美国围产期感染艾滋病毒的青少年线粒体相关指标和胰岛素抵抗的纵向变化。

IF 3.9 3区 生物学 Q2 CELL BIOLOGY
Greg S. Gojanovich , Wendy Yu , Zhongli J. Zhang , Denise L. Jacobson , Tzy-Jyun Yao , Jennifer Jao , Daniel E. Libutti , Mitchell E. Geffner , Mariana Gerschenson , for the Pediatric HIV/AIDS Cohort Study
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引用次数: 0

摘要

艾滋病毒感染及其治疗与线粒体功能障碍和新陈代谢失调有关。然而,围产期感染艾滋病病毒的青少年(YPHIV)的氧化磷酸化活性[复合体I(C1)和复合体IV(C4)]或静脉乳酸/丙酮酸比率(LPR)的纵向变化及其与胰岛素抵抗(IR)的关系仍不清楚。我们用两年时间测量了静脉 LPR、血细胞中 C1 和 C4 的活性以及胰岛素抵抗的稳态模型评估(HOMA-IR)。在 YPHIV 与围产期感染艾滋病毒但未感染的青少年之间,我们观察到线粒体相关指标和 IR 存在有限的纵向差异。各组之间在 C1、C4 或 HOMA-IR 方面没有系统性差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Longitudinal changes in mitochondrial-associated measures and insulin resistance in youth with perinatally-acquired HIV in the U.S

HIV infection and its treatment are associated with mitochondrial dysfunction and metabolic derangement. However, longitudinal changes in oxidative phosphorylation activities [Complex I (C1) and Complex IV (C4)], or venous lactate/pyruvate ratios (LPR), and their relationships with insulin resistance (IR), remain unclear in youth living with perinatally-acquired HIV (YPHIV). We measured venous LPR, C1, and C4 activities in blood cells and homeostatic model assessment for IR (HOMA-IR) over two years. Limited longitudinal differences in mitochondrial-related measures and IR were observed in YPHIV vs youth perinatally HIV-exposed but uninfected. There were no systematic differences in C1, C4, or HOMA-IR between the groups.

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来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
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