Further Aspects on the Characterization of High and Very Low Density Lipoproteins in Patients with Liver Disease

Seidel, D.; Greten, H.; Geisen, H. P.; Wengeler, H; Wieland, H.

doi:10.1111/j.1365-2362.1972.tb00662.x

Cited by 68 publications

(14 citation statements)

References 23 publications

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“…4), a mechanism which is important for plasma lipoprotein metabolism. The hypertriglyceridaemia of cholestasis may be caused by such a mechanism, a view which is supported by the observation that these apolipoproteins are either absent or drastically reduced in VLDL particles obtained from patients with cholestasis (25,27).…”

Section: Cholestasis and Hypercholesterolaemiamentioning

confidence: 48%

“…These unusual particles are heterogeneous in size, ranging from 30 nm to 80 nm, and are thus much larger than normal LDL (20 -25 nm). Dietary studies have indicated that these particles are remnants derived from a disturbed catabolism of chylomicrons (25). Their accumulation may be caused by reduced plasma lipolytic activity and/or by a disturbed hepatic uptake due to an Inhibition of the apolipoprotein E receptor.…”

Section: Hypertriglyceridaemiamentioning

confidence: 99%

“…Electrophoresis of lipoproteins in liver disease reveals a typicäl pattern of only one, often broadened, band in the ß-position, which masks a heterogeneity which can only be elucidated by the employment of various analyticäl techniques (25). Drastic changes in the concentration of apolipoproteins.…”

Section: The Abnormal Lipoprotein Profile In Liver Diseasementioning

confidence: 99%

“…From this observation i t may be concluded that the diminished plasma concentration of apolipoprotein A found in liver patients is primarily due to its accelerated catabolism, rather than to ä disturbed synthesis, äs described for Tangier disease, a primary deficiency of HDL (49). The apolipoprotein A-I and apolipoprotein A-II in the plasma of patients with liver disease often show a complete dissociation and they lose much of their lipid binding capacity (25). It is possible that the dissociation of the two apolipoprotein A sübünits is a inajor reason for their accelerated catabolism and this may well result from a disturbed generation of mature HDL from nascent HDL in the plasma of such patients, emphasizing the general importanee of the structural properties of a lipoprotein with respect to its metabolism.…”

Section: Hdl and A-lipoproteinsmentioning

confidence: 99%

“…The -lipoproteins cannöt be visualized on lipoprotein electropherograms (25,27). Ultracentrifugal and Chromatographie analysis, höwever, reveal the presence of lipoproteins in this density class but with an unusual degree of heterogeneity.…”

Section: Hdl and A-lipoproteinsmentioning

confidence: 99%

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Lipoproteins in Liver Disease

Seidel

1987

Clinical Chemistry and Laboratory Medicine

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Summary:Liver disease is associated with profound and characteristic changes in lipoprotein composition and metabolism. The most pronounced alterations are the Formation of lipoprotein-X in intra-and extrahepatic cholestasis, the decrease of apolipoproteins A-I and A-II and the increase of apolipoprotein E. These alterations impair the activities of both lipoprotein lipase and lecithin : cholesterol acyltransferase. They are also responsible for an abnormal receptor mediated uptake of the lipoproteins from plasma. The abnormal lipid and apolipoprotein composition of the lipoproteins in liver disease % appears to affect various important functions of cell membranes. The understanding of how these changes occur and their significance in the pathogenesis of other metabolic disturbances secondary to the abnormal lipid metabolism are important challenges for future research.

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Section: Cholestasis and Hypercholesterolaemiamentioning

confidence: 48%

Section: Hypertriglyceridaemiamentioning

confidence: 99%

Section: The Abnormal Lipoprotein Profile In Liver Diseasementioning

confidence: 99%

Section: Hdl and A-lipoproteinsmentioning

confidence: 99%

Section: Hdl and A-lipoproteinsmentioning

confidence: 99%

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Lipoproteins in Liver Disease

