Low density lipoprotein metabolism in hypertriglyceridemic and normolipidemic patients with coronary heart disease

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Abstract

The turnover rates of low density lipoprotein-apolipoprotein B (LDL-apoB) were determined in 32 men with coronary heart disease (CHD) and 11 control men with normal plasma lipids. Thirty patients with CHD had normal levels of LDL-cholesterol (LDL-C); of these patients, 9 had hypertriglyceridemia and 21 had normal plasma lipids. Mean concentrations of total cholesterol and LDL-C were similar among the control subjects and CHD patients, although the latter had significantly lower HDL-C. In control subjects, transport rates and fractional catabolic rates (FCR) of LDL-B were 10.6 ± 0.5 (SEM) mg/kg-day and 0.31 ± 0.01 pools/day, respectively. In 10 hypertriglyceridemic patients with CHD, transport rates were 21.7 ± 1.7 mg/kg-day, and FCRs averaged 0.56 ± 0.006 pools/day; both were significantly higher than norml (P < 0.05). Six normolipidemic patients also had abnormally high transport rates of LDL-apoB (19.4 ± 2.8 mg/kg-day) and FCRs (0.51 ± 0.03 pools/day); again both were higher than normal. The remaining 16 normolipidemic patients with CHD had normal transport rates (9.9 ± 0.6 mg/kg-day) and FCRs (0.28 ± 0.01 pools/day). Thus, hypertriglyceridemic patients with CHD and a portion of normolipidemic patients with CHD were characterized by increases in both transport and fractional catabolic rate of LDL-apoB; these abnormalities in LDL metabolism may have contributed to their coronary heart disease. However, the majority of normolipidemic patients with CHD did not show a distinct defect in their LDL metabolism.

Original languageEnglish (US)
Pages (from-to)115-126
Number of pages12
JournalJournal of Lipid Research
Volume26
Issue number1
StatePublished - 1985

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LDL Lipoproteins
Metabolism
Coronary Disease
Apolipoproteins B
LDL Cholesterol
Lipids
Plasmas
Hypertriglyceridemia
Cholesterol
Defects
Scanning electron microscopy

ASJC Scopus subject areas

  • Endocrinology

Cite this

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title = "Low density lipoprotein metabolism in hypertriglyceridemic and normolipidemic patients with coronary heart disease",
abstract = "The turnover rates of low density lipoprotein-apolipoprotein B (LDL-apoB) were determined in 32 men with coronary heart disease (CHD) and 11 control men with normal plasma lipids. Thirty patients with CHD had normal levels of LDL-cholesterol (LDL-C); of these patients, 9 had hypertriglyceridemia and 21 had normal plasma lipids. Mean concentrations of total cholesterol and LDL-C were similar among the control subjects and CHD patients, although the latter had significantly lower HDL-C. In control subjects, transport rates and fractional catabolic rates (FCR) of LDL-B were 10.6 ± 0.5 (SEM) mg/kg-day and 0.31 ± 0.01 pools/day, respectively. In 10 hypertriglyceridemic patients with CHD, transport rates were 21.7 ± 1.7 mg/kg-day, and FCRs averaged 0.56 ± 0.006 pools/day; both were significantly higher than norml (P < 0.05). Six normolipidemic patients also had abnormally high transport rates of LDL-apoB (19.4 ± 2.8 mg/kg-day) and FCRs (0.51 ± 0.03 pools/day); again both were higher than normal. The remaining 16 normolipidemic patients with CHD had normal transport rates (9.9 ± 0.6 mg/kg-day) and FCRs (0.28 ± 0.01 pools/day). Thus, hypertriglyceridemic patients with CHD and a portion of normolipidemic patients with CHD were characterized by increases in both transport and fractional catabolic rate of LDL-apoB; these abnormalities in LDL metabolism may have contributed to their coronary heart disease. However, the majority of normolipidemic patients with CHD did not show a distinct defect in their LDL metabolism.",
author = "Vega, {Gloria L} and Beltz, {W. F.} and Grundy, {Scott M}",
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T1 - Low density lipoprotein metabolism in hypertriglyceridemic and normolipidemic patients with coronary heart disease

AU - Vega, Gloria L

AU - Beltz, W. F.

AU - Grundy, Scott M

PY - 1985

Y1 - 1985

N2 - The turnover rates of low density lipoprotein-apolipoprotein B (LDL-apoB) were determined in 32 men with coronary heart disease (CHD) and 11 control men with normal plasma lipids. Thirty patients with CHD had normal levels of LDL-cholesterol (LDL-C); of these patients, 9 had hypertriglyceridemia and 21 had normal plasma lipids. Mean concentrations of total cholesterol and LDL-C were similar among the control subjects and CHD patients, although the latter had significantly lower HDL-C. In control subjects, transport rates and fractional catabolic rates (FCR) of LDL-B were 10.6 ± 0.5 (SEM) mg/kg-day and 0.31 ± 0.01 pools/day, respectively. In 10 hypertriglyceridemic patients with CHD, transport rates were 21.7 ± 1.7 mg/kg-day, and FCRs averaged 0.56 ± 0.006 pools/day; both were significantly higher than norml (P < 0.05). Six normolipidemic patients also had abnormally high transport rates of LDL-apoB (19.4 ± 2.8 mg/kg-day) and FCRs (0.51 ± 0.03 pools/day); again both were higher than normal. The remaining 16 normolipidemic patients with CHD had normal transport rates (9.9 ± 0.6 mg/kg-day) and FCRs (0.28 ± 0.01 pools/day). Thus, hypertriglyceridemic patients with CHD and a portion of normolipidemic patients with CHD were characterized by increases in both transport and fractional catabolic rate of LDL-apoB; these abnormalities in LDL metabolism may have contributed to their coronary heart disease. However, the majority of normolipidemic patients with CHD did not show a distinct defect in their LDL metabolism.

AB - The turnover rates of low density lipoprotein-apolipoprotein B (LDL-apoB) were determined in 32 men with coronary heart disease (CHD) and 11 control men with normal plasma lipids. Thirty patients with CHD had normal levels of LDL-cholesterol (LDL-C); of these patients, 9 had hypertriglyceridemia and 21 had normal plasma lipids. Mean concentrations of total cholesterol and LDL-C were similar among the control subjects and CHD patients, although the latter had significantly lower HDL-C. In control subjects, transport rates and fractional catabolic rates (FCR) of LDL-B were 10.6 ± 0.5 (SEM) mg/kg-day and 0.31 ± 0.01 pools/day, respectively. In 10 hypertriglyceridemic patients with CHD, transport rates were 21.7 ± 1.7 mg/kg-day, and FCRs averaged 0.56 ± 0.006 pools/day; both were significantly higher than norml (P < 0.05). Six normolipidemic patients also had abnormally high transport rates of LDL-apoB (19.4 ± 2.8 mg/kg-day) and FCRs (0.51 ± 0.03 pools/day); again both were higher than normal. The remaining 16 normolipidemic patients with CHD had normal transport rates (9.9 ± 0.6 mg/kg-day) and FCRs (0.28 ± 0.01 pools/day). Thus, hypertriglyceridemic patients with CHD and a portion of normolipidemic patients with CHD were characterized by increases in both transport and fractional catabolic rate of LDL-apoB; these abnormalities in LDL metabolism may have contributed to their coronary heart disease. However, the majority of normolipidemic patients with CHD did not show a distinct defect in their LDL metabolism.

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