Radioimmunoassay of human plasma lecithin-cholesterol acyltransferase.

Albers, John J.; Adolphson, Janet L.; Chen, C H

doi:10.1172/jci110006

Cited by 134 publications

(34 citation statements)

References 28 publications

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“…Both these differences are highly statistically significant (/?<0.001). FERHDL values were significantly higher in men and women with hyperlipidemia (p<0.01) and in those with proven CAD (/xO.OOl) compared with their respective controls ( Table 4 for individual [1][2][3][4][5][6][7][8] (32±12.1%/hr) compared with 15 men with familial hypercholesterolemia (20.3±4.4%/hr) or three men with hypertriglyceridemia (23.1±4.9%/hr). In hyperlipidemic women, the FERHDL value was highest in the three women with hypertriglyceridemia (25±6.9%/hr), compared with 19 heterozygotes for familial hypercholesterolemia (14.6±5.3%/hr) or five with familial combined hyperlipidemia (18.6±8.7%/hr).…”

Section: Resultsmentioning

confidence: 99%

Cholesterol esterification rates in very low density lipoprotein- and low density lipoprotein-depleted plasma. Relation to high density lipoprotein subspecies, sex, hyperlipidemia, and coronary artery disease.

Dobiášová¹,

Stríbrná²,

Sparks³

et al. 1991

Arterioscler Thromb

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The fractional rate of cholesterol esterification in very low density lipoprotein-and low density lipoprotein-depleted plasma (FERgoJ was studied in normolipidemic subjects and in individuals with hyperlipidemia and proven coronary artery disease (CAD). The FERnm, was significantly higher than the FER in whole plasma and was significantly higher in normal men than in normal women. In addition, men and women with primary hyperlipidemia had significantly

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Section: Resultsmentioning

confidence: 99%

Cholesterol esterification rates in very low density lipoprotein- and low density lipoprotein-depleted plasma. Relation to high density lipoprotein subspecies, sex, hyperlipidemia, and coronary artery disease.

Dobiášová¹,

Stríbrná²,

Sparks³

et al. 1991

Arterioscler Thromb

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“…LCAT mass was measured by radioimmunoassay by Dr. S.M. Marcovina (University of Washington School of Medicine; Seattle, WA) (13). CER were calculated from the rate of the esterification of [ 3 H]cholesterol and plasma free cholesterol (FC) levels as described previously (14,15).…”

Section: Methodsmentioning

confidence: 99%

An intronic mutation in a lariat branchpoint sequence is a direct cause of an inherited human disorder (fish-eye disease).

Kuivenhoven¹,

Weibusch²,

Pritchard³

et al. 1996

J. Clin. Invest.

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The first step in the splicing of an intron from nuclear precursors of mRNA results in the formation of a lariat structure. A distinct intronic nucleotide sequence, known as the branchpoint region, plays a central role in this process. We here describe a point mutation in such a sequence. Three sisters were shown to suffer from fish-eye disease (FED), a disorder which is caused by mutations in the gene coding for lecithin:cholesterol acyltransferase (LCAT). Sequencing of the LCAT gene of all three probands revealed compound heterozygosity for a missense mutation in exon 4 which is reported to underlie the FED phenotype, and a point mutation located in intron 4 (IVS4:T-22C). By performing in vitro expression of LCAT minigenes and reverse transcriptase PCR on mRNA isolated from leukocytes of the patient, this gene defect was shown to cause a null allele as the result of complete intron retention. In conclusion, we demonstrated that a point mutation in a lariat branchpoint consensus sequence causes a null allele in a patient with FED. In addition, our finding illustrates the importance of this sequence for normal human mRNA processing. Finally, this report provides a widely applicable strategy which ensures fast and effective screening for intronic defects that underlie differential gene expression.

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“…32 -3* Lecithin cholesterol acyltransferase (LCAT) was measured by double antibody radioimmunoassay. 35 HDL subfractions were analyzed by a two-step precipitation technique. 38 Gidez et al 36 found that the results obtained by their technique for determining HDL,C were highly correlated with the results from both analytical ultracentrifugation (n = 17, r = 0.92) and preparative ultracentrifugation (n = 295, r = 0.91).…”

Section: Laboratory Methodsmentioning

confidence: 99%

Epidemiological correlates of high density lipoprotein subfractions, apolipoproteins A-I, A-II, and D, and lecithin cholesterol acyltransferase. Effects of smoking, alcohol, and adiposity.

Haffner¹,

Applebaum-Bowden²,

Wahl³

et al. 1985

Arteriosclerosis

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122

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Recent data suggest that the protection against ischemic heart disease afforded by high density lipoprotein (HDL) cholesterol (C) may be concentrated in the HDL 2 subfraction. To examine the behavioral correlates of the HDL subfractions, we recalled 33 men and 17 women of a random sample from the Pacific Northwest Bell Telephone Company Health Survey. Adiposity and very low density lipoprotein (VLDL) triglyceride were negatively correlated with HDL 2 C. Smoking was not correlated with HDL 2 C, but was negatively correlated with HDL 3 C (men, r s = -0.635, p = 0.001; women, r s = -0.534, p -0.014); this relationship was independent of alcohol consumption, adiposity, and VLDL triglyceride. Alcohol consumption was also more strongly related to HDL 3 C (men, r s = 0.248, p = 0.082; women, r s = 0.586, p = 0.007). Lecithin cholesterol acyltransferase (LCAT) mass was negatively related with HDL 2 C, but was positively correlated with HDL 3 C and apolipoprotein A-ll. Smoking was negatively correlated with LCAT mass. Since it is believed that HDL 3 C is not associated with the risk of ischemic heart disease and since both smoking and alcohol consumption may mainly affect HDL 3 C, the current study suggests that the increase in risk of ischemic heart disease with smoking and the possible decrease with alcohol consumption may be mediated through mechanisms other than their effects on HDLC. (Arteriosclerosis 5:169-177, March/April 1985)

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Radioimmunoassay of human plasma lecithin-cholesterol acyltransferase.

Cited by 134 publications

References 28 publications

Cholesterol esterification rates in very low density lipoprotein- and low density lipoprotein-depleted plasma. Relation to high density lipoprotein subspecies, sex, hyperlipidemia, and coronary artery disease.

Cholesterol esterification rates in very low density lipoprotein- and low density lipoprotein-depleted plasma. Relation to high density lipoprotein subspecies, sex, hyperlipidemia, and coronary artery disease.

An intronic mutation in a lariat branchpoint sequence is a direct cause of an inherited human disorder (fish-eye disease).

Epidemiological correlates of high density lipoprotein subfractions, apolipoproteins A-I, A-II, and D, and lecithin cholesterol acyltransferase. Effects of smoking, alcohol, and adiposity.

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