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Antiretroviral Treatment Reduces Very-Low-Density Lipoprotein and Intermediate-Density Lipoprotein Apolipoprotein B Fractional Catabolic Rate in Human Immunodeficiency Virus-Infected Patients with Mild Dyslipidemia

Departments of HIV and Chemical Pathology (M.Sh., S.D., R.C., P.N.), University Hospitals Birmingham, Birmingham B29 6JF, United Kingdom; and Department of Diabetes and Endocrinology (M.St., F.S.-M., N.C.J., W.J., A.M.U.), St. Thomas’ Hospital, GKT School of Medicine, Kings College, London, SE1 7EH, United Kingdom

Address all correspondence and requests for reprints to: Margot Umpleby, Department of Diabetes and Endocrinology, 4th Floor, N Wing, St. Thomas Hospital, Lambeth Palace Road, London SE1 7EH, United Kingdom. E-mail: margot.umpleby{at}kcl.ac.uk.

The relationship between antiretroviral treatment of HIV infection, body fat distribution, insulin resistance, and very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) apolipoprotein-B (apoB) kinetics was investigated in 55 HIV-infected patients taking two nucleoside analogs plus either a protease inhibitor (n = 15) or a nonnucleoside reverse transcriptase inhibitor (n = 25), 15 antiretroviral therapy-naive patients, and 12 HIV-negative controls.

Compared with the controls, high-density lipoprotein cholesterol was reduced in all groups (P < 0.01). Plasma triglyceride was increased in patients taking protease inhibitors (P < 0.05). VLDL and IDL apoB fractional catabolic rate (FCR) was lower in all treatment groups (P < 0.05) compared with controls. Trunk fat, VLDL apoB absolute secretion rate, and insulin resistance were not different between groups. Peripheral fat was lower in the treated patients (P < 0.05) and correlated with duration of therapy (r = –0.55; P < 0.001). There was a positive correlation between peripheral fat and VLDL apoB FCR (P = 0.002) and IDL apoB FCR (P = 0.002) and a negative correlation with VLDL apoB pool size, VLDL cholesterol, and triglyceride (P < 0.03; P < 0.01; P < 0.002).

These results suggest that mild dyslipidemia resulting from antiretroviral therapy is caused by a decrease in VLDL and IDL apoB FCR, which is associated with a loss of peripheral fat.

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