BIOMAT Database Logo BIOMAT Database Logo

Catabolism of very-low-density lipoproteins in subjects with broad beta disease: comparison with endogenous hypertriglyceridemia. 1982

R S Kushwaha, and A Chait, and W R Hazzard

The catabolic rates of VLDL apo-B from subjects with broad beta disease (type III hyperlipoproteinemia) and from subjects with endogenous hypertriglyceridemia (type IV hyperlipoproteinemia) were compared in recipients with these disorders. In subjects with broad beta disease, disappearance of autologous VLDL apo-B was slower than that of isologous VLDL apo-B from subjects with a type IV lipoprotein pattern (FCR 0.049 +/- 0.03 hr-1 for autologous vs. 0.068 +/- 0.035 for isologous, n = 6, p less than 0.05). However, the FCRs of autologous and isologous VLDL apo-B in subjects with type IV hyperlipoproteinemia were the same (0.110 +/- 0.051 hr-1 for autologous vs. 0.110 +/- 0.063 for isologous, n = 4, p = NS). In vitro studies suggested that 125I-VLDL from subjects with endogenous hypertriglyceridemia retained most of the smaller peptides (87.5% +/- 1.8 apo E and 75.7% +/- 1.6 apo C) when incubated with plasma from subjects with broad beta disease. By contrast, 125I-labeled IDLs from subjects with broad beta disease exchanged these lipoproteins rapidly (retaining only 7.9% +/- 0.03 apo-E and 8.2% +/- 0.3 apo-C) when incubated with plasma from subjects with endogenous hypertriglyceridemia. Similarly, beta-VLDL isolated from a subject with broad beta disease by preparative electrophoresis, when incubated with plasma from a subject with endogenous hypertriglyceridemia, exchanged its apo-E with the normal VLDL (56% being recovered in VLDL of alpha2 mobility). Normal VLDL, however, retained most (93.3%) of its VLDL apo-E radioactivity when incubated with plasma from a subject with broad beta disease. These observations suggest that the abnormal composition of autologous VLDL may in part be responsible for its delayed clearance in subjects with broad beta disease.

UI MeSH Term Description Entries
D006952 Hyperlipoproteinemia Type III An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides. Autosomal Recessive Hypercholesterolemia,Broad Beta Disease,Dysbetalipoproteinemia,Dysbetalipoproteinemia, Familial,Familial Dysbetalipoproteinemia,Familial Hypercholesterolemia with Hyperlipemia,Hypercholesterolemia, Autosomal Recessive,Hyperlipoproteinemia, Broad-beta,Hyperlipoproteinemia, Type III,Autosomal Recessive Hypercholesterolemias,Broad-beta Hyperlipoproteinemia,Hyperlipoproteinemia, Broad beta,Hyperlipoproteinemias, Type III,Recessive Hypercholesterolemia, Autosomal,Type III Hyperlipoproteinemia,Type III Hyperlipoproteinemias
D006953 Hyperlipoproteinemia Type IV A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits. Hyperprebetalipoproteinemia,Hypertriglyceridemia, Familial,Carbohydrate Inducible Hyperlipemia,Carbohydrate-Inducible Hyperlipemia,Familial Hyperlipoproteinemia Type 4,Familial Type IV Hyperlipoproteinemia,Hyper prebeta lipoproteinemia,Hyperlipoproteinemia, Type IV,Carbohydrate Inducible Hyperlipemias,Carbohydrate-Inducible Hyperlipemias,Familial Hypertriglyceridemia,Hyperlipemia, Carbohydrate Inducible,Hyperlipemia, Carbohydrate-Inducible,Hyperlipemias, Carbohydrate Inducible,Hyperlipemias, Carbohydrate-Inducible,Hyperlipoproteinemias, Type IV,Inducible Hyperlipemia, Carbohydrate,Inducible Hyperlipemias, Carbohydrate,Type IV Hyperlipoproteinemia,Type IV Hyperlipoproteinemias,Type IV, Hyperlipoproteinemia
D008077 Lipoproteins, LDL A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues. Low-Density Lipoprotein,Low-Density Lipoproteins,beta-Lipoprotein,beta-Lipoproteins,LDL(1),LDL(2),LDL-1,LDL-2,LDL1,LDL2,Low-Density Lipoprotein 1,Low-Density Lipoprotein 2,LDL Lipoproteins,Lipoprotein, Low-Density,Lipoproteins, Low-Density,Low Density Lipoprotein,Low Density Lipoprotein 1,Low Density Lipoprotein 2,Low Density Lipoproteins,beta Lipoprotein,beta Lipoproteins
D008079 Lipoproteins, VLDL A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues. Pre-beta-Lipoprotein,Prebeta-Lipoprotein,Prebeta-Lipoproteins,Very Low Density Lipoprotein,Very-Low-Density Lipoprotein,Very-Low-Density Lipoproteins,Lipoprotein VLDL II,Lipoproteins, VLDL I,Lipoproteins, VLDL III,Lipoproteins, VLDL1,Lipoproteins, VLDL2,Lipoproteins, VLDL3,Pre-beta-Lipoproteins,Lipoprotein, Very-Low-Density,Lipoproteins, Very-Low-Density,Pre beta Lipoprotein,Pre beta Lipoproteins,Prebeta Lipoprotein,Prebeta Lipoproteins,VLDL Lipoproteins,VLDL1 Lipoproteins,VLDL2 Lipoproteins,VLDL3 Lipoproteins,Very Low Density Lipoproteins
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D002784 Cholesterol The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. Epicholesterol
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults

