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Hitoshi Hama - One of the best experts on this subject based on the ideXlab platform.
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Surfactant-Based Homogeneous Assay for the Measurement of Triglyceride Concentrations in VLDL and Intermediate-Density Lipoprotein
Clinical Chemistry, 2005Co-Authors: Masahiko Okada, Yasuhiko Noguchi, Tomohiro Saito, Hajime Yoshimura, Hiroko Sasaki, Hitoshi HamaAbstract:Background: Existing studies have demonstrated the clinical significance of triglyceride content in VLDL (VLDL-TG) and Intermediate-Density Lipoprotein (IDL-TG). We developed a homogeneous assay protocol to directly measure VLDL-TG. Methods: Possible reagents and conditions for measuring VLDL-TG were comprehensively tested, and the “best” combination was determined. Healthy persons were instructed to consume a fatty meal after 15-h overnight fasting. Serum VLDL-TG + IDL-TG concentrations were measured using the proposed method. Patients with serum LDL-cholesterol concentrations ≥3.62 mmol/L (140 mg/dL) were administered simvastatin at a daily dose of 5 mg, and serum VLDL-TG concentrations were then measured. Results: The combination of 2 nonionic surfactants played an important role in differentiating VLDL and IDL from other Lipoproteins, probably via specific interactions with phospholipids and apoLipoproteins. The regression line of the proposed method ( y ) and the ultracentrifugal assay ( x ) was: y = 0.98 x + 0.31 mmol/L ( r = 0.98; n = 73; P
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surfactant based homogeneous assay for the measurement of triglyceride concentrations in vldl and Intermediate Density Lipoprotein
Clinical Chemistry, 2005Co-Authors: Masahiko Okada, Yasuhiko Noguchi, Tomohiro Saito, Hajime Yoshimura, Hiroko Sasaki, Taeko Ito, Hitoshi HamaAbstract:Background: Existing studies have demonstrated the clinical significance of triglyceride content in VLDL (VLDL-TG) and Intermediate-Density Lipoprotein (IDL-TG). We developed a homogeneous assay protocol to directly measure VLDL-TG. Methods: Possible reagents and conditions for measuring VLDL-TG were comprehensively tested, and the “best” combination was determined. Healthy persons were instructed to consume a fatty meal after 15-h overnight fasting. Serum VLDL-TG + IDL-TG concentrations were measured using the proposed method. Patients with serum LDL-cholesterol concentrations ≥3.62 mmol/L (140 mg/dL) were administered simvastatin at a daily dose of 5 mg, and serum VLDL-TG concentrations were then measured. Results: The combination of 2 nonionic surfactants played an important role in differentiating VLDL and IDL from other Lipoproteins, probably via specific interactions with phospholipids and apoLipoproteins. The regression line of the proposed method ( y ) and the ultracentrifugal assay ( x ) was: y = 0.98 x + 0.31 mmol/L ( r = 0.98; n = 73; P <0.05). The difference between postprandial total TG and VLDL-TG concentrations was statistically significant ( P <0.05). After 8 weeks of therapy with simvastatin, total TG and LDL-cholesterol concentrations were 13.6% and 26.3% lower, respectively ( P <0.05), whereas VLDL-TG did not show any significant decrease. Conclusion: Our homogeneous method can measure TG content in VLDL and IDL.
Borge G Nordestgaard - One of the best experts on this subject based on the ideXlab platform.
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Intermediate Density Lipoprotein cholesterol as the best Lipoprotein predictor of atherosclerosis severity in the Watanabe Heritable Hyperlipidemic rabbit.
Atherosclerosis, 1997Co-Authors: Borge G Nordestgaard, Birgit Agerholm-larsen, Per Ibsen, Jorgen Fischer Hansen, Birgit Fischer Hansen, Alicja Mortensen, Knud KjeldsenAbstract:a Department of Clinical Biochemistry, Rigshospitalet, Uni6ersity of Copenhagen, Copenhagen, Denmark b Department of Clinical Biochemistry, Herle6 Hospital, Uni6ersity of Copenhagen, Herle6 Ring6ej 75, DK-2730 Herle6, Denmark c Department of Pathology, H6ido6re Hospital, Uni6ersity of Copenhagen, Copenhagen, Denmark d Department of Cardiology, H6ido6re Hospital, Uni6ersity of Copenhagen, Copenhagen, Denmark e Institute of Toxicology, National Food Agency of Denmark, Denmark
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Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits.
