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Biomedical subjects

G F Watts

Publications and source records attributed to G F Watts.

At least 37 records · Page 2Linked to original sources
PubMed2003

Comparison of intraperitoneal and posterior subcutaneous abdominal adipose tissue compartments as predictors of VLDL apolipoprotein B-100 kinetics in overweight/obese men.

AIMS: The influence of different regional adipose tissue (AT) compartments on insulin resistance and dyslipidaemia may account for variations in risk of diabetes and cardiovascular disease. The purpose of this study was to examine the association of intraperitoneal and posterior subcutaneous abdominal AT with very-low-density lipoprotein apolipoprotein B-100 (VLDL-apoB) kinetics in overweight/obese men. METHODS: Intraperitoneal, anterior subcutaneous and posterior subcutaneous abdominal AT mass (IPATM, ASAATM and PSAATM respectively) were quantified in 51 overweight/obese men using magnetic resonance imaging. Hepatic secretion of VLDL-apoB was measured using an intravenous infusion of 1-[13C]-leucine. Isotopic enrichment of VLDL-apoB was measured using gas chromatography mass spectrometry and a multicompartmental model used to estimate VLDL-apoB metabolic parameters. Insulin resistance was estimated by homeostasis model assessment (HOMA) score. RESULTS: In univariate analysis, IPATM, ASAATM and PSAATM were significantly associated with HOMA score (r = 0.554, 0.425 and 0.440 respectively; p < 0.01). Intraperitoneal abdominal AT mass was also associated with plasma triglycerides (r = 0.292, p < 0.05), VLDL-apoB concentrations (r = 0.407, p < 0.01) and VLDL-apoB secretion (r = 0.390, p < 0.05). Intraperitoneal abdominal AT mass remained significantly associated with VLDL-apoB secretion (r = 0.344, p < 0.05) and HOMA score (r = 0.368, p < 0.01) after adjusting for total body fat. In multiple regression analysis including IPATM, non-esterified fatty acids and age, IPATM was the best predictor of VLDL-apoB secretion (R2 = 17%, p < 0.01) and HOMA score (R2 = 32%, p < 0.001). None of the fat compartments were significantly associated with VLDL-apoB catabolism. CONCLUSIONS: In overweight/obese men the intraperitoneal AT mass is a better predictor of VLDL-apoB secretion and insulin resistance than either posterior or anterior subcutaneous abdominal AT mass.

Abdomen↗
PubMed2003

Waist circumference, waist-to-hip ratio and body mass index as predictors of adipose tissue compartments in men.

BACKGROUND: The accumulation of fat in visceral and posterior subcutaneous adipose tissue compartments is highly correlated with the metabolic abnormalities that contribute to increased risk of diabetes mellitus and cardiovascular disease. AIM: To determine which of waist circumference (WC), waist-to-hip ratio (WHR) and body mass index (BMI) was the best predictor of intraperitoneal and posterior subcutaneous abdominal adipose tissue mass in men. METHODS: We studied 59 free-living men with a wide range of BMI. WC, WHR and BMI were determined using standard methods. Intraperitoneal, retroperitoneal, anterior subcutaneous and posterior subcutaneous abdominal adipose tissue masses (IPATM, RPATM, ASAATM and PSAATM, respectively) were quantified using magnetic resonance imaging. RESULTS: In univariate regression analysis, WC, WHR and BMI were all significantly and positively correlated (all p < 0.05) with IPATM, RPATM, ASAATM and PSAATM. To assess the relative strength of these associations, we used non-nested regression models. There was no significant difference between WC and WHR in predicting IPATM and RPATM; WC was a stronger predictor of ASAATM (p < 0.001) and PSAATM (p < 0.001) than WHR; WC was also a stronger predictor of IPATM (p = 0.042) and RPATM (p = 0.045) than BMI, but the relative strengths of WC and BMI in predicting ASSATM and PSAATM did not different significantly (p > 0.05); there was no significant difference between BMI and WHR in predicting IPATM and RPATM (p>0.05), but BMI was a stronger predictor of ASAATM (p = 0.036) and PSAATM (p < 0.001) than WHR. DISCUSSION: In men WC is the anthropometric index that most uniformly predicts the distribution of adipose tissue among several fat compartments in the abdominal region, there apparently being little value in measuring WHR or BMI.

Abdomen↗
PubMed2003

Endothelial function in HIV-infected patients receiving protease inhibitor therapy: does immune competence affect cardiovascular risk?

