Sebaceous gland atrophy in the rat after a portacaval shunt.
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Biomedical subjects
F Magne
Publications and source records attributed to F Magne.
Chronic biliary drainage corrects liver atrophy induced by portacaval shunt in the rat.
Portacaval shunt induces a severe liver atrophy. The relative liver hypertrophy induced by chronic biliary drainage was studied by electron microscopy. Rats with either portacaval or sham portacaval shunt had a 4-day chronic bile fistula. Compared with rats not submitted to chronic bile fistula, liver weight/body weight ratio increased from 1.84 to +/- 0.12 to 3.54 +/- 0.48 (p less than 0.05) in portacaval shunt and from 3.52 +/- 0.15 to 3.64 +/- 0.40 (p less than 0.05) in sham portacaval shunt (controls). Chronic bile fistula stimulated bile acid synthesis in the two groups. Furthermore, the initial low bile flow observed in portacaval shunt (rats) reached control values after chronic bile fistula. Ultrastructural abnormalities observed in portacaval shunt: atrophy of the hepatocyte mainly related to the atrophy of the rough and smooth endoplasmic reticulum, irregularity of the nucleus, dilatation of the nuclear envelope and of the rough endoplasmic reticulum, and swelling of mitochondria, were greatly modified by chronic bile fistula. The hepatocyte size increased, mitochondria appeared smaller than normal, the nuclear envelope and the rough endoplasmic reticulum were not dilated, and the rough and smooth endoplasmic reticulum were expanded. Chronic bile fistula had no noticeable effect on the liver in sham portacaval shunt. Either stimulation of bile salts synthesis or removal of bile salts, which could be toxic for the atrophic liver, are possible explanations for the relative hypertrophy of the liver.
Animals↗
[Metabolism of bile salts. 2 - The cholanopathies (author's transl)].
A better understanding of the mechanisms of bile acid metabolism, coupled with advances in methodology, has shown the major part played by bile salts in the pathogenesis of several diseases, such as cholesterol cholelithiasis, secretory diarrhoea and/or steatorrhoea associated with diseases of the small intestine, etc. This in turn has helped to develop effective medical treatments for some of these conditions. Considerable progress has also been made in determining the abnormalities in bile acid metabolism found in parenchymal and cholestatic liver diseases and in rare conditions associated with inborn errors in bile acid synthesis. The clinician's approach to diagnosis and treatment has thus been thoroughly modified by improved knowledge of bile acid metabolism.
Bile Acids and Salts↗
[Metabolism of bile salts. 1. Control of synthesis (author's transl)].
Bile acids, which are essential to the digestion of fat, are synthetized in the liver from cholesterol, and changes in synthesis usually parallel changes in cholesterol synthesis. Mainly located in the gallbladder and intestine, they circulate several times a day between these two organs (enterohepatic circulation). The pool of bile salts remains constant, the amount synthetized daily being equal to those lost through the faeces. Bile acid synthesis is controlled by a feed-back mechanism represented by the amount of bile salts reaching the sinusoidal membranes of liver cells.
Animals↗