Severely dysregulated disposal of postprandial triacylglycerols exacerbates hypertriacylglycerolemia in HIV lipodystrophy syndrome

Background: The pathogenesis of hypertriacylglycerolemia, a characteristic feature of HIV lipodystrophy syndrome (HLS), is incompletely understood. One mechanism is accelerated lipolysis in the fasted state, but the severity of the hypertriacylglycerolemia suggests that additional underlying abnorma...

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Published in:	The American journal of clinical nutrition Vol. 81; no. 6; pp. 1405 - 1410
Main Authors:	Sekhar, R.V, Jahoor, F, Pownall, H.J, Rehman, K, Gaubatz, J, Iyer, D, Balasubramanyam, A
Format:	Journal Article
Language:	English
Published:	Bethesda, MD American Society for Clinical Nutrition 01-06-2005 American Society for Clinical Nutrition, Inc
Subjects:	acquired immunodeficiency syndrome Antiretroviral Therapy, Highly Active - adverse effects Area Under Curve Biological and medical sciences Carbon Dioxide - analysis Carbon Dioxide - metabolism Carbon Isotopes Case-Control Studies cholesteryl esters Chromatography, Thin Layer Chylomicrons - chemistry Diet diet-related diseases dietary fat Dietary Fats - administration & dosage Dietary Fats - pharmacokinetics enzyme activity Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology HIV HIV Infections - complications HIV Infections - drug therapy HIV-Associated Lipodystrophy Syndrome - etiology HIV-Associated Lipodystrophy Syndrome - metabolism Human immunodeficiency virus Humans hyperlipidemia hypertriglyceridemia Hypertriglyceridemia - etiology Hypertriglyceridemia - metabolism insulin resistance Lipid Metabolism Lipids Lipolysis lipoprotein lipase Male Medical disorders Oxidation Oxidation-Reduction pathogenesis Postprandial Period postprandial state Triglycerides - administration & dosage Triglycerides - metabolism Triglycerides - pharmacokinetics Vertebrates: anatomy and physiology, studies on body, several organs or systems Viral Load Human Skin disease Enzyme Postprandial fat oxidation Esterases Lipoprotein lipase Lipolysis Carboxylic ester hydrolases Ester Triacylglycerol Fat Hydrolases Lipodystrophy Oxidation Adipose tissue disorders cholesteryl ester
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Summary:	Background: The pathogenesis of hypertriacylglycerolemia, a characteristic feature of HIV lipodystrophy syndrome (HLS), is incompletely understood. One mechanism is accelerated lipolysis in the fasted state, but the severity of the hypertriacylglycerolemia suggests that additional underlying abnormalities may exist in the disposal of dietary fat. Objective: Our objective was to investigate abnormalities in dietary fat disposal in the pathogenesis of hypertriacylglycerolemia in HLS. Design: We studied 6 nondiabetic men with HLS and 6 men without HIV matched for age and body mass index as control subjects for 8 h after consumption of an isocaloric meal containing 2 g labeled [13C3]tripalmitin. Chylomicron-triacylglycerol disposal was estimated from labeled [13C1]palmitate in the plasma chylomicron fraction, and [13C1]palmitate oxidation was estimated from the 13CO2 enrichment in the breath and CO2 production, over 8 h after the meal. Results: HLS patients had significantly elevated concentrations of fasting plasma triacylglycerols in both chylomicron (average + SE: 100.3 +/- 49.5 compared with 29.2 +/- 2.2 mg/dL; P < 0.01) and VLDL (82.4 +/- 39.0 compared with 10.8 +/- 2.8 mg/dL; P < 0.01) fractions. Chylomicron-triacylglycerol-derived [13C1]palmitate disposal was markedly lower in the HLS patients (3.09 +/- 0.41 compared with 6.42 +/- 0.18 mmol [13C1]palmitate/8 h; P < 0.001) in the 8-h postmeal period. Further, HLS patients had lowered storage of chylomicron-triacylglycerols (0.74 +/- 0.38 compared with 5.05 +/- 0.16 mmol; P < 0.0001) and elevated plasma [13C1]palmitate concentrations (2.01 +/- 0.27 compared with 1.18 +/- 0.16 mmol; P < 0.05) 8 h after the meal. Conclusions: Patients with HLS have key defects that markedly impair postprandial disposal and storage of chylomicron-triacylglycerols. These defects contribute significantly to hypertriacylglycerolemia in HLS.
Bibliography:	http://hdl.handle.net/10113/1999 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0002-9165 1938-3207
DOI:	10.1093/ajcn/81.6.1405