Related Publications

R S Kushwaha, and A Chait, and W R Hazzard
Compositional and metabolic heterogeneity of alpha 2- and beta-very-low-density lipoproteins in subjects with broad beta disease and endogenous hypertriglyceridemia.
November 1985, Metabolism: clinical and experimental,
R S Kushwaha, and A Chait, and W R Hazzard
Catabolism of alpha2-and beta-very low density lipoproteins in normal and hyperlipidemic subjects.
January 1981, Transactions of the Association of American Physicians,
R S Kushwaha, and A Chait, and W R Hazzard
Broad-beta disease versus endogenous hypertriglyceridemia: levels and lipid composition of chylomicrons and very low density lipoproteins during fat-free feeding and alimentary lipemia.
July 1975, Metabolism: clinical and experimental,
R S Kushwaha, and A Chait, and W R Hazzard
The catabolism of very low density lipoproteins.
August 1985, Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire,
R S Kushwaha, and A Chait, and W R Hazzard
The spectrum of electrophoretic mobility of very low density lipoproteins: role of slower migrating species in endogenous hypertriglyceridemia (type IV hyperlipoproteinemia) and broad-beta disease (type III).
August 1975, The Journal of laboratory and clinical medicine,
R S Kushwaha, and A Chait, and W R Hazzard
Catabolism of very low density lipoproteins in experimental nephrosis.
October 1984, The Journal of clinical investigation,
R S Kushwaha, and A Chait, and W R Hazzard
Hypertriglyceridemia in Watanabe heritable hyperlipidemic rabbits was associated with increased production and reduced catabolism of very-low-density lipoproteins.
January 2009, Pathobiology : journal of immunopathology, molecular and cellular biology,
R S Kushwaha, and A Chait, and W R Hazzard
Abnormal lipid composition of very low density lipoproteins in diagnosis of broad-beta disease (type 3 hyperlipoproteinemia).
November 1972, Metabolism: clinical and experimental,
R S Kushwaha, and A Chait, and W R Hazzard
Catabolism of human very-low-density lipoproteins in monkeys: the appearance of human very-low-density lipoprotein peptides in monkey high-density lipoproteins.
July 1972, Biochimica et biophysica acta,
R S Kushwaha, and A Chait, and W R Hazzard
Impaired catabolism of very low-density lipoprotein-triglyceride in a family with primary hypertriglyceridemia.
April 1985, Metabolism: clinical and experimental,
Copied contents to your clipboard!