Diabetologia, 1997Co-Authors: Borge G Nordestgaard, Birgit Agerholm-larsen, S. StenderAbstract:To examine the hypothesis that hyperinsulinaemia promotes atherosclerosis, cholesterol-fed rabbits were injected subcutaneously with 6 i.u. of human insulin (n = 16) or placebo (n = 20) daily for 24 weeks; injection of insulin resulted in hyperinsulinaemia for up to 16 h after injection. Compared to placebo rabbits, insulin-treated rabbits had higher levels of insulin antibodies in plasma, similar levels of Intermediate Density, low Density and high Density Lipoprotein cholesterol and similar activities of hepatic and Lipoprotein lipase in post-heparin plasma, but lower levels of plasma C-peptide, blood glucose, postprandial plasma triglycerides, plasma cholesterol and very low Density Lipoprotein cholesterol. On univariate analysis, with and without adjustment for differences in plasma cholesterol levels between the two groups, there were no significant differences in extent or severity of atherosclerosis between insulin and placebo rabbits. Furthermore, after combining the results from all the rabbits to examine plasma insulin levels and the other variables mentioned above as predictors of atherosclerosis severity, plasma insulin level was not a predictor, on univariate or multiple linear regression analysis; the first ranked independent predictors were postprandial Intermediate Density Lipoprotein cholesterol in the arch, and postprandial plasma triglyceride in both the thoracic and abdominal aorta. These results suggest that exogenous hyperinsulinaemia does not promote atherogenesis in cholesterol-fed rabbits, but that postprandial levels of Intermediate Density Lipoprotein cholesterol or plasma triglycerides may be involved in atherogenesis.
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letter to the editors Intermediate Density Lipoprotein cholesterol as the best Lipoprotein predictor of atherosclerosis severity in the watanabe heritable hyperlipidemic rabbit
1997Co-Authors: Borge G Nordestgaard, Per Ibsen, Jorgen Fischer Hansen, Birgit Fischer Hansen, Alicja Mortensen, Birgit Agerholmlarsen, Knud KjeldsenAbstract:Dear Editors,Zilversmit proposed that atherogenesis might be apostprandial phenomena [1], implying that chylomicronremnants and even very low Density Lipoprotein(VLDL) remnants, the so-called Intermediate Densitylipoprotien (IDL) particles, may share with low DensityLipoprotein (LDL) the ability to cause atherosclerosis.This hypothesis has gained strength over the years [2,3].Familial hypercholesterolemia (FH), a disordercaused by defects in the LDL-receptor leading to highLDL levels and premature atherosclerosis [4], repre-sents an important observation supporting a role forLDL as the most atherogenic Lipoprotein. Both LDLand IDL levels are, however, elevated in patients withFH [4]. The relative role of these two Lipoproteins or ofchylomicron remnants in promoting atherosclerosis inFH, is at present unknown.In the present study we took advantage of the exis-tence of an animal model of FH, the Watanabe Herita-ble Hyperlipidemic (WHHL) rabbit that also hasdefective LDL-receptors [4], to examine the relativeimportance of chylomicron remnants, IDL and LDL inatherogenesis: fasting (24 h after last meal) and post-prandial (2–4 h after the daily meal) levels of choles-terol and triglycerides (CHOD-PAP and GPO- PAP,Boehringer Mannheim) in total plasma, and in theVLDL (
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IDL, VLDL, chylomicrons and atherosclerosis.
European Journal of Epidemiology, 1992Co-Authors: Borge G Nordestgaard, Anne Tybjærg-hansenAbstract:In humans with the Lipoprotein lipase deficiency disorder large amounts of chylomicrons and large very low-Density Lipoprotein (VLDL) accumulate in plasma. In spite of this, atherosclerosis does not seem to develop at an accelerated rate, suggesting that these Lipoproteins do not promote atherogenesis. In humans with dysbetaLipoproteinemia remnant Lipoproteins (Intermediate Density Lipoprotein (IDL) plus B-VLDL) accumulate in plasma and these particles may therefore be the factor causing accelerated atherosclerosis in this disorder.
