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16. Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin1[S]

Author

Thongtang, Nuntakorn, Diffenderfer, Margaret R., Ooi, Esther M. M., Barrett, P. Hugh R., Turner, Scott M., Le, Ngoc-Anh, Brown, W. Virgil, and Schaefer, Ernst J.

Subjects
Male, Proteomics, Hyperlipidemia, Familial Combined, nutritional and metabolic diseases, Humans, lipids (amino acids, peptides, and proteins), Female, Cholesterol, LDL, Middle Aged, Particle Size, Rosuvastatin Calcium, Research Articles
Abstract

Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL.

Published
2017

23. Elevated Remnant Cholesterol in 25-Hydroxyvitamin D Deficiency in the General Population:Mendelian Randomization Study

Author

Ooi, Esther M, Afzal, Shoaib, Nordestgaard, Børge G, Ooi, Esther M, Afzal, Shoaib, and Nordestgaard, Børge G

Abstract

BACKGROUND: Low plasma 25-hydroxyvitamin D [25(OH)D] levels are associated with high cardiovascular risk. This may be because that low 25(OH)D levels are associated with high levels of atherogenic lipoproteins, but whether these 2 risk factors are genetically associated is unknown. We tested this hypothesis.METHODS AND RESULTS: Using a Mendelian randomization approach, potential genetic associations between plasma levels of atherogenic lipoproteins and 25(OH)D were examined in ≤85,868 white, Danish individuals in whom we genotyped for variants affecting plasma levels of 25(OH)D, nonfasting remnant cholesterol, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol. Lipoprotein levels were measured in all and 25(OH)D levels in 31,435. A doubling in nonfasting remnant cholesterol levels was observationally and genetically associated with -6.0%(95% confidence interval [CI], -6.5% to -5.5%) and -8.9% (95% CI, -15% to -2.3%) lower plasma 25(OH)D levels. For low-density lipoprotein-cholesterol levels, corresponding values were -4.6% (95% CI, -5.4% to -3.7%) observationally and -11% (95% CI, -29% to +6.9%) genetically. In contrast, a halving in high-density lipoprotein-cholesterol levels was observationally associated with -1.5% (95% CI, -2.2% to -0.7%) lower but genetically associated with +20% (95% CI, +7.4% to +34%) higher plasma 25(OH)D levels. Plasma levels of lipoprotein(a) and 25(OH)D did not associate. Finally, low 25(OH)D levels did not associate genetically with levels of remnant and low-density lipoprotein-cholesterol.CONCLUSIONS: Genetically elevated nonfasting remnant cholesterol is associated with low 25(OH)D levels, whereas genetically reduced high-density lipoprotein-cholesterol is not associated with low 25(OH)D levels. These findings suggest that low 25(OH)D levels observationally is simply a marker for elevated atherogenic lipoproteins and question a role for vitamin D supplementation in the prevention of cardiovas

Published
2014

26. Association of apolipoprotein M with high-density lipoprotein kinetics in overweight-obese men

Author

Ooi, Esther M M, Watts, Gerald F, Chan, Dick C, Nielsen, Lars B, Plomgaard, Peter, Dahlbäck, Bjorn, Barrett, P Hugh R, Ooi, Esther M M, Watts, Gerald F, Chan, Dick C, Nielsen, Lars B, Plomgaard, Peter, Dahlbäck, Bjorn, and Barrett, P Hugh R