BACKGROUND: The use of HIV protease inhibitors (PIs) as a component of combination antiretroviral therapy in HIV-infected patients has been associated with dyslipidaemia, but its significance as a risk factor for cardiovascular disease is unclear. Endothelial dysfunction is an early phase of atherogenesis that may be assessed non-invasively with ultrasonography in vivo. AIM: To evaluate vascular function and investigate potential determinants of endothelial dysfunction of the peripheral circulation in PI-treated, HIV-infected men with dyslipidaemia. DESIGN: Observational, case-control study. METHODS: We studied 24 HIV-infected, PI-treated men with dyslipidaemia and 24 normolipidaemic, healthy male controls matched for age and body mass index. Brachial artery endothelial function was studied using high-resolution ultrasound and computerized edge-detection software. This non-invasive technique measured post-ischaemic flow-mediated dilatation (FMD), and the endothelium-independent vasodilatory response to glyceryl trinitrate (GTN). RESULTS: Within the HIV patient group, FMD was significantly associated with percentage of 'naïve' CD4 + 45RA + T cells (p = 0.03), while plasma lipid/lipoprotein and insulin levels, body mass, and smoking status did not correlate with endothelial function. FMD was not significantly different between the study group and the controls. CONCLUSIONS: The atherogenic potential of PI-associated dyslipidaemia may be attenuated in HIV-infected patients with decreased immune competence, reflecting a possible contribution of cell-mediated immune responses to the pathogenesis of atherosclerosis.

Adult↗
PubMed2003

Vascular function of forearm microcirculation in postmenopausal women with type 2 diabetes: potential benefit of hormone replacement therapy?

OBJECTIVE: To study the potential effects of hormone replacement therapy (HRT) on vascular function of the peripheral circulation in postmenopausal women with type 2 diabetes. METHODS: Seventeen premenopausal women aged 47.4 +/- 4.4 years (PreM), 23 nondiabetic postmenopausal women aged 59.4 +/- 7.0 years (PM), 15 postmenopausal women with type 2 diabetes aged 60.3 +/- 7.2 years (PMD) and 12 postmenopausal women with type 2 diabetes using HRT aged 61.2 +/- 4.0 years (PMDHRT) were studied. Vascular function of the peripheral circulation was investigated by measuring hyperemic responses of the forearm microcirculation following an ischemic stimulus using venous occlusion, strain-gauge plethysmography. Fasting lipids, glucose and glycated hemoglobin (HbA1c) were also measured. RESULTS: Forearm vascular function was significantly impaired in the PMD group: maximal blood flow (ml/100 ml/min) was 15.23 +/- 8.19 vs. 28.21 +/- 12.30 (PreM), 23.62 +/- 6.62 (PM) and 23.37 +/- 5.78 (PMDHRT) (p = 0.004); flow debt (ml/100 ml) was 3.99 +/- 2.83 vs. 7.40 +/- 4.92 (PreM), 5.66 +/- 3.67 (PM) and 8.57 +/- 4.84 (PMDHRT) (p = 0.0018); vascular resistance (mmHg/ml/100 ml/min) was 11.90 +/- 9.02 vs. 5.04 +/- 2.41 (PreM), 5.55 +/- 2.69 (PM) and 5.96 +/- 1.88 (PMDHRT) (p = 0.003). Fasting lipids, HbA1c and body mass index were not significantly different between the two diabetic groups. CONCLUSIONS: Postmenopausal women with diabetes have abnormal vascular function of resistance arteries that may improve with HRT. HRT may therefore reduce cardiovascular risk in postmenopausal women with type 2 diabetes, and a clinical end-point trial is warranted to test this hypothesis.

Adult↗
PubMed2002

Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus.