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Intermediate Density Lipoprotein levels are strong predictors of the extent of aortic atherosclerosis in the st thomas s hospital rabbit strain
Atherosclerosis, 1991Co-Authors: Borge G Nordestgaard, Barry LewisAbstract:Abstract This study assessed nonfasting cholesterol and triglyceride in plasma and in Lipoproteins as predictors of the extent of aortic atherosclerosis in 2 similar groups of rabbits from the St. Thomas's Hospital strain; the Lipoprotein classes studied in the 2 groups were very low (VLDL), Intermediate (IDL), low (LDL), and high Density Lipoprotein (HDL), and Sf > 60 Lipoprotein, Sf 12–60 Lipoprotein, LDL and HDL, respectively. These rabbits exhibit elevated plasma levels of VLDL, IDL, and LDL, with plasma cholesterol and triglyceride of up to 23 mmol/1 and 7 mmol/l, respectively, and with up to 100% of the aortic intima bearing atherosclerosis-like lesions. In group 1 rabbits ( n = 25), univariate linear regression showed that cholesterol in plasma, LDL, IDL and in VLDL each were positively associated with the extent of aortic atherosclerosis. In group 2 rabbits ( n = 20), cholesterol in plasma, LDL and Sf 12–60, but not in Sf > 60 Lipoprotein, was consistently positively associated with the extent of aortic atherosclerosis. Neither plasma triglyceride, triglyceride in Lipoprotein fractions nor HDL cholesterol was associated consistently with the extent of atherosclerosis. Using step-up multiple linear regression among Lipoprotein lipids, IDL and Sf 12–60 Lipoprotein cholesterol were the most powerful independent predictors of the extent of aortic atherosclerosis in the 2 groups of rabbits. LDL cholesterol was the only other independent predictor. The results suggest that remnant Lipoproteins, whether defined as IDL or Sf 12–60 Lipoprotein, play an important causal role in atherosclerosis under conditions where plasma levels of these Lipoproteins are elevated.
Tatsuo Hosoya - One of the best experts on this subject based on the ideXlab platform.
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delayed in vivo catabolism of Intermediate Density Lipoprotein and low Density Lipoprotein in hemodialysis patients as potential cause of premature atherosclerosis
Arteriosclerosis Thrombosis and Vascular Biology, 2005Co-Authors: Katsunori Ikewaki, Keio Okubo, Benjamin Dieplinger, Evi Trenkwalder, Michael E. Frischmann, Juergen R Schaefer, Horst Schweer, Tatsuo Hosoya, Seibu Mochizuki, Florian KronenbergAbstract:Objective— Premature cardiovascular disease is the leading cause of death in patients with end-stage renal disease treated by hemodialysis (HD). Low-Density Lipoprotein (LDL) levels are not general...
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Delayed In Vivo Catabolism of Intermediate-Density Lipoprotein and Low-Density Lipoprotein in Hemodialysis Patients as Potential Cause of Premature Atherosclerosis
Arteriosclerosis Thrombosis and Vascular Biology, 2005Co-Authors: Katsunori Ikewaki, Keio Okubo, Benjamin Dieplinger, Evi Trenkwalder, Michael E. Frischmann, Juergen R Schaefer, Horst Schweer, Tatsuo Hosoya, Seibu Mochizuki, Florian KronenbergAbstract:Objective— Premature cardiovascular disease is the leading cause of death in patients with end-stage renal disease treated by hemodialysis (HD). Low-Density Lipoprotein (LDL) levels are not generally increased in HD patients, but their LDL metabolism is still poorly understood. We therefore investigated the in vivo metabolism of apoB-containing Lipoproteins in two different ethnic populations of HD patients and controls. Methods and Results— We performed stable isotope kinetic studies using a primed constant infusion of deuterated leucine in 12 HD patients and 13 healthy controls. Tracer/tracee ratio of apoB was determined by means of gas chromatography/mass spectrometry, and the modeling program SAAMII was used to estimate the fractional catabolic rate (FCR) of apoB. Mean LDL-apoB plasma concentrations were almost identical in both groups (HD: 95±30 mg/dL, controls: 91±40 mg/dL), whereas LDL-apoB FCR was 50% lower in HD patients as compared with controls (0.22±0.12 days−1 versus 0.46±0.20 days−1, P =0.001) with concomitantly decreased production rates of LDL. Compared with controls, Intermediate-Density Lipoprotein (IDL)-apoB FCR was 65% lower (2.87±1.02 days−1 versus 8.89±4.94 days−1, P =0.014), accompanied by 1.5-fold higher IDL-apoB levels in HD. Very low-Density Lipoprotein metabolism was similar in both study groups. Conclusions— In vivo catabolism of LDL and IDL is severely impaired in HD patients but misleadingly masked by normal plasma cholesterol levels. The resulting markedly prolonged residence times of both IDL and LDL particles might thus significantly contribute to the well-documented high risk for premature cardiovascular disease in HD patients.