Abstract

Udgivelsesdato: 2010-May, OBJECTIVE: The aim of this study was to investigate associations between plasma apoM concentration and HDL apoA-I and apoA-II kinetics in 60 overweight-obese, insulin resistant men. METHODS: Plasma apoM concentration was determined using a sandwich ELISA with two monoclonal antibodies (CV<5%). The kinetics of HDL apoA-I and apoA-II were measured using intravenous administration of D(3)-leucine, gas chromatography-mass spectrometry and multi-compartmental modeling. RESULTS: Plasma apoM was inversely associated with body mass index and positively associated with plasma total cholesterol, LDL cholesterol and HDL cholesterol (p<0.05). There were no associations between plasma apoM and plasma triglyceride, NEFA, insulin, glucose, HOMA score or adiponectin concentrations. Plasma apoM was positively associated with both apoA-I and apoA-II concentrations (r=0.406, p<0.01 and r=0.510, p<0.01, respectively) and negatively associated with HDL apoA-I and apoA-II fractional catabolic rate (FCR) (r=-0.291, p=0.03 and r=-0.291, p=0.026, respectively). No significant associations were observed between plasma apoM and HDL apoA-I and apoA-II production rate. In multivariate regression models, both plasma apoM and triglycerides were significant, independent predictors of HDL apoA-I FCR (adjusted R(2)=16%, p<0.01) and HDL apoA-II FCR (adjusted R(2)=14%, p<0.01). CONCLUSION: ApoM may be a significant, independent predictor of HDL apoA-I and apoA-II catabolism in overweight-obese, insulin resistant men.

Published
2009

29. Regulation of lipoprotein transport in the metabolic syndrome : impact of statin therapy

Author

Ooi, Esther M. M., University of Western Australia.School of Medicine and Pharmacology, Ooi, Esther M. M., and University of Western Australia.School of Medicine and Pharmacology

Abstract

[Truncated abstract] The metabolic syndrome is characterized by cardiovascular risk factors including dyslipidemia, insulin resistance, visceral obesity, hypertension and diabetes. The dyslipidemia of the metabolic syndrome includes elevated plasma triglyceride and apolipoprotein (apo) B levels, accumulation of small, dense low-density lipoprotein (LDL) particles and low high-density lipoprotein (HDL) cholesterol concentration. However, the precise mechanisms for this dyslipoproteinemia, specifically low plasma HDL cholesterol, are not well understood. This thesis therefore, focuses on HDL, its structure, function and metabolism. However, lipoprotein metabolism is a complex interconnected system, which includes forward and reverse cholesterol transport pathways. Hence, this thesis also examines and discusses the metabolism of apoB-containing lipoproteins. This thesis tests the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that lipid regulating therapies can improve these kinetic abnormalities. The aims were first, to compare and establish the clinical, metabolic and kinetic differences between metabolic syndrome and lean subjects; and second, to determine the regulatory effects of statin therapy, specifically, rosuvastatin on lipoprotein transport in the metabolic syndrome. Five observation statements were derived from the general hypothesis and examined in the studies described below. The findings are presented separately as a series of original publications. Study 1 Twelve men with the metabolic syndrome and ten lean men were studied in a case-control setting. ... These findings explain the HDL raising effects of rosuvastatin in the metabolic syndrome. Collectively, these studies suggest that the dyslipidemia of the metabolic syndrome results from increased production rates of VLDL and LDL particles, reduced fractional catabolic rates of these lipoproteins, together with accelerated catabolism of HDL particles. Treatmen, Thesis (Ph.D.)--University of Western Australia, 2007

Published
2007

39. Effect of Ezetimibe on Hepatic Fat, Inflammatory Markers, and Apolipoprotein B-100 Kinetics in Insulin-Resistant Obese Subjects on a Weight Loss Diet.

Author

Chan, Dick C., Watts, Gerald F., Gan, Seng Khee, Ooi, Esther M. M., and Barrett, P. Hugh R.