AIM/HYPOTHESIS: We assessed whether dietary supplementation with coenzyme Q(10) improves endothelial function of the brachial artery in patients with Type II (non-insulin-dependent) diabetes mellitus and dyslipidaemia. METHODS: A total of 40 patients with Type II diabetes and dyslipidaemia were randomized to receive 200 mg of coenzyme Q(10) or placebo orally for 12 weeks. Endothelium-dependent and independent function of the brachial artery was measured as flow-mediated dilatation and glyceryl-trinitrate-mediated dilatation, respectively. A computerized system was used to quantitate vessel diameter changes before and after intervention. Arterial function was compared with 18 non-diabetic subjects. Oxidative stress was assessed by measuring plasma F(2)-isoprostane concentrations, and plasma antioxidant status by oxygen radical absorbance capacity. RESULTS: The diabetic patients had impaired flow-mediated dilation [3.8 % (SEM 0.5) vs 6.4 % (SEM 1.0), p = 0.016], but preserved glyceryl-trinitrate-mediated dilation, of the brachial artery compared with non-diabetic subjects. Flow-mediated dilation of the brachial artery increased by 1.6 % (SEM 0.3) with coenzyme Q(10) and decreased by -0.4 % (SEM 0.5) with placebo (p = 0.005); there were no group differences in the changes in pre-stimulatory arterial diameter, post-ischaemic hyperaemia or glyceryl-trinitrate-mediated dilation response. Coenzyme Q(10) treatment resulted in a threefold increase in plasma coenzyme Q(10) (p < 0.001) but did not alter plasma F(2)-isoprostanes, oxygen radical absorbance capacity, lipid concentrations, glycaemic control or blood pressure. CONCLUSION/INTERPRETATION: Coenzyme Q(10) supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes. The mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress, an effect that might not be reflected by changes in plasma F(2)-isoprostane concentrations.

Antioxidants↗
PubMed2002

Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes.

OBJECTIVE: Our objective was to assess effects of dietary supplementation with coenzyme Q10 (CoQ) on blood pressure and glycaemic control in subjects with type 2 diabetes, and to consider oxidative stress as a potential mechanism for any effects. SUBJECTS AND DESIGN: Seventy-four subjects with uncomplicated type 2 diabetes and dyslipidaemia were involved in a randomised double blind placebo-controlled 2x2 factorial intervention. SETTING: The study was performed at the University of Western Australia, Department of Medicine at Royal Perth Hospital, Australia. INTERVENTIONS: Subjects were randomly assigned to receive an oral dose of 100 mg CoQ twice daily (200 mg/day), 200 mg fenofibrate each morning, both or neither for 12 weeks. MAIN OUTCOME MEASURES: We report an analysis and discussion of the effects of CoQ on blood pressure, on long-term glycaemic control measured by glycated haemoglobin (HbA(1c)), and on oxidative stress assessed by measurement of plasma F2-isoprostanes. RESULTS: Fenofibrate did not alter blood pressure, HbA(1c), or plasma F2-isoprostanes. There was a 3-fold increase in plasma CoQ concentration (3.4+/-0.3 micro mol/l, P<0.001) as a result of CoQ supplementation. The main effect of CoQ was to significantly decrease systolic (-6.1+/-2.6 mmHg, P=0.021) and diastolic (-2.9+/-1.4 mmHg, P=0.048) blood pressure and HbA(1c) (-0.37+/-0.17%, P=0.032). Plasma F2-isoprostane concentrations were not altered by CoQ (0.14+/-0.15 nmol/l, P=0.345). CONCLUSIONS: These results show that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F2-isoprostanes. SPONSORSHIP: This study was supported by a grant from the NH&MRC, Australia.

Antioxidants↗
PubMed2002

Factorial study of the effects of atorvastatin and fish oil on dyslipidaemia in visceral obesity.

BACKGROUND: Dyslipidaemia may account for increased risk of cardiovascular disease in central obesity. Pharmacotherapy is often indicated in these patients, but the optimal approach remains unclear. We investigated the effects of atorvastatin and fish oil on plasma lipid and lipoprotein levels, including remnant-like particle-cholesterol and apolipoprotein C-III, in dyslipidaemic men with visceral obesity. METHODS: We carried out a 6-week randomized, placebo-controlled, 2 x 2 factorial intervention study of atorvastatin (40 mg day(-1)) and fish oil (4 g day(-1)) on plasma lipids and lipoproteins in 52 obese men (age 53 +/- 1 years, BMI 33.7 +/- 0.55 kg m(-2)) with dyslipidaemia and insulin resistance. Treatment effects were analysed by general linear modelling. RESULTS: Atorvastatin had significant main effects in decreasing triglycerides (-0.38 +/- 0.02 mmol L(-1), P = 0.002), total cholesterol (-1.89 +/- 0.17 mmol L(-1), P = 0.001), LDL-cholesterol (-1.78 +/- 0.14 mmol L(-1), P = 0.001), remnant-like particle-cholesterol (-0.08 +/- 0.04 mmol L(-1), P = 0.035), apolipoprotein B (-49 +/- 4 mg dL(-1), P = 0.001), apolipoprotein C-III (-12.6 +/- 6.1 mg L(-1), P = 0.044) and in increasing HDL-cholesterol (+0.10 +/0- 0.04 mmol L(-1), P = 0.007). Fish oil had significant main effects in decreasing triglycerides (-0.38 +/- 0.11 mmol L(-1), P = 0.002) and in increasing HDL-cholesterol (+0.07 +/- 0.04 mmol L(-1), P = 0.041). There were no significant changes in weight or insulin resistance during the study. CONCLUSIONS: Atorvastatin and fish oil have independent and additive effects in correcting dyslipidaemia in viscerally obese men. Improvement in abnormalities in remnant lipoproteins may occur only with use of atorvastatin. Combination treatment with statin and fish oil may, however, offer an optimal therapeutic approach for globally correcting dyslipidaemia in obesity.