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Role of hepatic lipase in Intermediate-Density Lipoprotein and small, dense low-Density Lipoprotein formation in hemodialysis patients
Kidney International, 1999Co-Authors: Keiko Oi, Soichi Sakai, Yoshindo Kawaguchi, Tsutomu Hirano, Tatsuo HosoyaAbstract:Role of hepatic lipase in Intermediate-Density Lipoprotein and small, dense low-Density Lipoprotein formation in hemodialysis patients. Background It has been reported that remnant Lipoproteins and small, dense low-Density Lipoproteins (LDLs) are risk factors for cardiovascular disease. To determine whether these risk factors are present in hemodialysis (HD) patients who are suffering from a high incidence of atherosclerotic vascular disease, we measured concentrations of remnant Lipoproteins and LDL particle diameter in HD patients and compared these with controls. We also measured Lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) that play important roles in the generation of remnant Lipoproteins and small, dense LDL, and we correlated these changes with plasma Lipoprotein abnormalities in HD patients. Methods Lipoproteins were separated by ultracentrifugation. Apoprotein B in very low-Density Lipoprotein (VLDL), and Intermediate-Density Lipoprotein (IDL) fractions were measured by a sensitive enzyme-linked immunosorbent assay method. The average LDL particle diameter was measured by gradient gel electrophoresis. Results Plasma triglyceride, total cholesterol, and high-Density Lipoprotein (HDL) cholesterol concentrations were comparable between HD patients and controls, whereas LDL cholesterol was significantly lower in HD patients. The average LDL particle diameter was not significantly different between HD patients and controls. LDL particle diameter was inversely related to plasma triglyceride concentrations in all of the subjects. VLDL triglyceride, VLDL cholesterol, and VLDL apoprotein B were comparable between HD patients and controls. IDL triglyceride, IDL cholesterol, and IDL apoprotein B concentrations were all significantly increased in HD patients compared with those in controls. LPL mass was not altered, but HTGL activity was significantly decreased in HD patients. The HTGL activity was inversely related to IDL concentrations. Conclusions These results suggest that a prominent characteristic of Lipoprotein abnormalities in HD patients is a marked increase in IDL particle number. In addition, small, dense LDL is not associated with uremic dyslipidemia. Because HTGLs promote the conversion from IDL to LDL and the generation of lipid-poor LDL, a decrease in HTGL activity may contribute to the accumulation of IDL particle and may prevent small, dense LDL formation in HD patients.
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Role of hepatic lipase in Intermediate-Density Lipoprotein and small, dense low-Density Lipoprotein formation in hemodialysis patients.
Kidney international. Supplement, 1999Co-Authors: Keiko Oi, Soichi Sakai, Yoshindo Kawaguchi, Tsutomu Hirano, Tatsuo HosoyaAbstract:It has been reported that remnant Lipoproteins and small, dense low-Density Lipoproteins (LDLs) are risk factors for cardiovascular disease. To determine whether these risk factors are present in hemodialysis (HD) patients who are suffering from a high incidence of atherosclerotic vascular disease, we measured concentrations of remnant Lipoproteins and LDL particle diameter in HD patients and compared these with controls. We also measured Lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) that play important roles in the generation of remnant Lipoproteins and small, dense LDL, and we correlated these changes with plasma Lipoprotein abnormalities in HD patients. Lipoproteins were separated by ultracentrifugation. Apoprotein B in very low-Density Lipoprotein (VLDL), and Intermediate-Density Lipoprotein (IDL) fractions were measured by a sensitive enzyme-linked immunosorbent assay method. The average LDL particle diameter was measured by gradient gel electrophoresis. Plasma triglyceride, total cholesterol, and high-Density Lipoprotein (HDL) cholesterol concentrations were comparable between HD patients and controls, whereas LDL cholesterol was significantly lower in HD patients. The average LDL particle diameter was not significantly different between HD patients and controls. LDL particle diameter was inversely related to plasma triglyceride concentrations in all of the subjects. VLDL triglyceride, VLDL cholesterol, and VLDL apoprotein B were comparable between HD patients and controls. IDL triglyceride, IDL cholesterol, and IDL apoprotein B concentrations were all significantly increased in HD patients compared with those in controls. LPL mass was not altered, but HTGL activity was significantly decreased in HD patients. The HTGL activity was inversely related to IDL concentrations. These results suggest that a prominent characteristic of Lipoprotein abnormalities in HD patients is a marked increase in IDL particle number. In addition, small, dense LDL is not associated with uremic dyslipidemia. Because HTGLs promote the conversion from IDL to LDL and the generation of lipid-poor LDL, a decrease in HTGL activity may contribute to the accumulation of IDL particle and may prevent small, dense LDL formation in HD patients.
