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. 2013 Sep;29(9):1211-7.
doi: 10.1089/AID.2012.0354.

Short communication: The relationship between mitochondrial dysfunction and insulin resistance in HIV-infected children receiving antiretroviral therapy

Tanvi S Sharma  1 , Denise L Jacobson, Lynn Anderson, Mariana Gerschenson, Russell B Van Dyke, Elizabeth J McFarland, Tracie L Miller; Pediatric HIV/AIDS Cohort Study (PHACS)
Collaborators, Affiliations

Short communication: The relationship between mitochondrial dysfunction and insulin resistance in HIV-infected children receiving antiretroviral therapy

Tanvi S Sharma et al. AIDS Res Hum Retroviruses. 2013 Sep.

Abstract

Mitochondrial abnormalities may lead to metabolic complications in HIV-infected children who have been receiving long-term antiretroviral treatment. We conducted a matched, case-control study comparing 21 HIV-infected children with insulin resistance (cases) to 21 HIV-infected children without insulin resistance (controls) to assess differences in mitochondrial DNA (mtDNA) copies/cell and oxidative phosphorylation NADH dehydrogenase (C1) and cytochrome c oxidase (C4) enzyme activities in peripheral blood mononuclear cells. MtDNA copies/cell tended to be lower in cases, and fasting serum glucose levels were inversely and significantly correlated with C1 enzyme activity, more so in cases. Larger pediatric studies should evaluate mitochondrial etiologies of insulin resistance and determine the role of antiretroviral therapies or HIV infection on mitochondrial dysfunction.

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Figures

FIG. 1.
FIG. 1.
Difference in mitochondrial DNA (mtDNA) copy number between cases and controls.
See this image and copyright information in PMC

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