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Insulin resistance in HIV-infected youth is associated with decreased mitochondrial respiration
Jody K Takemoto1, Tracie L Miller, Jiajia Wang
1aDepartment of Pharmaceutical Sciences, Ben and Maytee Fisch College of Pharmacy, The University of Texas at Tyler, Tyler, Texas bDepartment of Pediatrics, University of Miami, Miller School of Medicine, Miami, Florida cCenter for Biostatistics in AIDS Research, Harvard T.H. Chan School of Public Health, Boston, Massachusetts dThe Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, California eTulane University School of Medicine, New Orleans, Louisiana fDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii, USA.
Insights
Perinatally HIV-infected youth with insulin resistance (IR) show reduced mitochondrial respiration. This suggests impaired cellular energy production may contribute to IR in this population.
Area of Science:
- Biochemistry
- Cellular Biology
- Pediatric Endocrinology
Background:
- Insulin resistance (IR) is a growing concern in perinatally HIV-infected youth.
- Mitochondrial dysfunction is implicated in metabolic disorders, but its role in HIV-associated IR is not well understood.
Purpose of the Study:
- To investigate the relationship between insulin resistance (IR) and mitochondrial respiration in perinatally HIV-infected youth.
- To determine if impaired mitochondrial function is associated with IR in this cohort.
Main Methods:
- A case-control study involving perinatally HIV-infected youth (Tanner stages 2-5) from the Pediatric HIV/AIDS Cohort Study.
- Insulin resistance defined by homeostatic model of assessment for IR (HOMA-IR) ≥ 4.0.
- Mitochondrial respiration assessed using a novel, high-throughput oximetry method in peripheral blood mononuclear cells.
Main Results:
- Youth with IR (IR+) exhibited significantly higher BMI and metabolic analytes (glucose, insulin, lipids, lactate/pyruvate) compared to those without IR (IR-).
- Mitochondrial respiration markers, including basal, ATP production, proton leak, maximal, and spare respiration capacity, were significantly lower in the IR+ group.
- Non-mitochondrial respiration did not differ between groups, and results remained consistent after age adjustment.
Conclusions:
- Perinatally HIV-infected youth with insulin resistance demonstrate diminished mitochondrial respiration.
- Disordered mitochondrial respiration may represent a key mechanistic pathway contributing to insulin resistance in HIV-infected youth.
Objective:
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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