Atorvastatin↗
PubMed2002

Effect of Simvastatin on markers of triglyceride-rich lipoproteins in familial hypercholesterolaemia.

BACKGROUND: We have previously shown elevated fasting plasma concentrations of intestinal remnants, as reflected by apolipoprotein (apo) B-48 and remnant-like particle-cholesterol (RLP-C) in patients with heterozygous familial hypercholesterolaemia (FH). We now investigate the effect of an HMG-CoA reductase inhibitor (simvastatin) on chylomicron remnant metabolism using the measurement of fasting apoB-48 and RLP-C in FH patients after long- and short-term simvastatin therapy and after a wash-out period. We also piloted the response of a breath test, involving the measurement of the fractional catabolic rate (FCR) of an intravenously injected chylomicron remnant-like emulsion labeled with cholesteryl (13)C-oleate. METHODS: Fifteen FH patients were studied after > 6 months 40 mg day(-1) simvastatin treatment (long-term), a wash-out period (4 weeks), and 4 weeks of simvastatin treatment (short-term). Apolipoprotein B-48 was determined by SDS-PAGE and Western blotting/enhanced chemiluminescence and RLP-C by an immunoseparation assay. The FCR of the chylomicron remnant-like emulsion was determined from the appearance of (13)CO(2) in the breath and by multicompartmental mathematical modelling. RESULTS: Both long- and short-term treatment with simvastatin were associated with decreases in the plasma concentration of apoB-48 (P < 0.05) and RLP-C (P < 0.001), but there was no significant change in the FCR of the emulsion. CONCLUSIONS: We suggest that long- and short-term treatments with simvastatin have comparable effects in decreasing the plasma concentration of triglyceride-rich remnants in heterozygous FH, as measured by fasting apoB-48 and RLP-C. The mechanisms for this may involve decreased production of hepatic and possibly intestinal lipoproteins, and/or up-regulation of hepatic receptor clearance pathways, but these changes are apparently not associated with a change in remnant clearance as measured kinetically by the (13)CO(2) breath test.

Apolipoprotein B-48↗
PubMed2002

High-density lipoprotein metabolism in familial hypercholesterolaemia: significance, mechanisms, therapy.

AIM: To assess the significance, mechanisms and therapy of impaired high-density lipoprotein (HDL) metabolism in patients with heterozygous familial hypercholesterolaemia (FH). METHODS: Review of epidemiological, metabolic and clinical literature with synthetic analysis of data referring to HDL. PRINCIPAL FINDINGS AND SYNTHESIS: Low HDL is a powerful risk factor for coronary artery disease (CAD) in FH. Low HDL in FH is a metabolic sequel of insulin resistance, which is the central feature of the visceral accumulation of adipose tissue acquired in later life. Insulin resistance increases hepatic secretion of triglycerides that subsequently results in remodelling of holo-HDL particles and enhanced catabolism of apolipoprotein A-I. Gene-gene and gene-environment interactions may contribute to the pathogenesis of low HDL in FH. Low HDL may also point to other cardiovascular risk factors, such as hyper-remnantaemia, increased small dense low-density lipoproteins (LDL), procoagulopathy and vascular insulin resistance. Visceral obesity should be vigorously identified and treated in FH. Judicious addition of fish oils, niacin and fibrates to a statin may be required to optimise HDL metabolism. Extracorporeal removal of LDL cholesterol should aim not to extract HDL from plasma. CONCLUSIONS: With the increasing incidence of obesity in the community, the metabolic syndrome will overmanifest in patients with FH. Impaired HDL metabolism is an important consequence of this syndrome for FH patients, because it will per se or in collusion with other associated risk factors accelerate the progression of atherosclerosis and CAD. Dysregulation of HDL metabolism principally results from hepatic insulin resistance and remodelling of HDL particles. Obesity should be prevented and aggressively treated in FH and use of a safe combination drug regimen considered to correct the dysmetabolism of HDL in these patients.