Masahiko Okada - One of the best experts on this subject based on the ideXlab platform.
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Surfactant-Based Homogeneous Assay for the Measurement of Triglyceride Concentrations in VLDL and Intermediate-Density Lipoprotein
Clinical Chemistry, 2005Co-Authors: Masahiko Okada, Yasuhiko Noguchi, Tomohiro Saito, Hajime Yoshimura, Hiroko Sasaki, Hitoshi HamaAbstract:Background: Existing studies have demonstrated the clinical significance of triglyceride content in VLDL (VLDL-TG) and Intermediate-Density Lipoprotein (IDL-TG). We developed a homogeneous assay protocol to directly measure VLDL-TG. Methods: Possible reagents and conditions for measuring VLDL-TG were comprehensively tested, and the “best” combination was determined. Healthy persons were instructed to consume a fatty meal after 15-h overnight fasting. Serum VLDL-TG + IDL-TG concentrations were measured using the proposed method. Patients with serum LDL-cholesterol concentrations ≥3.62 mmol/L (140 mg/dL) were administered simvastatin at a daily dose of 5 mg, and serum VLDL-TG concentrations were then measured. Results: The combination of 2 nonionic surfactants played an important role in differentiating VLDL and IDL from other Lipoproteins, probably via specific interactions with phospholipids and apoLipoproteins. The regression line of the proposed method ( y ) and the ultracentrifugal assay ( x ) was: y = 0.98 x + 0.31 mmol/L ( r = 0.98; n = 73; P
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surfactant based homogeneous assay for the measurement of triglyceride concentrations in vldl and Intermediate Density Lipoprotein
Clinical Chemistry, 2005Co-Authors: Masahiko Okada, Yasuhiko Noguchi, Tomohiro Saito, Hajime Yoshimura, Hiroko Sasaki, Taeko Ito, Hitoshi HamaAbstract:Background: Existing studies have demonstrated the clinical significance of triglyceride content in VLDL (VLDL-TG) and Intermediate-Density Lipoprotein (IDL-TG). We developed a homogeneous assay protocol to directly measure VLDL-TG. Methods: Possible reagents and conditions for measuring VLDL-TG were comprehensively tested, and the “best” combination was determined. Healthy persons were instructed to consume a fatty meal after 15-h overnight fasting. Serum VLDL-TG + IDL-TG concentrations were measured using the proposed method. Patients with serum LDL-cholesterol concentrations ≥3.62 mmol/L (140 mg/dL) were administered simvastatin at a daily dose of 5 mg, and serum VLDL-TG concentrations were then measured. Results: The combination of 2 nonionic surfactants played an important role in differentiating VLDL and IDL from other Lipoproteins, probably via specific interactions with phospholipids and apoLipoproteins. The regression line of the proposed method ( y ) and the ultracentrifugal assay ( x ) was: y = 0.98 x + 0.31 mmol/L ( r = 0.98; n = 73; P <0.05). The difference between postprandial total TG and VLDL-TG concentrations was statistically significant ( P <0.05). After 8 weeks of therapy with simvastatin, total TG and LDL-cholesterol concentrations were 13.6% and 26.3% lower, respectively ( P <0.05), whereas VLDL-TG did not show any significant decrease. Conclusion: Our homogeneous method can measure TG content in VLDL and IDL.