Subjects
FATTY liver, INFLAMMATION, WEIGHT loss, EZETIMIBE, FAT cells
Abstract

OBJECTIVE -- Nonalcoholic fatty liver disease is highly prevalent in obese and type 2 diabetic individuals and is strongly associated with dyslipidemia and inflammation. Weight loss and/or pharmacotherapy are commonly used to correct these abnormalities. RESEARCH DESIGN AND METHODS -- We performed a 16-week intervention trial of a hypocaloric, low-fat diet plus 10 mg/day ezetimibe (n = 15) versus a hypocaloric, low-fat diet alone (n = 10) on intrahepatic triglyceride (IHTG) content, plasma high sensitivity-C-reactive protein (hs-CRP), adipocytokines, and fetuin-A concentrations and apolipoprotein (apo)B-100 kinetics in obese subjects. ApoB-100 metabolism was assessed using stable isotope tracer kinetics and compartmental modeling; liver and abdominal fat contents were determined by magnetic resonance techniques. RESULTS -- Both weight loss and ezetimibe plus weight loss significantly (all P < 0.05) reduced body weight, visceral and subcutaneous adipose tissues, insulin resistance and plasma triglycerides, VLDL-apoB-100, apoC-III, fetuin-A, and retinol-binding protein-4 and increased plasma adiponectin concentrations. Compared with weight loss alone, ezetimibe plus weight loss significantly (all P < 0.05) decreased IHTG content (-18%), plasma hs-CRP (-53%), interleukin-6 (-24%), LDL cholesterol (-18%), campesterol (-59%), and apoB-100 (-14%) levels, with a significant increase in plasma lathosterol concentrations (+ 43 %). The LDL-apoB-100 concentration also significantly fell with ezetimibe plus weight loss (-12 %), chiefly owing to an increase in the corresponding fractional catabolic rate (+29%). The VLDL-apoB-100 secretion rate fell with both interventions, with no significant independent effect of ezetimibe. CONCLUSIONS -- Addition of ezetimibe to a moderate weight loss diet in obese subjects can significantly improve hepatic steatosis, inflammation, and LDL-apoB-100 metabolism. [ABSTRACT FROM AUTHOR]

Published
2010
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41. Dose-Dependent Effect of Rosuvastatin on VLDL-Apolipoprotein C-III Kinetics in the Metabolic Syndrome.

Author

Ooi, Esther M. M., Watts, Gerald F., Chan, Dick C., Chen, Meifania M., Nestel, Paul J., Sviridov, Dmitri, and Barrett, P. Hugh R.

Subjects
*DRUG efficacy, *STATINS (Cardiovascular agents), *APOLIPOPROTEINS, *PROTEIN metabolism, *METABOLIC syndrome, *PLACEBOS
Abstract

OBJECTIVE -- Dysregulated apolipoprotein (apo)C-III metabolism may account for hypertriglyceridemia and increased cardiovascular risk in the metabolic syndrome. This study investigated the dose-dependent effect of rosuvastatin on VLDL apoC-III transport in men with the metabolic syndrome. RESEARCH DESIGN AND METHODS -- Twelve men with the metabolic syndrome were studied in a randomized double-blind crossover trial of 5-week intervention periods with placebo, 10 mg rosuvastatin, or 40 mg rosuvastatin, with 2-week placebo washouts between each period. VLDL apoC-III kinetics were examined using a stable isotope method and compartmental modeling at the end of each intervention period. RESULTS -- Compared with placebo, there was a significant dose-dependent reduction with rosuvastatin in plasma triglyceride and VLDL apoC-III concentrations. Rosuvastatin significantly (P < 0.05) increased VLDL apoC-III fractional catabolic rate (FCR) and decreased its production rate, with a significant (P < 0.05) dose-related effect. With 40 mg rosuvastatin, changes in VLDL apoC-III concentration were inversely associated with changes in VLDL apoC-III FCR and positively associated with VLDL apoC-III production rate (P < 0.05). Changes in VLDL apoC-III concentration and production rate were positively correlated with changes in VLDL apoB concentration and production rate and inversely correlated with VLDL apoB FCR (P < 0.05). Similar associations were observed with 10 mg rosuvastatin but were either less or not statistically significant. CONCLUSIONS -- In this study, rosuvastatin decreased the production and increased the catabolism of VLDL apoC-III, a mechanism that accounted for the significant reduction in VLDL apoC-III and triglyceride concentrations. This has implications for the management of cardiometabolic risk in obese subjects with the metabolic syndrome. [ABSTRACT FROM AUTHOR]

Published
2008
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42. Dietary plant sterols supplementation does not alter lipoprotein kinetics in men with the metabolic syndrome.

