Horm Metab Res 2009; 41(11): 840-845
DOI: 10.1055/s-0029-1225625
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Effect of L-Acetylcarnitine on Body Composition in HIV-related Lipodystrophy

S. Benedini1 , 2 , G. Perseghin1 , 2 , 3 , I. Terruzzi1 , P. Scifo3 , 4 , P. L. Invernizzi2 , A. Del Maschio3 , 5 , A. Lazzarin6 , L. Luzi1 , 2 , 3
  • 1Metabolism and Nutrition Unit, San Raffaele Scientific Institute, via Olgettina, Milan, Italy
  • 2Department of Sport Sciences, Nutrition and Health, Faculty of Exercise Sciences, Universita’ degli Studi di Milano, Milan, Italy
  • 3Clinical Spectroscopy, San Raffaele Scientific Institute, via Olgettina, Milan, Italy
  • 4Nuclear Medicine, San Raffaele Scientific Institute, via Olgettina, Milan, Italy
  • 5Diagnostic Radiology, San Raffaele Scientific Institute, via Olgettina, Milan, Italy
  • 6Divisions of Infectious Diseases, San Raffaele Scientific Institute, via Olgettina, Milan, Italy
Further Information

Publication History

received 17.02.2009

accepted 02.06.2009

Publication Date:
13 July 2009 (online)


This study examined the impact of L-acetylcarnitine treatment on metabolic parameters and body composition in patients with lipodystrophy syndrome secondary to antiretroviral treatment in human immunodeficiency virus (HIV) infection. A total of 9 HIV-1 infected patients with lipodystrophy syndrome (4F/5M, age 41±5 years, HIV duration 8±2 years, BMI 23.7±3.4 kg/m2, on protease inhibitors and nucleoside analogue Reverse Transcriptase inhibitors) were evaluated before and after 8 months of therapy with L-acetylcarnitine (2 g/die) and 9 matched healthy subjects served as control subjects. In all patients fasting plasma glucose, insulin concentrations (for evaluation of surrogate indexes of insulin sensitivity), lipid profile, lipid oxidation (by indirect calorimetry), body composition (by DEXA), and intramyocellular triglyceride (IMCL) content of the calf muscles (by 1 H NMR spectroscopy) were assessed. After this therapy, in HIV-1 patients, the IMCL content of the soleus had significantly decreased (p=0.03). Plasma FFAs (0.79±0.31 to 0.64±0.25; p<0.05) and Respiratory Quotient (0.83±0.18 to 0.72±0.16; p<0.03) also decreased. Insulin sensitivity was significantly lower prior (HOMA-IS 0.56±0.30) and nonstatistically different than controls after therapy (0.72±0.49 vs. 0.78±0.42) whilst the percentage of fat in the legs increased (p=0.05). Eight months of L-acetylcarnitine treatment increased lipid oxidation, decreased intramyocellular triglyceride content, and induced a more physiological distribution of fat deposits.



L. Luzi, MD 

Head, Clinical Research Unit II

Laboratory of Amino Acids and Stable Isotopes

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