Abstract
Mitochondrial dysfunction is widely reported in various diseases and contributes to their pathogenesis. We assessed the effect of cocoa flavanols supplementation on mitochondrial function and whole metabolism, and we explored whether the mitochondrial deacetylase sirtuin-3 (Sirt3) is involved or not. We explored the effects of 15 days of CF supplementation in wild type and Sirt3-/- mice. Whole-body metabolism was assessed by indirect calorimetry, and an oral glucose tolerance test was performed to assess glucose metabolism. Mitochondrial respiratory function was assessed in permeabilised fibres and the pyridine nucleotides content (NAD+ and NADH) were quantified. In the wild type, CF supplementation significantly modified whole-body metabolism by promoting carbohydrate use and improved glucose tolerance. CF supplementation induced a significant increase of mitochondrial mass, while significant qualitative adaptation occurred to maintain H2O2 production and cellular oxidative stress. CF supplementation induced a significant increase in NAD+ and NADH content. All the effects mentioned above were blunted in Sirt3-/- mice. Collectively, CF supplementation boosted the NAD metabolism that stimulates sirtuins metabolism and improved mitochondrial function, which likely contributed to the observed whole-body metabolism adaptation, with a greater ability to use carbohydrates, at least partially through Sirt3.
Highlights
There were no changes in locomotor activity.cocoa flavanols (CF) mice showed a significant increase of whole-body energy expenditure by 15 ± 15% (p = 0.042; Figure 1C)
While a muscle-specific knock-out would have been preferable over the whole-body Sirt3 KO mice used in our study, our results suggest that CF improves NAD metabolism, and Sirt3 is involved in this supplementation-induced mitochondrial electron transport chain activity improvement
CF supplementation for 15 days leads to mitochondrial function improvements in oxidative and glycolytic muscles
Summary
Mitochondria are subcellular organelles that are involved in multiple cellular functions, such as energy transduction through mitochondrial oxidative phosphorylation and in mitochondrial hydrogen peroxide production or mitochondrial-mediated cell death activation [1,2,3]. Emerging evidence suggests that mitochondrial dysfunction is involved in many pathologies and plays a central role in their pathogenesis [4]. Our group reported mitochondrial impairment in patients with type 1 diabetes long before clinical complications [5]. A decrease of mitochondrial oxidative capacity occurs with aging even in healthy people [6]. Identifications of strategies to mitigate these dysfunctions
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