May 1, 2000Arteriosclerosis Thrombosis and Vascular Biology

In Vivo Metabolism of ApoB, ApoA-I, and VLDL Triglycerides in a Form of Hypobetalipoproteinemia Not Linked to the ApoB Gene

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Why the study?

Does a novel form of FHBL linked to chromosome 3p21.1-2 alter the in vivo kinetics of apoB, apoA-I, and VLDL triglycerides compared to normolipidemic relatives?

Structured PICO

Does a novel form of FHBL linked to chromosome 3p21.1-2 alter the in vivo kinetics of apoB, apoA-I, and VLDL triglycerides compared to normolipidemic relatives?

Population

9 subjects from the F kindred, including 4 affected with familial hypobetalipoproteinemia (FHBL) linked to chromosome 3p21.1-2 and 5 normolipidemic relatives

Intervention

In vivo kinetic study using deuterated leucine and deuterated glycerol to label apolipoproteins and triglycerides

Comparator

Normolipidemic relatives

Outcome

Fractional catabolic rates (FCRs) and production rates of apoB, apoA-I, and VLDL triglyceridessurrogate

Decreased secretion of apoB-containing lipoproteins and hypercatabolism of LDL account for low apoB and cholesterol levels in this novel form of FHBL.

Discussion

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Implication

Supports apoB kinetic defects as mechanism in novel FHBL; leaves open applicability to other hypobetalipoproteinemia variants.

Cite This Study

Elias et al. (2000) studied this question.

synapsesocial.com/papers/6a1eded2cbc03da829ac866e https://doi.org/10.1161/01.atv.20.5.1309

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In Vivo Metabolism of ApoB, ApoA-I, and VLDL Triglycerides in a Form of Hypobetalipoproteinemia Not Linked to the ApoB Gene

Structured PICO

Discussion

Implication

Cite This Study

In Vivo Metabolism of ApoB, ApoA-I, and VLDL Triglycerides in a Form of Hypobetalipoproteinemia Not Linked to the ApoB Gene

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider