Key result
VLDL tracer studies reveal markedly depressed fractional catabolic rates of apo-B in type V hyperlipoproteinemia.
Why the study?
The metabolic abnormalities of apolipoproteins in VLDL in primary type V hyperlipoproteinaemia were not fully characterized.
Observational (n=3)
Type V hyperlipoproteinaemia appears to be largely due to impaired rates of formation and breakdown of apo-B in VLDL.
Supports catabolic defect in type V hyperlipoproteinaemia; leaves open confirmation in larger studies.
The metabolism of the apolipoproteins of very low density lipoprotein (VLDL) was studied in three subjects with primary type V hyperlipoproteinaemia (HLP) after injection of autologous 125I‐labelled VLDL of Sf 100–400. The fractional disappearance rate of total radioactivity was stable during the two‐week period of study. Transfer of apolipoprotein C (apo‐C) from VLDL to high density lipoprotein (HDL) occurred both in vivo and in vitro upon mixing the labelled VLDL preparation with serum and significant amounts of 125I‐labelled apoli‐poprotein B (apo‐B) and apo‐C were recovered in the chylomicron fraction (Sf >400) in both situations. The time‐courses of the disappearance of specific activity from VLDL (Sf 20–400) and its appearance in low density lipoprotein (LDL) are consistent with apo‐B in VLDL (VLDL‐B) being the precursor of that in LDL. In comparison to studies in which the whole VLDL class (Sf 20–400) was labelled, the rate of synthesis of VLDL‐B was slightly decreased and the fractional rates of catabolism (FCRs) of apo‐B in VLDL and in the whole spectrum of VLDL+chylomicrons were markedly depressed. In turn, the rate of formation of LDL was low, and its FCR was probably slightly decreased. The findings are consistent with the belief that in these three subjects the type V HLP is to a great extent due to impaired rates of formation and breakdown of apo‐B in VLDL. They do not exclude the possibility that the disorder is also caused by an increased rate of formation of chylomicrons.
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Ballantyne et al. (1977) conducted an observational in Primary type V hyperlipoproteinaemia (n=3). Autologous 125I-labelled VLDL of Sf 100-400 vs. Whole VLDL class (Sf 20-400) labelling was evaluated on Fractional disappearance rate of total radioactivity and apolipoprotein metabolism. In 3 subjects with type V hyperlipoproteinaemia, 125I-labelled VLDL tracer studies revealed markedly depressed fractional catabolic rates of apo-B in VLDL compared to whole VLDL labelling.
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