Hepatobiliary transport of hepatic 3‐hydroxy‐3‐methylglutaryl coenzyme a reductase inhibitors conjugated with bile acids

Ernst Petzinger, Lutz Nickau, Jurgen A. Horz, Siegfried Schulz, Gunther Wess, Alfons Enhsen, Eugen Falk, Karl‐Heinz Baringhaus, Heiner Glombik, Axel Hoffmann, Stefan Müllner, Georg Neckermann, Werner Kramer – 1 December 1995 – To obtain prodrugs with affinity to liver parenchymal cells, the hepatic 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitors HR 780 and lovastatin (syn. mevinolin) were conjugated with the bile acids cholic acid, taurocholic acid, and glycocholic acid.

The natural history of nonalcoholic fatty liver: A follow‐up study

Mohd R. Teli, Oliver F. W. James, Alastair D. Burt, Mark K. Bennett, Christopher P. Day – 1 December 1995 – Nonalcohol‐induced fatty liver is widely believed to be a benign condition with little or no risk of disease progression. There have been occasional reports of progression to cirrhosis but none in the absence of preexisting fibrosis on the index biopsy specimen even when co‐existing hepatitis was present (steatohepatitis). From our histological database (1978 to 1985), we identified 161 patients with fatty liver seen at our institution and traced the case notes of 156.

Molecular dissection of the mitogenic effect of hepatocytes on cultured hepatic stellate cells

Axel M. Gressner, Birgit Lahme, Arnfried Brenzel – 1 November 1995 – The activation of proliferation of rat liver hepatic stellate cells (HSC) in cooperation with hepatocytes (PC) was studied using a coculture system and cell‐conditioned media, respectively. The proliferation of HSC was followed by incorporation of [3H] thymidine and BrdU into DNA and by DNA content per culture.

Choline deficiency: A cause of hepatic steatosis during parenteral nutrition that can be reversed with intravenous choline supplementation

Alan L. Buchman, Mark D. Dubin, Adib A. Moukarzel, Donald J. Jenden, Margareth Roch, Kathleen M. Rice, Jeff Gornbein, Marvin E. Ament – 1 November 1995 – Patients receiving long‐term total parenteral nutrition (TPN) develop hepatic steatosis as a complication. Our previous studies have shown this to be caused, at least in part, by choline deficiency. We studied four patients (1 man, 3 women) aged 50 ± 13 years who had low plasma‐free choline concentrations 4.8 ± 1.7 (normal, 11.4 ± 3.7 nmol/mL). The patients had received TPN for 9.7 ± 4.7 years.

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