Impaired insulin-stimulated glucose oxidation and free fatty acid suppression in patients with familial combined hyperlipidemia: A precursor defect for dyslipidemia?

Arteriosclerosis, Thrombosis, and Vascular Biology

Volumn 18, Issue 10, 1998, Pages 1548-1553

  Karjalainen, Leena ^a   Pihlajamäki, Jussi ^a   Karhapää, Pauli ^a   Laakso, Markku ^a  

^a UNIVERSITY OF EASTERN FINLAND   (Finland)

Author keywords

Familial combined hyperlipidemia; Glucose oxidation; Insulin; Insulin resistance; Nonoxidative glucose disposal

Indexed keywords

APOLIPOPROTEIN B; CHOLESTEROL; FATTY ACID; TRIACYLGLYCEROL; VERY LOW DENSITY LIPOPROTEIN;

ADULT; ARTICLE; CALORIMETRY; CHOLESTEROL BLOOD LEVEL; CLINICAL FEATURE; CONTROLLED STUDY; CORRELATION FUNCTION; DYSLIPIDEMIA; FAMILIAL HYPERLIPEMIA; FATTY ACID BLOOD LEVEL; FATTY ACID OXIDATION; FEMALE; GLUCOSE OXIDATION; HUMAN; HYPERLIPIDEMIA; INSULIN RESISTANCE; LIPID OXIDATION; MAJOR CLINICAL STUDY; MALE; PRIORITY JOURNAL; TRIACYLGLYCEROL BLOOD LEVEL;

EID: 0031662895     PISSN: 10795642     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.ATV.18.10.1548     Document Type: Article

References (12)

1. Goldstein J, Schrott H, Hazzard W, Bierman E, Motulsky A. Hyperlipidemia in coronary heart disease, II: genetic analysis of lipid levels in 176 families and delineation of a new inherited disorder, combined hyperlipidemia. J Clin Invest. 1973;52:1544-1568.
2. Nikkilä E, Aro A. A family study of lipids and lipoproteins in coronary heart disease. Lancet. 1973;I:954-958.
3. Janus E, Nicoll A, Turner P, Magill P, Lewis B. Kinetic basis of the primary hyperlipidemias: studies of apolipoprotein turnover in genetically defined subjects. Eur J Clin Invest. 1980;10:161-172.
4. Cortner J, Coates P, Bennett M, Cryer D, Le N. Familial combined hyperlipidemia: use of stable isotopes to demonstrate overproduction of very-low-density lipoprotein apolipoprotein B by the liver. J Inherit Metab Dis. 1991;14:915-922.
5. Venkatesan S, Cullen P, Pacy P, Halliday D, Scott J. Stable isotopes show a direct relation between VLDL apoB overproduction and serum triglyceride levels and indicate a metabolically and biochemically coherent basis for familial combined hyperlipidemia. Arterioscler Thromb. 1993;13: 1110-1118.
6. Taskinen M. Insulin resistance and lipoprotein metabolism. Curr Opin Lipid. 1995;6:153-160.
7. Hunt S, Wu L, Hopkins P, Stults B, Kuida H, Ramirez M, Lalouel J, Williams R. Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia: study of Utah patients with familial dyslipidemic hypertension. Arteriosclerosis. 1989; 9:335-344.
8. Castro-Cabezas M, de Bruin T, de Valk H, Shoulders C, Jansen H, Willem-Erkelens D. Impaired fatty acid metabolism in familial combined hyperlipidemia: a mechanism associating hepatic apolipoprotein B overproduction and insulin resistance. J Clin Invest. 1993;92:160-168.
9. Karhapää P, Voutilainen E, Malkki M, Laakso M. Obese men with type IIB hyperlipidemia are insulin resistant. Arterioscler Thromb. 1993;13: 1469-1475.
10. Aitman T, Godsland I, Farren B, Crook D, Wong J, Scott J. Defects in insulin action on fatty acid and carbohydrate metabolism in familial combined hyperlipidemia. Arterioscler Thromb Vase Biol. 1997;17: 748-754.
11. Bredie S, Cees J, Smits P, Stalenhoef A. Nonobese patients with familial combined hyperlipidemia are insulin resistant compared with their non-affected relatives. Arterioscler Thromb Vasc Biol. 1997;17:1465-1471.
12. Voutilainen E. Serum lipids and lipoproteins in male survivors of acute myocardial infarction and their first-degree relatives: a case-control study. Kuopio: Kuopio University Publications; 1992.