Insulin resistance in HIV-infected youth is associated with decreased mitochondrial respiration
Takemoto, Jody K.
Miller, Tracie L.
Geffner, Mitchell E.
Van Dyke, Russell B.
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CitationTakemoto, Jody K., Tracie L. Miller, Jiajia Wang, Denise L. Jacobson, Mitchell E. Geffner, Russell B. Van Dyke, and Mariana Gerschenson. 2016. “Insulin resistance in HIV-infected youth is associated with decreased mitochondrial respiration.” AIDS (London, England) 31 (1): 15-23. doi:10.1097/QAD.0000000000001299. http://dx.doi.org/10.1097/QAD.0000000000001299.
AbstractObjective: To identify relationships between insulin resistance (IR) and mitochondrial respiration in perinatally HIV-infected youth. Design: Case–control study. Methods: Mitochondrial respiration was assessed in perinatally HIV-infected youth in Tanner stages 2–5, 25 youth with IR (IR+) and 50 without IR (IR−) who were enrolled in the Pediatric HIV/AIDS Cohort Study. IR was defined as a homeostatic model of assessment for IR value at least 4.0. A novel, high-throughput oximetry method was used to evaluate cellular respiration in peripheral blood mononuclear cells. Unadjusted and adjusted differences in mitochondrial respiration markers between IR+ and IR− were evaluated, as were correlations between mitochondrial respiration markers and biochemical measurements. Results: IR+ and IR− youth were similar on age, sex, and race/ethnicity. Mean age was 16.5 and 15.6 years in IR+ and IR−, respectively. The IR+ group had significantly higher mean BMI and metabolic analytes (fasting glucose, insulin, cholesterol, triglycerides, and venous lactate and pyruvate) compared with the IR−. Mitochondrial respiration markers were, on average, lower in the IR+ compared with IR−, including basal respiration (417.5 vs. 597.5 pmol, P = 0.074), ATP production (11 513 vs. 15 202 pmol, P = 0.078), proton leak (584.6 vs. 790.0 pmol, P = 0.033), maximal respiration (1815 vs. 2399 pmol, P = 0.025), and spare respiration capacity (1162 vs. 2017 pmol, P = 0.032). Nonmitochondrial respiration did not differ by IR status. The results did not change when adjusted for age. Conclusion: HIV-infected youth with IR have lower mitochondrial respiration markers when compared to youth without IR. Disordered mitochondrial respiration may be a potential mechanism for IR in this population.
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