Comparison between the use of isopropanol and tetramethylurea for the solubilisation and quantitation of human serum very low density apollpoproteins

Holmouist, Leif; Carlson, Kerstin; Carlson, Lars A.

doi:10.1016/0003-2697(78)90444-x

Cited by 97 publications

(30 citation statements)

References 5 publications

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“…Each diet was from 2 to 3.5 wk long, enough time to induce new steady plasma triglyceride and cholesterol concentrations, based on values during the last 5 d of each study. Dietary details are shown in Table II (12). The lipoprotein was sterilized, tested to be pyrogen-free, and reinjected gCi total radioactivity).…”

Section: Methodsmentioning

confidence: 99%

Suppression by diets rich in fish oil of very low density lipoprotein production in man.

Nestel¹,

Connor²,

Reardon³

et al. 1984

J. Clin. Invest.

581

174

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A X bstract. The highly polyunsaturated fatty acids in fish oils lower the plasma triglyceride concentration. We have studied the effect of a diet rich in fish oil on the rate of production of the triglyceride-transporting very low density lipoprotein (VLDL). Seven subjects, five normal and two with hypertriglyceridemia received up to 30% of daily energy needs from a fish oil preparation that was rich in eicosapentaenoic acid and docosahexaenoic acid, w-3 fatty acids with five and six double bonds, respectively.Compared with a diet similarly enriched with safflower oil (in which the predominant fatty acid is the w-6 linoleic acid, with two double bonds), the fish oil diet lowered VLDL lipids and B apoprotein concentrations profoundly.High density lipoprotein lipids and Al apoprotein were also lowered, but the effect on low density lipoprotein (LDL) concentration was inconsistent.The daily production or flux of VLDL apoprotein B, calculated from reinjected autologous '25I-labeled lipoprotein, was substantially less in six subjects studied after 3 wk of fish oil, compared with after safflower oil. This effect on flux was more consistent than that on the irreversible fractional removal rate, which was increased in the four normolipidemic but inconsistent in the hyThis work was presented in part at

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Section: Methodsmentioning

confidence: 99%

Suppression by diets rich in fish oil of very low density lipoprotein production in man.

Nestel¹,

Connor²,

Reardon³

et al. 1984

J. Clin. Invest.

581

174

View full text Add to dashboard Cite

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“…Blood samples of 70 l were collected from the retro-orbital plexus at the specified time points after the injection. The plasma content of 125 I-labeled apoB was determined by measuring the 125 I content in the pellet obtained after propan-2-ol precipitation (23,24).…”

Section: In Vivo Turnover Studies Using [ 3 H]triglyceride-labeled Vlmentioning

confidence: 99%

ANGPTL3 Decreases Very Low Density Lipoprotein Triglyceride Clearance by Inhibition of Lipoprotein Lipase

Shimizugawa¹,

Ono

Shimamura

et al. 2002

Journal of Biological Chemistry

329

258

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KK/San is a mutant mouse strain established in our laboratory from KK obese mice. KK/San mice show low plasma lipid levels compared with wild-type KK mice despite showing signs of hyperglycemia and hyperinsulinemia. Recently, we identified a mutation in the gene encoding angiopoietin-like protein 3 (Angptl3) in KK/ San mice, and injection of adenoviruses encoding Angptl3 or recombinant ANGPTL3 protein to mutant KK/San mice raised plasma lipid levels. To elucidate the regulatory mechanism of ANGPTL3 on lipid metabolism, we focused on the metabolic pathways of triglyceride in the present study. Overexpression of Angptl3 in KK/San mice resulted in a marked increase of triglyceride-enriched very low density lipoprotein (VLDL). In vivo studies using Triton WR1339 revealed that there is no significant difference between mutant and wild-type KK mice in the hepatic VLDL triglyceride secretion rate. However, turnover studies using radiolabeled VLDL revealed that the clearance of 3 H-triglyceride-labeled VLDL was significantly enhanced in KK/San mice, whereas the clearance of 125 I-labeled VLDL was only slightly enhanced. In vitro analysis of recombinant protein revealed that ANGPTL3 directly inhibits LPL activity. These data strongly support the hypothesis that ANGPTL3 is a new class of lipid metabolism modulator, which regulates VLDL triglyceride levels through the inhibition of LPL activity.Hyperlipidemia is a major risk factor of coronary heart disease. Variations in human plasma lipid levels result from both genetic and environmental factors. Genetic factors account for more than 50% of the variation in plasma lipid levels in the human population (1-4). Naturally occurring mutations that affect lipid metabolism in mice have also been reported (5-7). In most cases, the mutated genes have not yet been identified, but elucidating the mutations could lead to the identification of the relevant genes.KK obese mice have a multigenic syndrome of moderate obesity and a diabetic phenotype that resembles human hereditary type 2 diabetes; they show signs of hyperinsulinemia, hyperglycemia, and hyperlipidemia (8 -10). We have found that KK mice in our laboratory (KK/San) have significantly low plasma lipid levels despite showing signs of hyperinsulinemia and hyperglycemia (11). Genetic analysis shows that the mutant phenotype of KK/San mice is inherited recessively as a Mendelian trait. We therefore named this locus hypl (for hypolipidemia). We observed the autosomal recessive hypl phenotype in the progeny of the KK/San strain and mapped the locus to the middle of chromosome 4. We identified a mutation in the gene encoding angiopoietin-like protein 3 (Angptl3) as the cause of the hypl trait (12). The mRNA of Angptl3 is predominantly localized in the liver. The expression of Angptl3 in KK/San mice was found to be 1/30 to 1/40 that of wild-type mice. Overexpression of Angptl3 using adenoviruses or by an intravenous injection of the recombinant protein in KK/San mice elicited a marked increase in circulating plasma total cholesterol...

