Mitochondrial damage in adipose tissue of untreated HIV-infected patients

Garrabou, Glòria; López, Sònia; Morén, Constanza; Martínez, Estebán; Fontdevila, Joan; Cardellach, Francesc; Gatell, Josep M.; Miró, Òscar

doi:10.1097/qad.0b013e3283423219

Cited by 51 publications

(36 citation statements)

References 32 publications

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“…Detections such as these provide metabolic information linked to patient health and could serve as a guide for the implementation of corrective therapy prior to the development of clinical symptoms. Key metabolic defects caused by HIV also include its ability to induce malnutrition, 18 disrupt the functioning of the mitochondria, 19,20 induce changes in body composition, fat distribution, changes in lipid, carbohydrate and protein metabolism. 14,16 Changes in body composition are largely attributed to an increase in the catabolic state of the host.…”

Section: Hiv-and Haart-associated Metabolic Changes (As Detected By Cmentioning

confidence: 99%

Metabonomic analysis of HIV-infected biofluids

2013

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Monitoring the progression of HIV infection to full-blown acquired immune deficiency syndrome (AIDS) and assessing responses to treatment will benefit greatly from the identification of novel biological markers especially since existing clinical indicators of disease are not infallible. Nuclear magnetic resonance spectroscopy (NMR) and mass spectrometry (MS) are powerful methodologies used in metabonomic analyses for an approximation of HIV-induced changes to the phenotype of an infected individual. Although early in its application to HIV/AIDS, (biofluid) metabonomics has already identified metabolic pathways influenced by both HIV and/or its treatment. To date, biofluid NMR and MS data show that the virus and highly active antiretroviral treatment (HAART) mainly influence carbohydrate and lipid metabolism, suggesting that infected individuals are susceptible to very specific metabolic complications. A number of well-defined biofluid metabonomic studies clearly distinguished HIV negative, positive and treatment experienced patient profiles from one another. While many of the virus or treatment affected metabolites have been identified, the metabonomics measurements were mostly qualitative. The identities of the molecules were not always validated neither were the statistical models used to distinguish between groups. Assigning particular metabolic changes to specific drug regimens using metabonomics also remains to be done. Studies exist where identified metabolites have been linked to various disease states suggesting great potential for the use of metabonomics in disease prognostics. This review therefore examines the field of metabonomics in the context of HIV/AIDS, comments on metabolites routinely detected as being affected by the pathogen or treatment, explains what existing data suggest and makes recommendations on future research.

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Section: Hiv-and Haart-associated Metabolic Changes (As Detected By Cmentioning

confidence: 99%

Metabonomic analysis of HIV-infected biofluids

2013

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“…73 More recently, Garrabou et al found significant mtDNA depletion and reduced mitochondrial oxidative function in adipocytes of HIVinfected ART-naïve individuals compared to uninfected controls. 74 The value of tissue mtDNA measurement has been questioned by Kim et al, 75 who confirmed findings of depleted mtDNA in adipose tissue of lipoatrophic HAART-treated patients, but found no decrease in mtDNA-dependent mitochondrial function and an actual compensatory increase in nuclear-driven mitochondrial biogenesis, suggesting that mtDNA depletion was not a good marker for mitochondrial function. In another cross-sectional study by Magaard et al, 34 mitochondrial DNA was lower in muscle biopsies from 24 patients with HIV on HAART than 10 ART-naïve HIV patients, but both groups demonstrated decreased PBL mtDNA compared to 11 healthy controls.…”

Section: Research History Of Nucleoside Reverse Transcriptase Inhibitmentioning

confidence: 81%

Mitochondrial dysfunction and human immunodeficiency virus infection

Watt

2011

Journal of Endocrinology, Metabolism and Diabetes of South Afri

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Human immunodeficiency virus (HIV) infection and the pharmacological treatment thereof have both been shown to affect mitochondrial function in a number of tissues, and each may cause specific organ pathology through specific mitochondrial pathways. HIV has been shown to kill various tissue cells by activation of mitochondrial apoptosis. Nucleoside analogues, used extensively to treat HIV infection, are known to influence a number of steps affecting mitochondrial DNA integrity. This review describes the basic physiology, pharmacology and pathophysiology of HIV infection and the nucleoside analogues regarding mitochondrial function and discusses the progress made in this field with respect to the measurement of these effects and the prediction of potential drug toxicity.Peer reviewed.

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“…In part this is because these drugs are often prescribed as one component of highly active antiretroviral cocktails of drugs, which also may be increasing mutational load. In addition, HIV infection itself can damage mitochondria [35,36] For both HepG2 and CCD-1112Sk cells, the frequency of mutations was higher for the AZT treated samples. 11A 24A 64T 80A 128C -382A -396C 181A 198G 295A 320A -345A 369A -382C -388A 369A -388A 382A -396C 388A CO 2 7830G 7918T -7966T -8117T 7982C 7982C-8019T 7985T 7986G ND1 3573A -3632A -3670A 3905G 3993C…”

Section: Discussionmentioning

confidence: 99%