D. C. Anderson - One of the best experts on this subject based on the ideXlab platform.
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The effect of bezafibrate on very low Density Lipoprotein (VLDL), Intermediate Density Lipoprotein (IDL), and low Density Lipoprotein (LDL) composition in type 1 diabetes associated with hypercholesterolaemia or combined hyperlipidaemia.
Atherosclerosis, 1992Co-Authors: P H Winocour, D Bhatagnar, M Ishola, Mike Mackness, Sharon Arrol, Paul N. Durrington, D. C. AndersonAbstract:Lipoprotein composition was examined in type 1 diabetic subjects with hypercholesterolaemia +/- hypertriglyceridaemia during a 3-month double-blind placebo controlled assessment of bezafibrate therapy. The predominant effect was on Lipoprotein lipid content. In those with hypercholesterolaemia alone, bezafibrate significantly reduced the cholesterol (particularly esterified cholesterol) and triglyceride content of large very low Density Lipoprotein (VLDL) (Svedberg flotation units (Sf) 60-400) in comparison to the placebo group (P less than 0.05), and a trend towards a reduction in free and esterified cholesterol within the Intermediate Density Lipoprotein fraction (IDL) (Sf 12-20) was noted. Low Density Lipoprotein (LDL) composition was unaltered and in general phospholipid and protein concentrations and cholesteryl ester/protein ratios within the Lipoprotein fractions were unaffected. Large VLDL cholesterol and triglyceride concentrations in those with combined hyperlipidaemia were significantly decreased following bezafibrate therapy, both in comparison to placebo-treated subjects and to baseline concentrations (P less than 0.05). An additional significant reduction in small VLDL (Sf 20-60) free cholesterol was recorded (P less than 0.05). Average reductions of large and small VLDL protein of 50-56% were not significant because of wide variation in responses. Bezafibrate had no effect on the abnormal composition of IDL and LDL, characteristic of Type 1 diabetes, regardless of whether or not hypertriglyceridaemia was associated with hypercholesterolaemia. Its major action was to lower VLDL lipid concentrations, but it may also reduce the lipid content of Intermediate Density Lipoprotein in Type 1 diabetes.
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The effect of bezafibrate on very low Density Lipoprotein (VLDL), Intermediate Density Lipoprotein (IDL), and low Density Lipoprotein (LDL) composition in Type 1 diabetes associated with hypercholesterolaemia or combined hyperlipidaemia
Atherosclerosis, 1992Co-Authors: P H Winocour, D Bhatagnar, M Ishola, Mike Mackness, Sharon Arrol, Paul N. Durrington, D. C. AndersonAbstract:Lipoprotein composition was examined in type 1 diabetic subjects with hypercholesterolaemia ± hypertriglyceridaemia during a 3-month double-blind placebo controlled assessment of bezafibrate therapy. The predominant effect was on Lipoprotein lipid content. In those with hypercholesterolaemia alone, bezafibrate significantly reduced the cholesterol (particularly esterified cholesterol) and triglyceride content of large very low Density Lipoprotein (VLDL) (Svedberg flotation units (Sf) 60–400) in comparison to the placebo group (P < 0.05), and a trend towards a reduction in free and esterified cholesterol within the Intermediate Density Lipoprotein fraction (IDL) (Sf 12–20) was noted. Low Density Lipoprotein (LDL) composition was unaltered and in general phospholipid and protein concentrations and cholesteryl ester/protein ratios within the Lipoprotein fractions were unaffected. Large VLDL cholesterol and triglyceride concentrations in those with combined hyperlipidaemia were significantly decreased following bezafibrate therapy, both in comparison to placebo-treated subjects and to baseline concentrations (P < 0.05). An additional significant reduction in small VLDL (Sf 20–60) free cholesterol was recorded (P < 0.05). Average reductions of large and small VLDL protein of 50–56% were not significant because of wide variation in responses. Bezafibrate had no effect on the abnormal composition of IDL and LDL, characteristic of Type 1 diabetes, regardless of whether or not hypertriglyceridaemia was associated with hypercholesterolaemia. Its major action was to lower VLDL lipid concentrations, but it may also reduce the lipid content of Intermediate Density Lipoprotein in Type 1 diabetes.