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“…Blood samples of 70 l were collected from the retro-orbital plexus at the indicated time points after the injection. The plasma content of 125 I-labeled apoB was determined by measuring the 125 I content in the pellet after propan-2-ol precipitation (23,24).…”

Section: Labeling and Removal Of 125 I-labeled Vldl In Vivomentioning

confidence: 99%

A decreased expression of angiopoietin-like 3 is protective against atherosclerosis in apoE-deficient mice

Ando¹,

Shimizugawa²,

Takeshita³

et al. 2003

Journal of Lipid Research

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KK/Snk mice (previously KK/San) possessing a recessive mutation ( hypl ) of the angiopoietin-like 3 ( Angptl3 ) gene homozygously exhibit a marked reduction of VLDL due to the decreased Angptl3 expression. Recently, we proposed that Angptl3 is a new class of lipid metabolism modulator regulating VLDL triglyceride (TG) levels through the inhibition of lipoprotein lipase (LPL) activity. In this study, to elucidate the role of Angptl3 in atherogenesis, we investigated the effects of hypl mutation against hyperlipidemia and atherosclerosis in apolipoprotein E knockout (apoEKO) mice. ApoEKO mice with hypl mutation (apoEKO-hypl ) exhibited a significant reduction of VLDL TG, VLDL cholesterol, and plasma apoB levels compared with apoEKO mice. Hepatic VLDL TG secretion was comparable between both apoE-deficient mice. Turnover studies revealed that the clearance of both [ 3 H]TG-labeled and 125 I-labeled VLDL was significantly enhanced in apoEKO-hypl mice. Postprandial plasma TG levels also decreased in apoEKO-hypl mice. Both LPL and hepatic lipase activities in the postheparin plasma increased significantly in apoEKO-hypl mice, explaining the enhanced lipid metabolism. Furthermore, apoEKO-hypl mice developed 3-fold smaller atherogenic lesions in the aortic sinus compared with apoEKO mice. Taken together, the reduction of Angptl3 expression is protective against hyperlipidemia and atherosclerosis, even in the absence of apoE, owing to the enhanced catabolism and clearance of TG-rich lipoproteins. The accrued evidence that lipid-lowering therapy limits the progression of atherosclerosis and reduces the events of coronary artery diseases is overwhelming (1, 2). The focus has been on the reduction of LDL cholesterol (3, 4). Recent studies have also pointed out the importance of reducing triglyceride (TG)-rich lipoproteins such as chylomicrons, VLDL, and their remnants, and of raising HDL cholesterol (5, 6). In addition, postprandial hypertriglyceridemia is mentioned as an independent risk factor for atherogenesis (7,8).In a colony of KK mice with mild obesity, hyperlipidemia, and diabetes, we found mutant mice (KK/Snk, previously KK/San) that were characterized by a significant decrease in plasma lipid levels, mainly due to the reduction of TG-rich lipoproteins, despite their obesity and diabetes. Genetic studies for the mutation, named hypolipidemia ( hypl ), in KK/Snk mice identified a 4 bp nucleotide insertion in exon 6 of a gene encoding angiopoietin-like 3 ( Angptl3 ), which causes a premature stop codon after a frameshift (9). Angptl3 is a secretory protein of 70 kDa expressed predominantly in the liver, and has a signal sequence, coiled-coil domain, and fibrinogen-like domain similar to those of other angiopoietin families (10, 11). In KK/Snk mice with the homozygous hypl mutation, Angptl3 expression was markedly decreased, probably due to the instability of mutant mRNA, resulting in a hypolipidemic trait (9). In contrast, adenovirus-mediated overexpression of Angptl3 or intravenous injection of the purified...

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Comparison between the use of isopropanol and tetramethylurea for the solubilisation and quantitation of human serum very low density apollpoproteins

Cited by 97 publications

References 5 publications

Suppression by diets rich in fish oil of very low density lipoprotein production in man.

Suppression by diets rich in fish oil of very low density lipoprotein production in man.

ANGPTL3 Decreases Very Low Density Lipoprotein Triglyceride Clearance by Inhibition of Lipoprotein Lipase

A decreased expression of angiopoietin-like 3 is protective against atherosclerosis in apoE-deficient mice

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