HIV-1 protease inhibitors induce an increase of triglyceride level in HIV-infected men without modification of insulin sensitivity: A longitudinal study

Citation
Jm. Petit et al., HIV-1 protease inhibitors induce an increase of triglyceride level in HIV-infected men without modification of insulin sensitivity: A longitudinal study, HORMONE MET, 32(9), 2000, pp. 367-372
Citations number
32
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
HORMONE AND METABOLIC RESEARCH
ISSN journal
00185043 → ACNP
Volume
32
Issue
9
Year of publication
2000
Pages
367 - 372
Database
ISI
SICI code
0018-5043(200009)32:9<367:HPIIAI>2.0.ZU;2-1
Abstract
We investigated longitudinally the effect of protease inhibitors (PI) on in sulin sensitivity, glycemia, and serum lipids in HIV-infected patients. Nin ety-one consecutive patients treated with PI for at least 12 months were in cluded in this study. Easting glycemia, lipid profile, insulinemia, CD4 T l ymphocytes, and plasma HIV-1 RNA were performed at baseline and on PI thera py. Insulin sensitivity and insulin secretion were measured by the homeosta sis model assessment (HOMA MODEL) using the fasting glucose and insulin con centrations. Triglycerides (+ 0.34 mmo/l, SD = 1.07, p = 0.001) and cholest erol (+ 1.07 mmol/l, SD = 1.21, p = 0.001) significantly increased on PI th erapy. Fasting glycemia, insulin sensitivity, and insulin secretion were no t modified after PI therapy. PI therapy significantly increased body mass i ndex (0.35 kg/m(2), p < 0.05). Serum lipid changes correlated with changes in the CD4+ cell count. Lipodystrophy was observed in 40.6% of patients tre ated with PI. Our longitudinal study found that PI therapy had no major imp act on fasting glycemia, insulin sensitivity, and insulin secretion. These findings are not consistent with previous cross-sectional studies, which di d not include baseline measurements before PI initiation. However, we obser ved a similar profile of lipid changes induced by PI therapy. These results suggest that PI could be responsible for the development of hypertriglycer idemia by a mechanism independent of insulin resistance which remains to be elucidated.