7th Conference - Abstract 42

Mitochondrial Fat Oxidation Is Not Reduced in HIV-Associated Dyslipidaemia

J. F. MORLESE¹*, L. J. WARE², M. KRUGER², A. POZNIAK¹, B. GAZZARD¹, A. A. JACKSON², and S. A. WOOTTON². ¹St. Stephen's Ctr., Chelsea and Westminster Hosp., London; and ²Inst. of Human Nutrition, Univ. of Southampton, UK

Dyslipidaemia in HIV-seropositive patients treated with highly active antiretroviral therapy (HAART) has been well described. The mechanisms responsible are not known, but mitochondrial damage due to nucleoside analogues has been proposed. Such damage would be expected to decrease fat oxidation in patients treated with HAART. We measured fat oxidation using a stable isotopic tracer methodology in subjects with and without HAART-associated dyslipidaemia.
After an overnight fast, six HIV-seropositive men currently treated with a protease inhibitor (PI)-containing HAART (five on stavudine and one on zidovudine) with fasting triacylglycerols >9.5 mmol/L (LI) and seven HIV-seropositive men who had never taken PI-containing HAART (NLI) and with normal triacylglycerol concentrations were given a test meal and (1-¹³C)palmitic acid to measure in vivo lipid oxidation. Recovery of tracer in breath as (¹³CO₂) was determined hourly for 6-h after the meal. Data were compared with age-matched healthy male controls.

* Significantly different from controls (p<0.05, Kruskal-Wallis test).

Net lipid oxidation was significantly greater in the dyslipidaemia group compared with the control group. There was no difference in the recovery of tracer between the three groups. Thus, the absence of a decrease in the amount of lipid oxidised in the dyslipidaemia group indicates that nucleoside associated mitochondrial damage may not be the major pathogenic mechanism.

Key Words: dyslipidaemia, fat oxidation, mitochondria