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Familial combined hyperlipidaemia: use of stable isotopes to demonstrate overproduction of very low-density lipoprotein apolipoprotein B by the liver.

作者信息

Cortner J A, Coates P M, Bennett M J, Cryer D R, Le N A

机构信息

Lipid-Heart Research Center, Children's Hospital of Philadelphia, PA 19104.

出版信息

J Inherit Metab Dis. 1991;14(6):915-22. doi: 10.1007/BF01800473.

DOI:10.1007/BF01800473
PMID:1779650
Abstract

We have assessed very low-density lipoprotein apolipoprotein B production, using [15N]glycine as an endogenous marker in a 9-hour primed constant infusion protocol, in four adult male subjects with familial combined hyperlipidaemia and in four normolipidaemic adult male controls. The mean very low-density lipoprotein apolipoprotein B absolute synthetic rate was significantly greater in the familial combined hyperlipidaemic subjects than in control subjects (26.31 +/- 8.37 vs 9.36 +/- 4.07 mg/kg per 24 h, p less than 0.05). These results confirm findings using exogenous radioisotope labelling techniques that very low-density lipoprotein apolipoprotein B production is significantly increased in most patients with familial combined hyperlipidaemia. A modified 9-hour protocol can be safely done repeatedly and in children and pregnant women.

摘要

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Integrated regulation of very low density lipoprotein triglyceride and apolipoprotein-B kinetics in man: normolipemic subjects, familial hypertriglyceridemia and familial combined hyperlipidemia.人类极低密度脂蛋白甘油三酯和载脂蛋白B动力学的综合调节:血脂正常受试者、家族性高甘油三酯血症和家族性混合型高脂血症。
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Kinetic bases of the primary hyperlipidaemias: studies of apolipoprotein B turnover in genetically defined subjects.
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The effect of lovastatin on very low-density lipoprotein apolipoprotein B production by the liver in familial combined hyperlipidaemia.洛伐他汀对家族性混合性高脂血症患者肝脏极低密度脂蛋白载脂蛋白B生成的影响。
J Inherit Metab Dis. 1993;16(1):127-34. doi: 10.1007/BF00711326.
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Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.家族性混合性高脂血症中脂肪酸代谢受损。一种将肝脏载脂蛋白B过量产生与胰岛素抵抗相关联的机制。
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原发性高脂血症的动力学基础:对基因明确个体载脂蛋白B周转率的研究
Eur J Clin Invest. 1980 Apr;10(2 Pt 1):161-72. doi: 10.1111/j.1365-2362.1980.tb02076.x.
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Very low density lipoprotein overproduction in genetic forms of hypertriglyceridaemia.遗传性高甘油三酯血症中极低密度脂蛋白的过度生成。
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