The degradation of very low density lipoprotein by the extrahepatic tissues of the rat

Suri, Bhim S.; Targ, Michael E.; Robinson, Donald S.

doi:10.1016/0005-2760(78)90076-0

Cited by 10 publications

(11 citation statements)

References 37 publications

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“…Instead, the curve in panel C rose to about the 60% level, suggesting that an appreciable portion of chylomicron remnant core lipid may have been removed extrahepatically. This interpretation is supported by our observation that in hepatectomized rabbits as much as 43% of chylomicron retinyl and cholesterol esters disappears from the circulation in 1 hour.38 Similarly, Suri et al 60 observed a 50% loss of VLDL protein and cholesterol from the circulation of supradiaphragmatic rats.…”

Section: Chylomicron Clearancesupporting

confidence: 76%

Atherogenesis: a postprandial phenomenon.

Zilversmit¹

1979

Circulation

1,589

746

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THE VIEW that coronary heart disease, or arteriosclerosis, is a multifactorial disease has always disturbed me -not because it isn't important to uncover the conditions that aggravate this disease, but because as a basis for scientific inquiry I feel that it may be a very long time before we can formulate a model that will be both scientifically sound as well as aesthetically pleasing.In some way nearly every process around us is mul tifactorial. Even a simple discussion about the weight of a gas can be conducted in multifactorial terms. The weight depends, of course, on its volume, pressure, temperature, molecular weight and the gravitational force. Even in this simple analysis at least flve factors determine the outcome of the inquiry. If we analyzed the question in terms of molecular, atomic or subatomic physics the number of factors involved in answering the inquiry would probably be increased manifold.Therefore, we should not be discouraged by the multitude of possible etiological and risk factors that compete for priority status. It is highly unlikely that we shall have to control each and every one of them to prevent the clinical manifestations of arteriosclerosis.However, it is still not possible to present a unitary view of the atherogenic process. Consequently, this presentation deals only with selected early manifestations of arterial pathology, i.e., lipid accumulation, and leans more heavily on my own work than is warranted by its importance. I shall, however, synthesize our findings with those of others in support of the view that arterial lipid accumulates as the result not only of abnormally high concentrations of low- density lipoproteins (LDL) in the blood plasma, but also as a consequence of the normal process of lipid absorption and transport. This normal process may be innocuous in persons who ingest low-fat diets, but is probably pathogenic in those who consume a diet rich in fat and cholesterol. Lipid and AtherosclerosisCholesterol and AtherosclerosisMost scientists working in the atherosclerosis area see cholesterol as a pivotal element in the etiology of cardiovascular disease. At least five areas of research contribute to this view. In 1910, Windaus' described the presence of cholesterol in the lesions of diseased arteries. Since then, many studies have confirmed that free and esterified cholesterol accumulate in the aorta, coronary arteries, cerebral vessels and other large arteries at different rates in different persons or in different population groups.2 In persons with premature, genetically determined hypercholesterolemia, arterial cholesterol accumulates more rapidly and clinical manifestations of cardiovascular disease appear earlier in life.3 Epidemiological studies have repeatedly shown high degrees of correlation between the intake of cholesterol and other lipids with the prevalence of coronary heart disease in various populations.2 Animal studies show, almost without exception, that experimentally induced hypercholesterolemia is followed by the accumulation of cholesterol in...

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Section: Chylomicron Clearancesupporting

confidence: 76%

Atherogenesis: a postprandial phenomenon.

Zilversmit¹

1979

Circulation

1,589

746

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“…The maintenance diet ofthe liver donors was replaced by a fructose-rich diet. (Suri et al, 1978) 3 days before the perfusion experiments in order to increase the output of VLDlipoprotein triacylglycerol and protein (Petersburg et al, 1975).…”

Section: Animalsmentioning

confidence: 99%

“…This was carried out by urea/polyacrylamide-gel electrophoresis as previously described (Suri et al, 1978), except that tetramethylurea was omitted from the samples, since delipidated apoproteins were loaded on the gels. The apoprotein solutions were first dialysed for 24h against several changes of 0.15M-NaCl solution containing 6M-urea.…”

