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  • Title: Dietary intake in HIV-infected men with lipodystrophy: relationships with body composition, visceral fat, lipid, glucose and adipokine metabolism.
    Author: Samaras K, Wand H, Law M, Emery S, Cooper DA, Carr A.
    Journal: Curr HIV Res; 2009 Jul; 7(4):454-61. PubMed ID: 19601783.
    Abstract:
    Highly active antiretroviral therapy (HAART) for HIV-infection is associated with lipodystrophy, insulin resistance, increased prevalence of disturbances in glucose tolerance and diabetes, hyperlipidemia and increased cardiovascular risk. Whether dietary intake influences total body fat, visceral fat, insulin resistance, glucose metabolism, lipid metabolism and circulating inflammatory markers in HIV-infected subjects with lipodystrophy is unclear and the focus of this report. We examined the dietary intake of 106 male HIV-infected HAART-recipients with lipodystrophy, enrolled in a study of the effects of rosiglitazone. All subjects had normal glucose tolerance. Dietary intakes were determined at study entry using Food Frequency Questionnaires and examined cross-sectionally against body composition by dual-energy Xray absorptiometry, visceral obesity by computed tomography, fasting glucose, insulin, lipids, adiponectin, leptin, insulin resistance (by HOMA). Energy underreporters were identified and excluded. After exclusion of underreporters (n = 22) we found no relationships between diet composition (% dietary fat, %carbohydrate) and BMI, %body fat and visceral adiposity (p>0.3). Only modest relationships were found between BMI and fat subtypes: polyunsaturated fats (g/day) (r = 0.14, p = 0.007), monounsaturated fat (g/d) (r = 0.06, p = 0.001), saturated fat (g/d) (r = 0.02, p<0.0001). Only saturated fat related to % total body fat (g/d: r = 0.08, p<0.0001, %energy intake: r = 0.16, p<0.0001). No nutrient related to visceral adiposity by CT. Dietary fat intake (expressed as a % of energy intake) was not related to total cholesterol, HDL cholesterol, triglycerides, fasting insulin, glucose, leptin, adiponectin or HOMA-IR (p>0.4). Fat subtype did not relate to fasting insulin, insulin resistance, total cholesterol, HDL, triglycerides, glucose, adiponectin. In conclusion, there are weak relationships between saturated fat intake and adiposity in HIV-infected subjects with lipodystrophy, using gold standard measures of body fat. There were no relationships between nutrient intake and visceral adiposity, any measure of glucose metabolism, insulin resistance or adipokines. Only interventional, prospective studies will determine whether any nutritional strategy can assist in ameliorating the metabolic complications associated with HIV lipodystrophy.
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