Studies on the regulation of cholesterol metabolism by low‐and high‐density lipoproteins in HepG2 cellsx

Subramanian Ranganathan, Bruce A. Kottke – 1 April 1989 – The uptake and degradation of low‐density lipoproteins and the esterification and synthesis of cholesterol were poorly down‐regulated by low‐density lipoproteins in HepG2 cells. Addition of low‐density lipoproteins to the cells increased the free and esterified cholesterol in the cells. The heavier fraction of high‐density lipoproteins enhanced the degradation of low‐density lipoproteins and cholesterol synthesis and decreased acyl CoA:cholesterol acyltransferase activity.

Impaired liver function in stable renal allograft recipients

Felix J. Frey, Heinz J. Schaad, Eberhard L. Renner, Fritz F. Horber, Brigitte M. Frey, Rudolf Preisig – 1 April 1989 – Hepatic failure as a cause of death is increased in stable renal allograft recipients when compared with patients on dialysis. In order to assess the magnitude and the natural history of the hepatic functional derangement, the kinetics of xenobiotics which are metabolized by cytosolic (galactose) or microsomal (prednisolone, cyclosporine A) enzymes were determined in 28 consecutive stable kidney transplant patients 1 month and 1 year after transplantation.

Colchicine treatment of cirrhosis: Questions

Norman D. Grace – 1 April 1989 – There is preliminary evidence that colchicine, an inhibitor of collagen synthesis, may be beneficial in the treatment of cirrhosis of the liver. To evaluate the use of colchicine (1 mg per day, five days per week) in the treatment of hepatic cirrhosis, we performed a randomized, double‐blind, placebo‐controlled trial in which 100 patients were followed for up to 14 years. Forty‐five patients had alcoholic cirrhosis, 41 had posthepatitic cirrhosis, and the remaining 14 had cirrhosis with various other causes.

Biochemical effects and zonal heterogeneity of peroxisome proliferation induced by perfluorocarboxylic acids in rat liver

Wilhelm W. Just, Karin Gorgas, Franz‐Ulrich Hartl, Petra Heinemann, Manfred Salzer, Hans Schimassek – 1 April 1989 – Rats were treated for 5 to 14 days with perfluoroacetate, perfluorobutyrate and perfluorooctanoate. Alterations in hepatic morphology with special reference to the peroxisomal compartment were investigated by light and electron microscopy following cytochemical staining of catalase activity with the alkaline 3,3′‐diaminobenzidine medium. All three compounds induced hepatomegaly and peroxisome proliferation.

Effect of repetitive low‐dose endotoxin on liver parenchymal and kupffer cell fibronectin release

Peter A. Vincent, Eshin Cho, Thomas M. Saba – 1 April 1989 – Repetitive low‐dose endotoxin, at a dose which will result in endotoxin tolerance, produces a marked but transient 2‐ to 3‐day increase in plasma fibronectin. This elevation of fibronectin appears to contribute to increased hepatic Kupffer cell phagocytic function observed with repetitive low‐dose endotoxin administration. Although numerous cell types synthesize fibronectin, hepatocytes are believed to be the major cell source of fibronectin in the plasma.

Modulation of hepatic ferrochelatase activity by dietary manipulation of mitochondrial phospholipid fatty acyl groups

Ann M. Kools, James G. Straka, Hazel D. Hill, Dorothy I. Whitmer, Ralph T. Holman, Joseph R. Bloomer – 1 April 1989 – Ferrochelatase is an enzyme bound to the inner mitochondrial membrane, which is important in heme biosynthesis. Activity of purified ferrochelatase is affected by the presence of certain fatty acids. In the present study, we examined whether the activity of ferrochelatase is altered by dietary manipulation of the composition of mitochondrial membrane phospholipid fatty acylgroups.

Benign recurrent intrahepatic cholestasis: A long‐term follow‐up study of two patients

Charles M. A. Bijleveld, Roel J. Vonk, Folkert Kuipers, Rick Havinga, John Fernandes – 1 April 1989 – Two brothers with benign recurrent intrahepatic cholestasis were studied over a period of 6 years. During this period, 11 episodes of cholestasis were observed, with a mean duration of 2.6 months (range: 2 weeks to 6 months). Once, both brothers developed cholestasis simultaneously. There was a prevalence for episodes of cholestasis in wintertime.

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