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H J Weis

Publications and source records attributed to H J Weis.

12 recordsLinked to original sources
PubMed1979

Tupaias (tree shrews)--a new animal model for gallstone research. II. Influence of fat, sugar, and cholesterol on bile composition.

The lipid composition of bile obtained from the gallbladder and from the liver of tupaias was determined. Compared to the gallbladder bile of man, the gallbladder bile of tupaias contains the same percentage of phospholipids (PL), one third of the cholesterol (CH), and 50% more total bile acids (TBA). The lithogenic index (LI) of the bile is about 0.2--0.3. No significant sex differences or diurnal variations are found in the composition of bile. The concentration of PL, CH, and TBA is found 5 to 8 times higher in the gallbladder bile than in the liver bile. The bile acid spectrum in tupaias equals that in man qualitatively and is similar quantitatively. In a feeding experiment, the influences of butter, cholesterol, butter plus cholesterol and sucrose on bile composition, clinicochemical serum values, and liver and gallbladder histology were studied. Groups of six animals each were fed the different diets over a 10-week period. In group A: 20% butter added to the standard diet, PL content was higher, the LI was unchanged. In group B: 2% cholesterol added to the standard diet, the CH value and the LI were elevated, CH crystals but no stones were found. In group C: 2% cholesterol and 20% butter in the standard diet, stone formation was observed. PL and CH values were higher than in group A and B, TBA values were lower. In group D: 50% sucrose added to the standard diet very low PL and TBA values were determined in the liver bile, resulting in elevated LIs. It is concluded that all three components of a diet, which had proven lithogenic in a preceding experiment (Schwaier, 1979a), contribute to gallstone formation.

Animals↗
PubMed1975

The interaction of various control mechanisms in determining the rate of hepatic cholesterogenesis in the rat.

In these studies rats were subjected to diurnal light-cycling, stress, fasting and the feeding of cholestyramine, beta-sitosterol and cholesterol in various combinations. In control animals exposed to light cycling for 2 weeks the rate of hepatic cholesterogenesis was 3.7 fold higher in the mid-dark than in the mid-light phase of the light cycle. The magnitude of this difference varied with the duration of light cycling and the size of the animals. Similarly, enhanced rates of cholesterol synthesis were seen in the mid-dark phase relative to the mid-light phase of the light cycle in rats where the base-line level of hepatic cholesterogenesis was increased by feeding cholestyramine (1.6-fold) or beta-sitosterol (2.9-fold) or was depressed by fasting (19-fold) or cholesterol feeding (2.1-fold). Restraining animals for 48 h also increased the rate of cholesterol synthesis in the liver; in control animals, this stress enhanced the level of cholesterogenesis seen at both the mid-light and mid-dark phases of the light cycle. In addition, both the effects of stress and of diurnal light cycling could be identified in groups of animals where base-line cholesterogenic activity was varied by fasting or by feeding cholestyramine, beta-sitosterol or cholesterol. These studies illustrate the complexity of the control of hepatic cholesterol synthesis and suggest that the final rate of cholesterogenesis may be the result of several different effectors modifying by different mechanisms the activity of beta-hydroxy-beta-methylglutaryl-CoA reductase.

Animals↗
PubMed1975

The kinetic characteristics of inhibition of hepatic cholesterogenesis by lipoproteins of intestinal origin.

In these studies intestinal lipoproteins were injected intravenously into recipient rats in order to study the kinetic characteristics of cholesterol uptake by the liver cell and inhibition of the cholesterol synthetic pathway. Net cholesterol uptake from circulating intestinal lipoproteins took place only in the liver, and only this tissue manifested inhibition of cholesterol syntheses. Cholesterol uptake by the liver, quantified by a rise in the cholesterol ester content, was a linear function of time and of the amount of lipoprotein cholesterol administered to the animals. Using groups of rats that were either fed cholesterol or injected intravenously with intestinal lipoproteins as a bolus or as a continuous infusion, there was generally a correlation between inhibition of the rate of cholesterol synthesis and the cholesterol ester content of the liver. However, there was no consistent quantitative relationship between these two variables suggesting either that cholesterol ester was not the immediate effector of the inhibition or, alternatively, that there was intracellular localization of the effector at the site of control of the rate-limiting enzyme in the cholesterogenic pathway.

Animals↗