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Altered Glycolytic Capacity, Not Mitochondrial Common Deletion, May Be Responsible For Age-Related Increases in Rat Intestinal Permeability


 Some evidence points to a link between aging-related increased intestinal permeability and mitochondrial dysfunction in in-vivo models. Several studies have also demonstrated age-related accumulation of the of specific deletion 4834-bp of “common” mitochondrial DNA (mtDNA) in various rat tissues and suggest that this deletion may disrupt mitochondrial metabolism. The present study aimed to investigate possible associations among the mtDNA common deletion, mitochondrial function, intestinal permeability, and aging in rats. Our data showed were no significant differences in the abundance of mtDNA4834 deletions in intestinal tissue between young adult ((4-month-old) and aged (24-month-old) rats). In addition, Spearman's correlation coefficients of measured parameters in serum samples for intestinal permeability did not correlate with deletion frequency and measured levels of mitochondrial energy function parameters. However, the tissue lactate/pyruvate ratio (L/P) was three times lower in old rats than in young rats. Additionally, there were significant negative correlations between intestinal permeability parameters and L/P ratios. Considering our findings showing that the intestinal tissues of aged rats are not prone to accumulate mtDNA common deletion, we suggest that this mutation does not explain the age-related increase in intestinal permeability. Some data support the thought that altered glycolytic capacity could be a possible mechanism linked to increased intestinal permeability with age.