Author

Ooi, Esther M. M., Watts, Gerald F., Barrett, P. Hugh R., Chan, Dick C., Clifton, Peter M., Juying Ji, and Nestel, Paul J.

Subjects
*STEROLS, *LIPOPROTEINS, *METABOLIC syndrome, *CHOLESTEROL, *APOLIPOPROTEINS
Abstract

Dietary plant sterols supplementation has been demonstrated in some studies to lower plasma total and LDL cholesterol in hypercholesterolemic subjects. The cholesterol lowering action of plant sterols remains to be investigated in subjects with the metabolic syndrome. In a randomized, crossover study of 2 x 4 week therapeutic periods with oral supplementation of plant sterols (2 g/day) or placebo, and two weeks placebo wash-out between therapeutic periods, we investigated the effects of dietary plant sterols on lipoprotein metabolism in nine men with the metabolic syndrome. Lipoprotein kinetics were measured using [D3]-leucine, gas chromatography-mass spectrometry and compartmental modeling. In men with the metabolic syndrome, dietary plant sterols did not have a significant effect on plasma concentrations of total cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, apolipoprotein (apo) B, apoA-I or apoA-II. There were no significant changes to VLDL-, IDL-, LDLapoB or apoA-I fractional catabolic rates and production rates between therapeutic phases. Relative to placebo, plasma campesterol, a marker of cholesterol absorption was significantly increased (2.53 ± 0.35 vs. 4.64 ± 0.59 μg/ml, p<0.05), but there was no change in plasma lathosterol, a marker of endogenous cholesterol synthesis. In conclusion, supplementation with plant sterols did not appreciably influence plasma lipid or lipoprotein metabolism in men with the metabolic syndrome. Future studies with larger sample size, stratification to low and high cholesterol absorbers and cholesterol balance studies are warranted. [ABSTRACT FROM AUTHOR]

Published
2007

44. Plasma apolipoprotein C-III metabolism in patients with chronic kidney disease

Author

Ooi, Esther M. M., Chan, Doris T., Watts, Gerald F., Chan, Dick C., Ng, Theodore W. K., Dogra, Gursharan K., Irish, Ashley B., and Barrett, P. Hugh R.

Abstract

Moderate chronic kidney disease (CKD) (defined by an estimated glomerular filtration rate of 30–60 ml/min) is associated with mild hypertriglyceridemia related to delayed catabolism of triglyceride-rich lipoprotein particles. Altered apolipoprotein C-III (apoC-III) metabolism may contribute to dyslipidemia in CKD. To further characterize the dyslipidemia of CKD, we investigated the kinetics of plasma apoC-III in 7 nonobese, nondiabetic, non-nephrotic CKD subjects and 7 age- and sex-matched healthy controls, using deuterated leucine ([5, 5, 5, 2H3]leucine), gas chromatography-mass spectrometry, and multicompartmental modeling. Compared with controls, CKD subjects had higher concentrations of plasma and VLDL triglycerides and plasma and VLDL apoC-III (P < 0.05). The increased plasma apoC-III concentration was associated with a decreased apoC-III fractional catabolic rate (FCR) (1.21 ± 0.15 vs. 0.74 ± 0.12 pools/day, P = 0.03). There were no differences between apoC-III production rates of controls and those of CKD subjects. In CKD subjects, plasma apoC-III concentration was significantly and negatively correlated with apoC-III FCR (r = –0.749, P = 0.05) but not with apoC-III production rate. Plasma apoC-III concentration was positively correlated with plasma and VLDL triglycerides and VLDL apoB concentrations and negatively correlated with VLDL apoB FCR (P < 0.05 for all). ApoC-III FCR was negatively correlated with plasma and VLDL triglycerides and VLDL apoB concentration and positively correlated with VLDL apoB FCR (P < 0.05 for all). Altered plasma apoC-III metabolism is a feature of dyslipidemia in moderate CKD. Modification of apoC-III catabolism may be an important therapeutic target for reducing cardiovascular disease risk in moderate CKD.