Seidel

1987

Clinical Chemistry and Laboratory Medicine

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Immunosuppressive Serum Factors in Viral Hepatitis. III. Prognostic Relevance of Rosette Inhibitory Factor and Serum Inhibition Factor in Acute and Chronic Hepatitis

et al. 1984

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Two immunosuppressive serum factors, serum inhibition factor (SIF) and rosette inhibitory factor (RIF), were studied in sera from patients with acute and chronic viral hepatitis. In a study of 30 patients with acute viral hepatitis, an association was found between RIF, SIF, and biochemical and virological parameters in 27 patients (90%), 25 of whom recovered completely; two had a protracted course. In three patients, the clinical course was not reflected by the immunosuppressive factors. In 26 patients with chronic persistent hepatitis, 3 had RIF and 7 had SIF of low activity. In patients with HBsAg-positive and -negative chronic active hepatitis, 32 of 47 had RIF and 24 had SIF. SIF activity was significantly increased in HBsAg positive as compared to -negative cases. There was no correlation between RIF and SIF activity at any stage of viral hepatitis. Although SIF was demonstrated in patients with various infectious and other inflammatory diseases, RIF was infrequently detected in nonviral liver disorders, and was not present in any of the nonhepatic diseases tested. It was confirmed that RIF is associated with the beta-lipoprotein fraction. RIF was easily separated from SIF by density gradient ultracentrifugation. The evaluation of SIF and RIF may be helpful in determining the outcome of acute viral hepatitis. In chronic hepatitis, RIF was a better indicator of disease activity than was SIF. These clinical data support previous findings that SIF may be related to the immune response whereas RIF is associated with liver cell damage.

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Lipoprotein Profiles in Chronic Alcoholics: Use of High-Density Lipoprotein Subspecies Levels to Differentiate Subpopulations

Sabesin

Weidman

1984

Hepatology

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Recent research in lipoprotein metabolism has revealed new important contributions of the liver to lipoprotein synthesis and metabolism in addition to its established role in triglyceride and very low-density lipoprotein (VLDL) formation. Examples of these contributions include: (i) the synthesis of apoproteins, which are constituents of lipoproteins and are essential co-factors in the activation of key enzymes involved in lipoprotein metabolism; (ii) synthesis and secretion of lecithin:cholesterol acyltransferase (LCAT), which is responsible, in man, for virtually all plasma cholesterol esterification; (iii) uptake and degradation of chylomil cron remnants, low-density lipoproteins (LDL) and high-density lipoproteins (HDL), and (iv) regulation of cholesterol homeostasis by synthesis of bile acids from cholesterol and excretion of cholesterol in bile. The importance of these hepatic contributions to lipoprotein metabolism is dramatically demonstrated by the profound derangements in lipoprotein concentration and composition which occur as a consequence of hepatocellular (1) or cholestatic (2) liver disease. These changes are largely secondary to abnormalities in lipoprotein synthetic and catabolic functions of the liver.Recent studies of patients with alcoholic hepatitis (3-9) provide evidence that hepatocellular injury is associated with the following alterations in plasma lipoprotein composition: (i) VLDL is relatively normal in lipid composition but deficient in apoproteins E and C; (ii) LDL contains mainly apoprotein (apo) B but is heterogeneous in size and enriched in triglyceride and deficient in esterified cholesterol, and (iii) HDL that is diminished in concentration, enriched in apo E and phospholipid, and deficient in apo A-I and esterified cholesterol. Using density gradient ultracentrifugal techniques, the abnormal HDL has been resolved into discoidal (apo E-rich) and spherical particles (apo A-I rich). Several studies (1, 10) documented low plasma LCAT activity in alcoholic liver disease associated with impaired cholesterol esterification. LCAT deficiency also occurs in nonalcoholic hepatocellular injury. Associated with LCAT deficiency is decreased plasma apo A-I, an activator of LCAT. The catabolism of apo A-I is increased in alcoholic hepatitis, providing a rationale for reduced plasma levels (11).

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Further Aspects on the Characterization of High and Very Low Density Lipoproteins in Patients with Liver Disease

Cited by 68 publications

References 23 publications

Lipoproteins in Liver Disease

Lipoproteins in Liver Disease

Immunosuppressive Serum Factors in Viral Hepatitis. III. Prognostic Relevance of Rosette Inhibitory Factor and Serum Inhibition Factor in Acute and Chronic Hepatitis

Lipoprotein Profiles in Chronic Alcoholics: Use of High-Density Lipoprotein Subspecies Levels to Differentiate Subpopulations

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