Perturbations of glucose metabolism associated with HIV infection in human intestinal epithelial cells

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Abstract
Objective: To analyse the effect of HIV-1 infection on the glucose metabolism of human intestinal epithelial cells. Methods: HT-29 cells were infected with HIV-1NDK and studied 3 weeks (acutely infected cells) or 9 months (chronically infected cells) post-infection. Perchloric acid extracts were analysed by high-resolution 1H, 31P and 13C nuclear magnetic resonance spectroscopy. Metabolite concentrations and specific 13C enrichments were quantified for chronically infected, acutely infected and control cells grown in Dulbecco's modified Eagle's medium containing natural-abundance or 1-13C-enriched glucose to determine significant differences between infected and non-infected cells. Results: Chronically HIV-infected cells showed alterations in glycerol-3-phosphate (+40%), fructose-1,6-diphosphate (−66%), uridine diphosphate glucuronic acid (−33%), lactate (+75%) and [1-13C]glucose (+181%) levels, and in specific lactate 3-13C enrichment (+19%) when compared with controls. Acutely infected cells exhibited decreased fructose-1,6-diphosphate (−58%) and increased nicotinamide adenine dinucleotide (+33%) levels relative to controls. Conclusion: HIV-1 infection results in a disturbance of glycolytic and oxidative activities in human intestinal epithelial cells. This finding supports the concept that HIV-1 may directly impair some metabolic functions of the intestinal epithelium, and that it can be considered a potential aetiological agent for HIV-associated enteropathy.