Published
2011

45. Effect of apolipoprotein E genotype on apolipoprotein B-100 metabolism in normolipidemic and hyperlipidemic subjects

Author

Ooi, Esther M. M., Janus, Edward D., Grant, Susan J., Sinclair, Lucia M. T., and R.Barrett, P. Hugh

Abstract

The effect of apolipoprotein (apo) E genotype on apoB-100 metabolism was examined in three normolipidemic apoE2/E2, five type III hyperlipidemic apoE2/E2, and five hyperlipidemic apoE3/E2 subjects using simultaneous administration of 131I-VLDL and 125I-LDL, and multi-compartmental modeling. Compared with normolipidemic apoE2/E2 subjects, type III hyperlipidemic E2/E2 subjects had increased plasma and VLDL cholesterol, plasma and VLDL triglycerides, and VLDL and intermediate density lipoprotein (IDL) apoB concentrations (P < 0.05). These abnormalities were chiefly a consequence of decreased VLDL and IDL apoB fractional catabolic rate (FCR). Compared with hyperlipidemic E3/E2 subjects, type III hyperlipidemic E2/E2 subjects had increased IDL apoB concentration and decreased conversion of IDL to LDL particles (P < 0.05). In a pooled analysis, VLDL cholesterol was positively associated with VLDL and IDL apoB concentrations and the proportion of VLDL apoB in the slowly turning over VLDL pool, and was negatively associated with VLDL apoB FCR after adjusting for subject group. VLDL triglyceride was positively associated with VLDL apoB concentration and VLDL and IDL apoB production rates after adjusting for subject group. A defective apoE contributes to altered lipoprotein metabolism but is not sufficient to cause overt hyperlipidemia. Additional genetic mutations and environmental factors, including insulin resistance and obesity, may contribute to the development of type III hyperlipidemia.

Published
2010

46. Relationships between changes in plasma lipid transfer proteins and apolipoprotein B-100 kinetics during fenofibrate treatment in the metabolic syndrome

Author

Watts, Gerald F., Ji, Juying, Chan, Dick C., Ooi, Esther M. M., Johnson, Anthony G., Rye, Kerry-Anne, and Barrett, P. Hugh R.

Abstract

The aim of the present study was to investigate the association between changes in apoB (apolipoprotein B-100) kinetics and plasma PLTP (phospholipid transfer protein) and CETP (cholesteryl ester transfer protein) activities in men with MetS (the metabolic syndrome) treated with fenofibrate. Eleven men with MetS underwent a double-blind cross-over treatment with fenofibrate (200 mg/day) or placebo for 5 weeks. Compared with placebo, fenofibrate significantly increased the FCRs (fractional catabolic rates) of apoB in VLDL (very-low-density lipoprotein), IDL (intermediate-density lipoprotein) and LDL (low-density lipoprotein) (all P<0.01), with no significant reduction (−8%; P=0.131) in VLDL-apoB PR (production rate), but an almost significant increase (+15%, P=0.061) in LDL-apoB PR. Fenofibrate significantly lowered plasma TG [triacylglycerol (triglyceride); P<0.001], the VLDL-TG/apoB ratio (P=0.003) and CETP activity (P=0.004), but increased plasma HDL (high-density lipoprotein)-cholesterol concentration (P<0.001) and PLTP activity (P=0.03). The increase in PLTP activity was positively associated with the increase in both LDL-apoB FCR (r=0.641, P=0.034) and PR (r=0.625, P=0.040), and this was independent of the fall in plasma CETP activity and lathosterol level. The decrease in CETP activity was positively associated with the decrease in VLDL-apoB PR (r=0.615, P=0.044), but this association was not robust and not independent of changes in PLTP activity and lathosterol levels. Hence, in MetS, the effects of fenofibrate on plasma lipid transfer protein activities, especially PLTP activity, may partially explain the associated changes in apoB kinetics.