Body Composition↗
PubMed2001

Endothelium-dependent and independent vasodilation studies at normoglycaemia in type I diabetes mellitus with and without microalbuminuria.

AIMS/HYPOTHESIS: We examined whether endothelial function is impaired in patients with Type I (insulin-dependent) diabetes mellitus under conditions of near-normoglycaemia compared with age-matched healthy control subjects. Our aim was to determine whether microalbuminuria is associated with endothelial dysfunction in Type I diabetes. METHODS: Endothelial function, measured as post-ischaemic flow-mediated dilatation of the brachial artery using ultrasound, was compared among 17 microalbuminuric and 17 normoalbuminuric diabetic patients, and 17 control subjects. Glyceryl trinitrate-mediated dilatation of the brachial artery was used to measure endothelium-independent function. All diabetic patients were studied at near-normoglycaemia, using insulin and 5 % dextrose infusions to maintain blood glucose between 3.5 and 8.0 mmol/l. RESULTS: Flow-mediated dilatation was significantly lower in microalbuminuric diabetic patients (3.2 +/- 0.3%) compared with normoalbuminuric diabetic patients (5.4 +/- 0.6%) and control subjects (7.9 +/- 0.6%, p < 0.001). Normoalbuminuric diabetic patients also had significantly lower flow-mediated dilatation than control subjects (p = 0.01). Glyceryl trinitrate mediated dilatation was significantly lower in the microalbuminuric patients compared with the control subjects (11.9 +/- 1.1% vs 20.0 +/- 1.2%, p = 0.001). Albumin excretion rate and glycated haemoglobin showed a significant negative independent correlation with flow-mediated dilatation (both p < 0.05). CONCLUSION/INTERPRETATION: Type I diabetic patients show endothelial dysfunction at near-normoglycaemia compared with the control subjects, and this abnormality is more marked in diabetic patients with microalbuminuria. Endothelial dysfunction in Type I diabetes is related to the albumin excretion rate and glycaemic control. The presence of endothelial dysfunction in normoalbuminuric diabetic patients suggests it could precede microalbuminuria as an early risk marker for cardiovascular disease.

Adolescent↗
PubMed2001

Clinical and biochemical features, molecular diagnosis and long-term management of a case of cerebrotendinous xanthomatosis.

Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive sterol storage disease characterised clinically by juvenile bilateral cataracts, progressive neurological dysfunction, and formation of tendon xanthomata. We describe the clinical and biochemical features, molecular diagnosis and long-term management of the first reported Australasian case of CTX. Molecular analysis confirmed the diagnosis of CTX and demonstrated that the patient was homozygous for a G-->A transition in the splice donor site of intron 4 of the sterol 27-hydroxylase gene. Serum cholestanol concentrations were decreased with the HMG-CoA reductase inhibitor simvastatin alone and greater reductions were achieved after the addition of the bile acid chenodeoxycholic acid; suggesting a synergistic effect of this combination. Despite serum cholestanol concentrations remaining within the low-normal range, there has been no significant improvement in mental and physical abilities or in EEG abnormalities with 5 years of treatment. Metabolism of radiolabeled 7-ketocholesterol to aqueous soluble products was absent in CTX-derived macrophages. Consistent with this finding, plasma 7 alpha-hydroxycholesterol, 7 beta-hydroxycholesterol, and 7-ketocholesterol concentrations were increased in the CTX subject compared with controls.

Achilles Tendon↗
PubMed2001

Chylomicron remnant metabolism in familial hypercholesterolaemia studied with a stable isotope breath test.

