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Short communication: The relationship between mitochondrial dysfunction and insulin resistance in HIV-infected

Tanvi S Sharma1, Denise L Jacobson, Lynn Anderson

  • 1Division of Infectious Diseases, Boston Children’s Hospital, Boston, Massachusetts 02115, USA. tanvi.sharma@childrens.harvard.edu

AIDS Research and Human Retroviruses
|June 8, 2013
PubMed

Insights

Mitochondrial dysfunction may contribute to insulin resistance in children with HIV on long-term antiretroviral therapy. Lower mitochondrial DNA copies and impaired enzyme activity were observed in children with insulin resistance.

Area of Science:

  • Pediatric Endocrinology
  • Infectious Diseases
  • Mitochondrial Medicine

Background:

  • HIV infection and long-term antiretroviral therapy (ART) are associated with metabolic complications.
  • Mitochondrial dysfunction is a potential mechanism underlying metabolic abnormalities.

Purpose of the Study:

  • To investigate the association between mitochondrial abnormalities and insulin resistance in HIV-infected children.
  • To compare mitochondrial DNA (mtDNA) levels and specific enzyme activities between HIV-infected children with and without insulin resistance.

Main Methods:

  • A matched case-control study design was employed.
  • 21 HIV-infected children with insulin resistance (cases) were compared to 21 HIV-infected children without insulin resistance (controls).
  • Mitochondrial DNA copies/cell and activities of NADH dehydrogenase (C1) and cytochrome c oxidase (C4) enzymes in peripheral blood mononuclear cells were assessed.

Main Results:

  • Mitochondrial DNA copies/cell tended to be lower in cases (children with insulin resistance).
  • Fasting serum glucose levels showed a significant inverse correlation with C1 enzyme activity, particularly pronounced in cases.
  • These findings suggest a link between mitochondrial dysfunction and insulin resistance in this cohort.

Conclusions:

  • Mitochondrial abnormalities may play a role in the development of insulin resistance in HIV-infected children undergoing long-term ART.
  • Further pediatric studies are warranted to elucidate the specific roles of HIV infection and antiretroviral therapies in causing mitochondrial dysfunction and subsequent metabolic complications.

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