Malnutrition vs calorie restriction: The effects on maternal nutrient reduction in cardiac fetal mitochondrial function

Mitochondrial metabolism and autophagy are two of the most metabolically active cellular processes, playing a crucial role in regulating organism longevity. In fact, both mitochondrial dysfunction or autophagy decline compromise cellular homeostasis and induce inflammation. Calorie restriction (CR) is the oldest strategy known to promote healthspan, and a plethora of CR mimetics have been used to emulate its beneficial effects. Herein, we discuss how CR and CR mimetics, by modulating mitochondrial metabolism or autophagic flux, prevent inflammatory processes, protect the intestinal barrier function, and dampen both inflammaging and neuroinflammation. We outline the effects of some compounds classically known as modulators of autophagy and mitochondrial function, such as NAD+ precursors, metformin, spermidine, rapamycin, and resveratrol, on the control of the inflammatory cascade and how these anti-inflammatory properties could be involved in their ability to increase resilience to age-associated diseases.

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Oxidative stress and mitochondrial function with aging - the effects of calorie restriction

Aging Cell ◽

10.1046/j.1474-9728.2003.00074.x ◽

2004 ◽

Vol 3 (1) ◽

pp. 7-12 ◽

Cited By ~ 132

Author(s):

B. J. Merry

Keyword(s):

Oxidative Stress ◽

Calorie Restriction ◽

Mitochondrial Function

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

10.1101/2021.07.13.452233 ◽

2021 ◽

Author(s):

Cícera Edna Barbosa David ◽

Aline Maria Brito Lucas ◽

Pedro Lourenzo Oliveira Cunha ◽

Yuana Ivia Ponte Viana ◽

Marcos Yukio Yoshinaga ◽

...

Keyword(s):

Fatty Acids ◽

Cardiac Hypertrophy ◽

Calorie Restriction ◽

Mitochondrial Function ◽

Cardiac Tissue ◽

Unsaturated Fatty Acids ◽

Saturated Fatty Acids ◽

Respiratory Control ◽

H2o2 Production

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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