Normalization of Triglycerides in Type IV Hyperlipoproteinemia Fails to Correct Low Levels of High-Density-Lipoprotein Cholesterol

Witztum, Joseph L.; Dillingham, Mary Ann; Giese, William E.; Bateman, Joyce; Diekman, Connie B.; Blaufuss, Elaine Kammeyer; Weidman, Stuart W.; Schonfeld, Gustav

doi:10.1056/nejm198010163031603

Cited by 61 publications

(10 citation statements)

References 33 publications

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“…These concurrent elevations are in contrast to the reciprocal relationship between HDL cholesterol and triglycerides seen in population studies 28 and the low HDL cholesterol levels observed in many patients with either endogenous or exogenous hypertriglyceridemia. 29 In spite of the low levels of LDL lipids in plasma, on zonal ultracentrifugation, the LDL populations in the plasma of the proband had normal flotation characteristics. 11 The results suggest that the proband's LDL was not unusual in its physicc.hemical properties.…”

Section: Discussionmentioning

confidence: 96%

Lipoproteins in familial hyperalphalipoproteinemia.

Patsch¹,

Kuisk²,

Glueck³

et al. 1981

Arteriosclerosis

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Familial hyperalphalipoproteinemia Is determined by a major gene and is characterized by high levels of high density lipoprotein cholesterol and longevity. To describe the plasma llpoprotelns in this condition more completely, a kindred consisting of the proband, her affected father, and her two affected brothers was studied. Fasting plasmas were analyzed for lipoprotein lipids by combined preparative ultracentrlfugal and precipitation methods. Levels of apollpoprotein A-l and apolipoproteln A-ll, the major apoproteins of high density lipoproteins, were assayed by radlolmmunoassay. The flotation properties of very low density, low density and high density lipoprotein were determined by zonal ultracentrlfugatlon, and the Isolated high density lipoprotein subtractions were characterized according to their Ilpid and apoprotein compositions. Total cholesterol of all subjects was normal, but trlglycerides were elevated (above the 90th percentile) In the two brothers.

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Section: Discussionmentioning

confidence: 96%

Lipoproteins in familial hyperalphalipoproteinemia.

Patsch¹,

Kuisk²,

Glueck³

et al. 1981

Arteriosclerosis

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“…In the early 1980s, obesity was reported to be positively associated with plasma TG levels in a number of studies (Cowan et al 1985;Phillips et al 1981;Albrink and Meigs 1964;Laskarzewski et al 1980), and a decrease in plasma TG level has been observed with weight loss (Witztum et al 1980). In one study reported by Laskarzewski et al (1980), obesity was found to be the strongest independent correlate for HTG.…”

Section: Discussionmentioning

confidence: 97%

Interaction between obesity and genetic polymorphisms in the apolipoprotein CIII gene and lipoprotein lipase gene on the risk of hypertriglyceridemia in Chinese

Teng

et al. 1997

Human Genetics

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To understand the effects of the interaction between genetic polymorphisms and obesity on the risk of hypertriglyceridemia (HTG), two polymorphisms, an SstI polymorphism on the apolipoprotein CIII gene and a HindIII polymorphism on the lipoprotein lipase gene, were analyzed in 339 Chinese subjects with (82 cases in the HTG group) or without HTG (257 cases in the control group). Our data revealed that the frequencies of obesity, the SstI minor allele (S2), and the HindIII major allele (H+) in the HTG group were significantly higher than in the control group. Subgroup analysis revealed that the association between these two polymorphisms and HTG occurred predominantly in nonobese subjects and in subjects with the less hypertriglyceridemic genotype of another polymorphism. Multivariate logistic regression analysis showed that all three risk factors (obesity, S2-containing chromosome, and H+ homozygosity) were associated with HTG, and an interaction was found between obesity and H+ homozygosity for the occurrence of HTG. The risk of HTG increased significantly with combinations of risk factors. Subjects can be divided into low or high risk groups for HTG using such combinations. These results provide evidence of interaction between obesity and the HindIII polymorphism of the lipoprotein lipase gene on the risk of HTG.

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“…Moreover, in the human study, the decrease in apoAI levels associated with HTG was only 12%, whereas in the mice it was 50% (Hayek et al 1993). Finally, in patients with HTG and low HDL-C, normalization of TGs by diet and drug therapy failed to elevate HDL-C (Witztum et al 1980;Falko et al 1979). Therefore, there may be other factors independent of apoCIII levels involved in the difference of HDL-C between hypertriglyceridemic patients and apoCIII Tg animal models.…”

Section: Discussionmentioning

confidence: 86%

Hypertriglyceridemia and delayed clearance of fat load in transgenic rabbits expressing human apolipoprotein CIII

et al. 2010

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Apolipoprotein CIII (apoCIII) has been implicated in hypertriglyceridemia and plasma apoCIII independently predicts risk for coronary heart disease. While hypertriglyceridemia in patients has been demonstrated to correlate with elevated plasma apoCIII levels and reduced lipoprotein lipase (LPL) activity, apoCIII transgenic mice show elevated LPL activity. In this study, we generated transgenic (Tg) rabbits expressing human apoCIII gene exclusively in liver and investigated the effect of apoCIII overexpression on lipid metabolism of rabbits. In comparison with non-Tg littermates, Tg rabbits had 3- and 3.2-fold increases in fed and fasted plasma triglycerides, respectively. In contrast, no significant differences were observed in plasma total cholesterol and high density lipoprotein cholesterol levels between Tg and non-Tg rabbits. Analysis of lipoprotein fractions revealed that elevated plasma triglyceride levels in Tg rabbits were mainly attributed to an increase in very low density lipoprotein/chylomicron-sized particles. Furthermore, Tg rabbits showed markedly delayed clearance of plasma triglycerides accompanied with significantly reduced LPL activity in post-heparin plasma compared to that in non-Tg controls. In conclusion, these results indicate apoCIII transgenic rabbits develop hypertriglyceridemia with similar mechanism in hypertriglyceridemic patients via delayed clearance of plasma triglycerides, and could be used as a valuable tool for the study of human hyperlipidemia in relation with atherosclerotic disorders.

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Normalization of Triglycerides in Type IV Hyperlipoproteinemia Fails to Correct Low Levels of High-Density-Lipoprotein Cholesterol

Cited by 61 publications

References 33 publications

Lipoproteins in familial hyperalphalipoproteinemia.

Lipoproteins in familial hyperalphalipoproteinemia.

Interaction between obesity and genetic polymorphisms in the apolipoprotein CIII gene and lipoprotein lipase gene on the risk of hypertriglyceridemia in Chinese

Hypertriglyceridemia and delayed clearance of fat load in transgenic rabbits expressing human apolipoprotein CIII

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