorie restriction. Altogether, our data demonstrate that hypertrophy changes the cardiac lipidome, causes mitochondrial disturbances and oxidative stress. All these changes are prevented by calorie restriction intervention in vivo. This study uncovers calorie restriction as a resource protect cardiac tissue and prevent cardiac hypertrophy-induced lipidomic remodeling.

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Functional changes induced by caloric restriction in cardiac and skeletal muscle mitochondria

Cited by 23 publications

References 43 publications

Impact of Dietary Restriction Regimens on Mitochondria, Heart, and Endothelial Function: A Brief Overview

Impact of Dietary Restriction Regimens on Mitochondria, Heart, and Endothelial Function: A Brief Overview

Regulation of Kidney Mitochondrial Function by Caloric Restriction

Calorie Restriction Maintains Mitochondrial Function and Redox Balance Avoiding Lipidomic Reprogramming during Isoproterenol-Induced Cardiac Hypertrophy

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