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HIV-associated fat redistribution syndrome is associated with marked acceleration of lipid turnover.

Sekhar RV, White Jr AC, Jahoor F, Visnegarwala F, Reeds PJ, Balasubramanyam B; Conference on Retroviruses and Opportunistic Infections.

Program Abstr 8th Conf Retrovir Oppor Infect Conf Retrovir Oppor Infect 8th 2001 Chic Ill. 2001 Feb 4-8; 8: 243 (abstract no. 663).

Baylor Coll of Med, Houston, Texas.

Background: Initial descriptions of fat redistribution syndrome in HIV patients focused on clinical manifestations, incidence, and risk factors. Few data are available on how lipid metabolism is actually altered. Methods: To characterize lipid kinetics in HIV patients with fat redistribution syndrome, stable isotope studies of triglyceride kinetics were performed in 6 subjects with HIV (on HAART [5 PI, 1 NNRTI based], with central obesity and peripheral fat wasting) and in 6 HIV- negative age-, gender-, and BMI-matched controls. Studies were performed in the fasted and fed states and included: 1) measurement of body composition using deuterated water, 2) measurement of triglyceride absorption and disposal using oral 13C-tripalmitin, and 3) measurement of glycerol and palmitate turnover using intravenous 13C-palmitate and 2H5-glycerol. Results: When compared to normal controls, patients with HIV-associated fat redistribution syndrome demonstrated decreased total body fat (19.5 +/- 1.79% vs. 24.6 +/- 1.82% of body mass). This decrease in total body fat was associated with a marked increase in whole-body lipolytic rates [total lipolysis (1.02 +/- 0.15 vs. 0.62 +/- 0.07 mmol/kg fat/h, p < 0.03) and net lipolysis (0.73 +/- 0.07 vs. 0.42 +/- 0.03 mmol/kg fat/h, p < 0.002)], together with significantly increased free fatty acid oxidation (0.48 +/- 0.08 vs. 0.27 +/- 0.03 mmol/kg fat/h) and re-esterification in both the adipocytes (1.41 +/- 0.41 vs. 0.70 +/- 0.15 mmol/kg fat/h) and the liver (0.55 +/- 0.05 vs. 0.31 +/- 0.03 mmol/kg fat/h, p < 0.001). Concomitant with the increased lipid turnover, fasting concentrations of both chylomicrons and VLDL-triglycerides were strikingly elevated (chylomicrons 57.5 +/- 34.1 vs. 14.0 +/- 2.48 mg/dl; VLDL triglycerides 44.0 +/- 33.4 vs. 7.0 +/- 0 mg/dl). Conclusions: These studies suggest that severe dysregulation of lipid kinetics occurs in HIV-associated fat redistribution, resulting in increases in both whole-body lipolysis and re-esterification as well as decreased triglyceride clearance. Thus, the main alterations in lipid metabolism in HIV-associated fat redistribution syndrome are increased turnover (lipolysis, oxidation, and re-esterification) and decreased triglyceride clearance rather than simple fat deposition.

Publication Types:
  • Meeting Abstracts
Keywords:
  • AIDS Vaccines
  • Acquired Immunodeficiency Syndrome
  • Antiretroviral Therapy, Highly Active
  • Body Composition
  • Case-Control Studies
  • Endocrine System Diseases
  • Fats
  • HIV Infections
  • HIV Seropositivity
  • Humans
  • Lipids
  • Lipolysis
  • Syndrome
  • Triglycerides
  • tripalmitin
  • very low density lipoprotein triglyceride
Other ID:
  • GWAIDS0006951
UI: 102244447

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