Chylomicron remnant metabolism was studied using a stable isotope breath test in 25 patients with familial hypercholesterolaemia (FH) (10 homozygotes, 15 heterozygotes), and in 15 normolipidaemic controls. A lipid emulsion mimicking the composition of chylomicron remnants and labelled with cholesteryl (13)C-oleate was injected intravenously; (13)CO(2) was measured subsequently in breath using isotope-ratio mass spectrometry. The fractional catabolic rate (pools/h) of the emulsion, derived from a compartmental model, did not differ significantly among the groups: homozygous FH mean 0.20 (S.E.M. 0.05), heterozygous FH 0.12 (0.02), controls 0.16 (0.03). We suggest that the catabolism of chylomicron remnants from plasma is not impaired in FH and that the hepatic uptake of these particles is not dependent on functional LDL receptors.

Adult↗
PubMed2001

Preliminary experience with a new stable isotope breath test for chylomicron remnant metabolism: a study in central obesity.

We aimed to investigate the metabolism of chylomicron remnants in the postabsorptive state employing a new stable isotope breath test in centrally obese men without overt hyperlipidaemia. Groups of 12 centrally obese and 12 non-obese men of similar age and with similar plasma cholesterol and triacylglycerol (triglyceride) levels were studied. The catabolism of chylomicron remnants was measured using an intravenous injection of a remnant-like emulsion containing cholesteryl [(13)C]oleate. Isotopic enrichment of (13)CO(2) in breath was determined using isotope-ratio mass spectrometry, and a multi-compartmental model (SAAM II program) was used to estimate the fractional catabolic rate (FCR) of the chylomicron remnant-like particles. The plasma concentrations of low-density lipoprotein (LDL)-cholesterol, non-high-density lipoprotein (HDL)-cholesterol and insulin were significantly higher (P<0.05) in the obese than the control subjects. The obese subjects had significantly lower HDL-cholesterol (P<0.05) and, in particular, a decreased FCR of the remnant-like particles compared with lean subjects (0.061+/-0.014 and 0.201+/-0.048 pools/h respectively; P=0.016). In the obese group, the FCR of remnant-like particles was inversely associated with the waist/hip ratio, and with plasma triacylglycerol, cholesterol, LDL-cholesterol and non-HDL-cholesterol levels. In multiple regression analysis, the waist/hip ratio was the best predictor of the FCR of the emulsion. In conclusion, this new test suggests that postabsorptive chylomicron remnant catabolism is impaired in centrally obese subjects without overt hyperlipidaemia. This defect may be due to the degree of adiposity.

Adult↗
PubMed2001

Elevated apolipoprotein B-48 and remnant-like particle-cholesterol in heterozygous familial hypercholesterolaemia.

Apolipoprotein B-48 (apoB-48) is a marker of triglyceride-rich lipoprotein (TRL) remnants of intestinal origin. Chylomicron remnants are causally related to atherosclerosis. We have shown previously that fasting plasma apoB-48 may predict postprandial lipaemia. Remnant-like particle-cholesterol (RLP-C) may also reflect TRL remnants. We aimed to determine whether subjects with heterozygous familial hypercholesterolaemia (FH) had an accumulation of remnants of intestinal origin, as reflected by fasting plasma apoB-48 and RLP-C levels. The fasting plasma concentrations of apoB-48 and RLP-C were measured in 15 subjects with heterozygous FH and 15 age- and sex-matched, normolipidaemic subjects. ApoB-48 was determined using SDS-PAGE and a western blotting/enhanced chemi-luminescence technique. RLP-C was measured using an immuno-separation assay. Serum apolipoprotein B-100 (apoB-100) levels were measured using immunonephelometry; lipids were assayed enzymatically. Compared with controls, FH subjects had significantly elevated plasma concentrations of apoB-48 (29.3 median, 16.7-45.1 mg L-1 range vs. 12.8, 7.3-28.6; P < 0.001) and RLP-C (16.2, 1.5-114.3 mg dL-1 vs. 8.5, 5.0-13.5; P = 0.003), as well as serum total apoB-100 (1.9, 1.3-2.6 g L-1 vs. 1.0, 0.3-1.3; P < 0.001), LDL-cholesterol (8.1, 4.6-10.4 mmol L-1 vs. 3.5, 2.4-4.4; P < 0.001) and triglyceride (1.5, 0.6-5.6 mmol L-1 vs. 1.0, 0.4-1.8; P = 0.018). There was no significant difference in HDL cholesterol. The findings suggest that patients with heterozygous FH have elevated plasma concentrations of TRL remnants, including those of intestinal origin. This may be a consequence of decreased clearance of these particles by the LDL-receptor.

Apolipoprotein B-48↗