Section: Polyacrylamide-gel Electrophoresismentioning

confidence: 99%

“…These are known to be formed through the metabolism of chylomicrons and VLD lipoproteins, but, although it has been suggested that the LD lipoproteins could be released from the liver after remnant degradation in the organ (Felts et al, 1975), this view has not been supported by any experimental evidence. Our recent work with the supradiaphragmatic rat (Suri et al, 1978) Eisenberg & Rachmilewitz, 1973;Glangeaud et al, 1977). These last will normally contain complexes of both hepatic and intestinal origin and some of them may already be partially degraded.…”

mentioning

confidence: 99%

“…) and proteins for use as molecular-weight markers were all purchased from Sigma (London) Chemical Co., Kingston upon Thames, Surrey, U.K. 2,5-Diphenyloxazole and 1,4-bis-(4-methyl-5-phenyloxazol-2-yl)benzene were obtained from Koch-Light Laboratories, Colnbrook, Bucks., U.K. Sources of all other materials used were as specified by Suri et al (1978).…”

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confidence: 99%

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The metabolic conversion of very-low-density lipoprotein into low-density lipoprotein by the extrahepatic tissues of the rat

Suri¹,

Targ²,

Robinson³

1979

Biochemical Journal

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1. The work reported was designed to provide quantitative information about the capacity of the extrahepatic tissues of the rat to degrade injected VLD lipoproteins (very-lowdensity lipoproteins, d< 1.006) to LD lipoproteins (low-density lipoproteins, d 1.006-1.063) and to study the fate of the different VLD-lipoprotein apoproteins during the degradative process. 2. Rat liver VLD lipoproteins, radioactively labelled in their protein moieties, were produced by the perfusion of the organ and were either injected into the circulation of the supradiaphragmatic rats or incubated in rat plasma at 370C. At a time (75 min) when approx. 90% of the triacylglycerol of the VLD lipoproteins had been hydrolysed, the supradiaphragmatic rats were bled and VLD lipoproteins, LD lipoproteins and HD lipoproteins (high-density lipoproteins, d 1.063-1.21) were separated from their plasma and from the plasma incubated in vitro. The apoproteins of each of the lipoprotein classes were resolved by gel-filtration chromatography into three main fractions, designated peaks I, II and III. 3. Incubation of the liver VLD lipoproteins in plasma in vitro led to the transfer of about 30 % of the total protein radioactivity to the HD lipoproteins. This transfer mainly involved the peak-II (arginine-rich and/or apo A-I) and peak-Ill (apo C) proteins. There was also a small transfer of radioactivity (about 5 % of the total) to the LD lipoproteins. 4. Injection of the liver VLD lipoproteins into the circulation of the supradiaphragmatic rat resulted in the transfer of about 15 % of the total VLD-lipoprotein radioactivity to the LD lipoproteins. This transfer involved mainly the peak-I (apo B) proteins and accounted for about 20% of the total apo B protein radioactivity of the injected VLD lipoproteins. When the endogenous plasma VLD lipoprotein was taken into account the transfer of apo B protein was about 35 %.5. The transfer of peak-Il protein radioactivity from the VLD to the HD lipoproteins was greater in the plasma of the supradiaphragmatic rat than in the incubated plasma, suggesting that there was a net transfer of peak-II apoproteins during the VLD lipoprotein degradation. The transfer of peak-III protein radioactivity was not greater in the plasma of the supradiaphragmatic rat, but there was a loss of this radioactivity from the circulation.

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Lipoproteine bei zeitlich unterschiedlicher Nahrungsaufnahme

Schneider

Tauber

1981

Klin Wochenschr

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The lipid infiltration theory of atherogenesis accepted, 24 h lipoprotein profiles may be more relevant than preprandial morning samples. Such profiles were performed in 12 metabolically healthy volunteers during two dietetic regimes identical in total food content but differing in the distribution over the day: form A meant an evening meal of 15% of total caloric intake, form B of 40%. After one week of each form, 24 h lipoprotein profiles differed significantly in the time course of triglyceride rich lipoproteins and in the mean values over 24 h in VLDL and LDL phospholipids and HDL cholesterol. These findings are cautiously interpreted as possible signs of differences in the catabolism of triglyceride rich lipoproteins, remnants and intermediate lipoproteins. The difference in HDL cholesterol which was higher in form A is discussed in the context of recent epidemiologic evidence.

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The degradation of very low density lipoprotein by the extrahepatic tissues of the rat

Cited by 10 publications

References 37 publications

Atherogenesis: a postprandial phenomenon.

Atherogenesis: a postprandial phenomenon.

The metabolic conversion of very-low-density lipoprotein into low-density lipoprotein by the extrahepatic tissues of the rat

Lipoproteine bei zeitlich unterschiedlicher Nahrungsaufnahme

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