Metabolic Research Center

Medicine and, Australia

Metabolic Research Center

Medicine and, Australia
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Ng T.W.K.,Metabolic Research Center | Ng T.W.K.,Baker IDI Heart and Diabetes Institute | Ooi E.M.M.,Metabolic Research Center | Watts G.F.,Metabolic Research Center | And 4 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2014

Context: Statins are effective cholesterol-lowering agents that reduce cardiovascular disease risk but also have pleiotropic effects that may extend to other lipid classes.Objective: The purpose of this article was to investigate, in a post hoc analysis, the dose-dependent effects of rosuvastatin on plasma sphingolipids and phospholipids in men with the metabolic syndrome.Methods: Subjects (n = 12) were studied in a randomized, double-blind, triple-crossover trial of a 5-week treatment period with placebo or rosuvastatin (10 or 40 mg/day) with 2-week washouts between treatments. Plasma sphingolipid profiling was determined by liquid chromatography electrospray ionization-tandem mass spectrometry.Results: Rosuvastatin at 10 mg/d (R10) and 40 mg/d (R40) significantly (all P < .001 unless stated otherwise) lowered plasma cholesterol (-34% and -42% [% change with R10 and with R40, respectively]), low-density lipoprotein cholesterol (-49% and -57%) and triglyceride (-24%, P =.03 and -42%) concentrations. Compared with placebo, R10 and R40 significantly decreased the plasma levels of total sphingolipids including those of ceramide (-33%and -37%), sphingomyelin (-27% and-31%), monohexosylceramide (-40% and-47%), dihexosylceramide (-31% and-34%), and trihexosylceramide (-29% and-31%), and GM3 gangliosides (-29% and-26%), lysophosphatidylcholine (-32% and-37%), alkylphosphatidylcholine (-19% and-19%), phosphatidylcholine (-17% and-19%), alkenylphosphatidylcholine (plasmalogen) (-20% and-22%), alkylphosphatidylethanolamine (-20%, P-.008 and-24%, P =.02), alkenylphosphatidylethanolamine (plasmalogen) (-24%, P =.003 and-23%, P =.007), phosphatidylglycerol (-24%, P =.07,-31%, P =.046), and phosphatidylinositol (-34% and-40%). No significant changes were found with phosphatidylethanolamine and phosphatidylserine. Significant dose effects were found with the majority of the plasma sphingolipids, whereas only phosphatidylcholine, lysophosphatidylcholine, alkylphosphatidylcholine, alkenylphosphatidylcholine (plasmalogen), and phosphatidylinositol had significant dose effects. Similar changes were found with plasma sphingolipids when results were normalized to the total phosphatidylcholine concentration.Conclusions: Rosuvastatin dose-dependently lowers plasma sphingolipids and phospholipids, independent of low-density lipoprotein lowering, in men with the metabolic syndrome. Copyright © 2014 by the Endocrine Society.


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Ooi E.M.M.,Tufts University | Ooi E.M.M.,Metabolic Research Center | Ooi E.M.M.,University of Western Australia | Russell B.S.,University of Cincinnati | And 9 more authors.
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2012

Objective-: We investigated the impact of lipoprotein lipase (LPL) gene mutations on apolipoprotein B (apoB)-100 metabolism. Methods and Results-: We studied 3 subjects with familial LPL deficiency; 14 subjects heterozygous for the LPL gene mutations Gly188Glu, Trp64Stop, and Ile194Thr; and 10 control subjects. Very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL)-apoB-100 kinetics were determined in the fed state using stable isotope methods and compartmental modeling. Compared with controls, familial LPL deficiency had markedly elevated plasma triglycerides and lower VLDL-apoB-100 fractional catabolic rate (FCR), IDL-apoB-100 FCR, VLDL-to-IDL conversion, and VLDL-apoB-100 production rate (P<0.01). Compared with controls, Gly188Glu had higher plasma triglyceride and VLDL-and IDL-apoB-100 concentrations and lower VLDL-and IDL-apoB-100 FCR (P<0.05). Plasma triglycerides were not different, but IDL-apoB-100 concentration and production rate and VLDL-to-IDL conversion were lower in Trp64Stop compared with controls (P<0.05). No differences between controls and Ile194Thr were observed. Conclusion-: Our results confirm that hypertriglyceridemia is a key feature of familial LPL deficiency. This is due to impaired VLDL-and IDL-apoB-100 catabolism and VLDL-to-IDL conversion. Single-allele mutations of the LPL gene result in modest to elevated plasma triglycerides. The changes in plasma triglycerides and apoB-100 kinetics are attributable to the effects of the LPL genotype. © 2012 American Heart Association, Inc.

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