Effect of Dietary Bioactive Compounds on Mitochondrial and Metabolic Flexibility
Abstract
:1. Introduction
- (1)
- Not all organs and systems respond in a similar way to an increase or decrease in energy availability. Differences are observed in insulin sensitivity in different organs during the development from an insulin resistance stage to a clinically type 2 diabetes stage. It seems that the onset of type 2 diabetes or other clinical complications are a consequence of the increase in the number of organs with reduced insulin sensitivity. In the clinical setting, it is common to observe a rapid shift from a non-pathological (subclinical) to a disease condition (Figure 1A) that is triggered after exceeding a metabolic checkpoint where the organism is unable to maintain homeostasis. For example, Figure 1B shows that the intake of a high-fat diet in mice is well regulated after two months, until a possible accumulation of factors that triggers a disease condition observed at Month 4 with a clinically-observed feature (unpublished observations); suggesting that, at a certain point, the homeostatic compensation is overwhelmed, and pathological conditions could be observed. Even though, it is interesting to note in the same Figure 1B that at four months of a high-fat diet, the basal glucose levels are the same, although the organism is unable to maintain normal glycemia levels; implying that, in stress conditions (glucose overload), the capacity of the system to rapidly maintain homeostasis is compromised; albeit, finally, a homeostatic condition is reached (fasting state).
- (2)
- In the same way, in the clinical setting, the effects of a mild reduction in body weight induce a rapid switch from a disease to a clinically non-pathological condition (Figure 1C). However, in this respect, frailty from this condition is also observed if an increase in body weight is observed. This implies that although most disease biomarkers are normalized during weight reduction programs, the metabolic system is unstable and liable to return to a disease condition. In other words, some organs still have metabolic inflexibility, explaining, in this way, the deleterious effects of “yo-yo” dieting.
- (3)
- The total recovery of the metabolic inflexibility condition will imply the normalization of metabolic flexibility in all organs. Thus, combined treatments with multiple mechanisms of action are required for a better handling of metabolic diseases.
2. Mitochondria Dynamic Regulation
3. Polyphenols and Mitochondria
4. ω-3 Fatty Acids and Mitochondria
5. Dietary Fiber, Gut Microbiota and Derived Colonic Fermentation Metabolites and Mitochondria
6. Conclusions
Acknowledgments
Conflicts of Interest
References
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Compound | Effect | Mechanism | Type of Study | Reference |
---|---|---|---|---|
Resveratrol | Increased number of mitochondria in liver and muscle | SIRT1 and PGC-1α activation | Animal model | [22] |
Quercetin | Increased mtDNA and cytochrome c content in muscle and brain | SIRT1 and PGC-1α activation | Animal model | [23] |
Epicatechin-rich cocoa | Mitochondrial biogenesis stimulation in muscle | SIRT1 and PGC-1α activation | Human study | [24] |
Coumestrol | Increased mitochondrial content in muscle cells | SIRT1 activation | Cell culture | [25] |
Quercetin, kaempferol, epicatechin | Inhibitors of H2O2 production by mitochondria | Inhibition of complex I activity | Cell culture | [26] |
Grape seed proanthocyanidin extract | Enhanced thermogenic capacity and improvement in mitochondrial function in brown and adipose tissue | Not described | Animal model | [27] |
Anthocyanins | Complex I activity recovery and increase in the rate of ATP synthesis | Functioning as electron carriers in a similar way as coenzyme Q1 | Isolated mitochondria | [28] |
Galangin | Modulation of the mitochondrial permeability transition pore | Decreased fluidity of the mitochondrial membrane | Isolated mitochondria | [29] |
Epigallocatechin | Modification in mitochondrial architecture | AMPKα activation | Animal model | [30] |
Product | Effect | Mechanism | Type of Study | Reference |
---|---|---|---|---|
Fish oil | Improvement in mitochondrial efficiency | Increased content or enhanced kinetics of ETC | Animal model | [38] |
Fish oil | Reduced body fat mass | Stimulation of lipid oxidation | Human study | [39] |
Fish oil | Decrease in insulinemia | Increased lipid oxidation | Human study | [40] |
DHA + EPA | Improve in mitochondrial ADP kinetics | Incorporation in mitochondrial membranes, displacing ω-6 species in several phospholipids population | Human study | [44] |
DHA + EPA | Decrease in H2O2 production | Increased tolerance to Ca2+-induced MPTP opening | Isolated mitochondria | [47] |
Fish oil | Improvement in ATP production in brain | Improvement in membrane fluidity | Animal model | [49] |
EPA and DHA | Increase in ATP and reduction in ROS levels in hepatocytes | Increase in the length of mitochondrial tubes by an increase in Mfn2 mRNA levels | Cell culture | [50] |
EPA | Restoration of skeletal muscle mitochondrial capacity | Increase in coupling efficiency of the ETC | Animal model | [51] |
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Serrano, J.C.E.; Cassanye, A.; Martín-Gari, M.; Granado-Serrano, A.B.; Portero-Otín, M. Effect of Dietary Bioactive Compounds on Mitochondrial and Metabolic Flexibility. Diseases 2016, 4, 14. https://doi.org/10.3390/diseases4010014
Serrano JCE, Cassanye A, Martín-Gari M, Granado-Serrano AB, Portero-Otín M. Effect of Dietary Bioactive Compounds on Mitochondrial and Metabolic Flexibility. Diseases. 2016; 4(1):14. https://doi.org/10.3390/diseases4010014
Chicago/Turabian StyleSerrano, Jose C. E., Anna Cassanye, Meritxell Martín-Gari, Ana Belen Granado-Serrano, and Manuel Portero-Otín. 2016. "Effect of Dietary Bioactive Compounds on Mitochondrial and Metabolic Flexibility" Diseases 4, no. 1: 14. https://doi.org/10.3390/diseases4010014