Sixth International Congress Drug Therapy in HIV Infection 17-21 November, 2002 Glasgow, UK

HIV infection itself induces multiple metabolic abnormalities: e.g. increases in resting energy expenditure and lipolysis, while glucose metabolism is characterized by increased insulin sensitivity. Combination antiretroviral therapy including protease inhibitors for the treatment of HIV-1-infected patients has been associated with the development of a fat redistribution syndrome, which may include both central fat accumulation and peripheral fat wasting. HIV-1- positive patients with lipodystrophy and concomitant HAART therapy have major disturbances in glucose metabolism: e.g. increased rates of postabsorptive glucose production; in addition, both the ability of insulin to suppress endogenous glucose production and to stimulate peripheral glucose uptake and its metabolic pathways is reduced. Lipolysis is not different from the values obtained in patients with no antiretroviral therapy. However, insulin’s ability to suppress lipolysis is diminished. These combined data indicate severe resistance with respect to multiple effects of insulin. Plasma norepinephrine concentrations are increased in patients with lipodystrophy, while plasma adrenaline is normal, indicating increased sympathetic activity. The fasting REE is lower and remains lower during epinephrine infusion in patients with lipodystrophy. This suggests that HAART-associated lipodystrophy, as a result of concomitant sympathetic stimulation of adipose tissue, has only minor effects on changes in lipolysis induced by HIV infection itself, but normalises REE. The absence of an increase in REE despite increased sympathetic activity could be explained by selective sympathetic stimulation of the adipose tissue, as this organ contributes little to basal REE. These data suggest that the HAART-induced fat redistribution could be due to selective sympathetic stimulation of certain fat depots and selective parasympathetic stimulation of other fat depots. The common denominator could be selective damage by HAART of autonomic nuclei projecting to these fat depots.

Presenting author: HP Sauerwein

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1 Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, Netherlands

2002-11-17
PL9-1

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