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Articles in PresS, published online ahead of print October 8, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00391.2001
Submitted on August 29, 2001
Accepted on September 17, 2002
1 Division of Infectious Diseases, Division of Diagnostic Radiology, Division of Nuclear Medicine, San Raffaele Scientific Institute, Milano, Italy; International Center for the Assessment of the Nutritional Status, Universita' degli Studi di Milano, Milano, Italy
2 Division of Infectious Diseases, Division of Diagnostic Radiology, Division of Nuclear Medicine, San Raffaele Scientific Institute, Milano, Italy
3 International Center for the Assessment of the Nutritional Status, Universita' degli Studi di Milano, Milano, Italy
* To whom correspondence should be addressed. E-mail: luzi.livio{at}hsr.it.
Antiretroviral therapy in HIV-positive patients can induce a lipodystrophy syndrome of peripheral fat wasting and central adiposity, dyslipidemia and insulin resistance. To test whether in this syndrome insulin resistance is associated with abnormal muscle handling of fatty acids 12 HIV-1 patients (8F/4M, age=26±2 ys, HIV duration=8±1 ys, BMI=22.0±1.0 kg/m2, on protease inhibitors and nucleoside-analogue reverse-transcriptase inhibitors) and 12 healthy subjects matched for anthropomorphic parameters, were studied with 1) dual energy X-ray absorption to assess body fat content, 2) localized 1H NMR spectroscopy of the calf muscles to assess intramyocellular lipid content (IMCL), 3) indirect calorimetry to assess basal metabolic rate and whole body glucose/lipid oxidation. HIV-1 patients had a total body fat content similar to that of controls (22±1 vs 23±2%; p=0.56), with a topographic fat re-distribution characterized by reduced fat content in the legs (18±2 vs 32±3%; p<0.01) and increased fat content in the trunk (25±2 vs 19±2%; p=0.03). In HIV positive patients fasting plasma glucose was similar to normals, but fasting plasma insulin (p=0.05) and C-peptide (p<0.01) concentrations were double than in normals, and insulin sensitivity, based on the logarithm and the reciprocal of the insulin-glucose product (QUICKI), was markedly impaired (0.341±0.011 vs 0.376±0.007; P=0.012). HIV-positive patients also had increased total plasma cholesterol (216±20 vs 174±9 mg/dl; p=0.05) and triglyceride (298±96 vs 87±11 mg/dl; p=0.03) concentrations. Muscular triglyceride content assessed by means of 1H NMR spectroscopy was higher in HIV patients in soleus (92±12 vs 42±5 AU; p<0.01) and tibialis anterior (26±6 vs 11±3 AU; p=0.04) muscles; in a stepwise regression analysis it was strongly associated with QUICKY (R2 = 0.27; P <0.0093). Even if the basal metabolic rate was comparable to that of normals, post-absorptive lipid oxidation was significantly impaired (0.30±0.07 vs 0.88±0.09 mg/[kg.min]; p<0.01). In conclusion, lipodystrophy in HIV-1 patients in antiretroviral treatment is associated with intramuscular fat accumulation, which may mediate the development of the insulin resistance syndrome.
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