Published
2006
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47. Regulatory Effects of Fenofibrate and Atorvastatin on Lipoprotein A-I and Lipoprotein A-I:A-II Kinetics in the Metabolic Syndrome.

Author

Chan, Dick C., Watts, Gerald F., Ooi, Esther M. M., Rye, Kerry-Anne, Ji, Juying, Johnson, Anthony G., and Barrett, P. Hugh R.

Subjects
FENOFIBRATE, STATINS (Cardiovascular agents), LIPOPROTEINS, METABOLIC syndrome, HIGH density lipoproteins, BLOOD lipoprotein metabolism, PLACEBOS, CROSSOVER trials
Abstract

OBJECTIVE -- Subjects with the metabolic syndrome have reduced HDL cholesterol concentration and altered metabolism of high-density lipoprotein (Lp)A-I and LpA-I:A-II particles. In the metabolic syndrome, fenofibrate and atorvastatin may have differential effects on HDL particle kinetics. RESEARCH DESIGN AND METHODS -- Eleven men with metabolic syndrome were studied in a randomized, double-blind, crossover trial of 5-week intervention periods with placebo, fenofibrate (200 mg/day), and atorvastatin (40 mg/day). LpA-I and LpA-I:A-II kinetics were examined using stable isotopic techniques and compartmental modeling. RESULTS-- Compared with placebo, fenofibrate significantly increased the production of both LpA-I:A-II (30% increase; P < 0.001) and apoA-II (43% increase; P < 0.001), accounting for significant increases of their corresponding plasma concentrations (10 and 23% increases, respectively), but it did not alter LpA-I kinetics or concentration. Atorvastatin did not significantly alter HDL concentration or the kinetics of HDL particles. CONCLUSIONS -- In the metabolic syndrome, fenofibrate, but not atorvastatin, influences HDL metabolism by increasing the transport of LpA-I:A-II particles. [ABSTRACT FROM AUTHOR]

Published
2009
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48. Lipoprotein (a) and Low‐density lipoprotein apolipoprotein B metabolism following apheresis in patients with elevated lipoprotein(a) and coronary artery disease.

Author

Ma, Louis, Waldmann, Elisa, Ooi, Esther M. M., Chan, Dick C., Barrett, Hugh P. R., Watts, Gerald F., and Parhofer, Klaus G.

Subjects
CORONARY disease, APOLIPOPROTEIN B, LIPOPROTEINS, LOW density lipoproteins, CARDIOVASCULAR diseases, METABOLISM
Abstract

Background: Lipoprotein apheresis effectively lowers lipoprotein(a) [Lp(a)] and low‐density lipoprotein (LDL) by approximately 60%‐70%. The rebound of LDL and Lp(a) particle concentrations following lipoprotein apheresis allows the determination of fractional catabolic rate (FCR) and hence production rate (PR) during non‐steady state conditions. We aimed to investigate the kinetics of Lp(a) and LDL apolipoprotein B‐100 (apoB) particles in patients with elevated Lp(a) and coronary artery disease undergoing regular apheresis. Patients and methods: A cross‐sectional study was carried out in 13 patients with elevated Lp(a) concentration (>500 mg/L) and coronary artery disease. Lp(a) and LDL‐apoB metabolic parameters, including FCR and PR were derived by the fit of a compartment model to the Lp(a) and LDL‐apoB concentration data following lipoprotein apheresis. Results: The FCR of Lp(a) was significantly lower than that of LDL‐apoB (0.39 [0.31, 0.49] vs 0.57 [0.46, 0.71] pools/day, P = 0.03) with no significant differences in the corresponding PR (14.80 [11.34, 19.32] vs 15.73 [11.93, 20.75] mg/kg/day, P = 0.80). No significant associations were observed between the FCR and PR of Lp(a) and LDL‐apoB. Conclusions: In patients with elevated Lp(a), the fractional catabolism of Lp(a) is slower than that of LDL‐apoB particles, implying that different metabolic pathways are involved in the catabolism of these lipoproteins. These findings have implications for new therapies for lowering apolipoprotein(a) and apoB to prevent atherosclerotic cardiovascular disease. [ABSTRACT FROM AUTHOR]

Published
2019
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49. Consumption of a whey protein-enriched diet may prevent hepatic steatosis associated with weight gain in elderly women

Author

Ooi, Esther M, Adams, L A, Zhu, Kun, Lewis, Joshua R, Kerr, Deborah Anne, Meng, Xingqiong, Solah, Vicky A, Devine, Amanda, Binns, Colin W, Prince, R L, Ooi, Esther M, Adams, L A, Zhu, Kun, Lewis, Joshua R, Kerr, Deborah Anne, Meng, Xingqiong, Solah, Vicky A, Devine, Amanda, Binns, Colin W, and Prince, R L

Abstract

Ooi E.M., Adams L.A., Zhu K., Lewis J.R., Kerr D.A., Meng X., Solah V., Devine A., Binns C.W., Prince R.L. (2015). Consumption of a whey protein-enriched diet may prevent hepatic steatosis associated with weight gain in elderly women. Nutrition, Metabolism and Cardiovascular Diseases, 25(4), 388-395. Available here

50. Fractional turnover of apolipoprotein(a) and apolipoprotein B-100 within plasma lipoprotein(a) particles in statin-treated patients with elevated and normal Lp(a) concentration.

Author

Ma L, Chan DC, Ooi EMM, Barrett PHR, and Watts GF

Subjects
Adolescent, Adult, Aged, Female, Humans, Hyperlipidemias blood, Kinetics, Lipoprotein(a) blood, Male, Middle Aged, Young Adult, Apolipoprotein B-100 metabolism, Apolipoproteins A metabolism, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Lipoprotein(a) metabolism
Abstract

Context: Lipoprotein(a) [Lp(a)] is a highly atherogenic lipoprotein characterized by apolipoprotein(a) [apo(a)] covalently bounded to apoB-100 (apoB). However, the metabolism of apo(a) and apoB within plasma Lp(a) particles in patients on statins remains unclear., Methods: The kinetics of Lp(a)-apo(a) and Lp(a)-apoB were determined in 20 patients with elevated Lp(a) (≥0.8 g/L; n = 10) and normal Lp(a) (≤0.3 g/L; n = 10) using stable isotope techniques and compartmental modeling. Plasma apo(a) concentration was measured using liquid chromatography-mass spectrometry. All patients were on statin therapy and were studied in the fasting state., Results: The fractional catabolic rate (FCR) of Lp(a)-apo(a) was not significantly different from that of Lp(a)-apoB in statin-treated patients with elevated or normal Lp(a) (P > 0.05 in both). Lp(a)-apo(a) FCR was significantly correlated with Lp(a)-apoB in patients with elevated and normal Lp(a) concentrations (r = 0.970 and r = 0.979, respectively; all P < 0.001) with Lin's concordance test showing substantial agreement between the FCRs of Lp(a)-apo(a) and Lp(a)-apoB in patients with elevated and normal Lp(a) concentrations (r c  = 0.978 and r c  = 0.966, respectively)., Conclusion: Our data indicate that the apo(a) and apoB proteins within Lp(a) particles have similar FCR and are therefore tightly coupled as an Lp(a) holoparticle in statin-treated patients with elevated and normal Lp(a) concentrations., (Copyright © 2019. Published by Elsevier Inc.)

Published
2019
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