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Biomedical subjects

A C Beynen

Publications and source records attributed to A C Beynen.

At least 325 records · Page 18Linked to original sources
PubMed1988

Assessment of discomfort in rats with hepatomegaly.

An attempt was made to assess discomfort in rats with hepatomegaly induced by feeding a high cholesterol, high cholate diet. After 8 weeks, the rats displayed a more than two-fold increase in liver weight when compared with controls fed a commercial diet. In a small open field test, behaviour of rats with hepatomegaly was similar to the controls. Of 9 parameters scored per rat, only the response to pressure on the right hypochondrium (tension of overlying muscles) scored higher than in control animals. There was considerable between-assessor variation in the assignment of scores. It is suggested, tentatively, that hepatomegaly in rats caused by cholesterol plus cholate feeding, may not cause extreme discomfort. Upon 'blind' palpation of control and test rats, an average of 60% of the rats with hepatomegaly were classified correctly.

Animals↗
PubMed1988

Atherosclerosis in the rat.

Rats are generally considered to be resistant to naturally occurring and experimentally induced atherosclerosis. In this review, data are presented which show that rats do develop arterial lesions. Spontaneous lesions can be detected microscopically only if a very large number of slides from different sites are screened. Heroic treatments, including extreme diets, hypothyreoidy, mechanical trauma of the arteries and hypertension, have been used to induce more easily detectable arterial lesions. Special strains of rats with increased susceptibility to atherogenesis have been developed. Although the induced atherosclerotic lesions in rats are generally quite different from those in man, the rat might be suitable to study specific aspects of atherosclerosis or to serve as a bioassay to identify factors promoting atherosclerosis.

Animals↗
PubMed1988

Interrelated effects of the type of dietary fat and carbohydrate on cholesterol metabolism in rats.

Rats were fed semipurified diets, differing in the amount of cholesterol and the sources of fat (corn oil or coconut fat) and carbohydrate (sucrose or starch). After 21 days dietary corn oil had induced higher serum cholesterol concentrations than did coconut fat, except for on diets with a high-cholesterol, high-sucrose background. On high-cholesterol diets containing coconut fat, dietary sucrose increased serum cholesterol, when compared with starch; with corn oil sucrose tended to lower serum cholesterol. Such a tendency was not seen on cholesterol-free diets. Cholesterol feeding caused a dramatic increase in liver cholesterol with all dietary carbohydrate-fat combinations. Liver cholesterol was higher in rats fed corn oil than in those fed coconut fat. The influence of the type of dietary carbohydrate on liver cholesterol was dependent on the type of fat and the amount of cholesterol in the diet. Thus effects of a single dietary component on serum and liver cholesterol in rats are strongly influenced by the background of the diet. This implies that published results of experiments on diet and cholesterol metabolism in rats cannot be compared readily.

Animals↗
PubMed1988

Dietary monounsaturated fatty acids and liver cholesterol.

Evidence is accumulating that diets rich in monounsaturated fatty acids might be of value in the treatment of hypercholesterolemia and prevention of coronary heart disease. This communication shows that such diets cause increased concentrations of liver cholesterol in rats and rabbits. It is not known whether this effect is harmful. Caution is warranted in extrapolating the animal data to man, but the possibility that monounsaturated fatty acids increase liver cholesterol in man should be considered.

Animals↗
PubMed1987

Dietary acetate and cholesterol metabolism in rats.

Rats were fed either cholesterol-free or high-cholesterol (1%, w/w) semipurified diets containing acetate (0.5%) or cholestyramine (0.44%) or both compounds for 29 days. The bile-acid binding resin, cholestyramine, did not affect serum and liver cholesterol, irrespective of whether the diet was cholesterol-free or contained cholesterol. In the cholesterol-free diets, acetate tended to lower the concentration of serum cholesterol, but did not influence liver cholesterol. When the diets contained cholesterol, acetate lowered liver cholesterol concentrations by about 20% both in the presence and absence of cholestyramine. Acetate did not affect the excretion of bile acids in feces. The mechanism by which acetate may partly counteract the increase in liver cholesterol seen after cholesterol feeding of rats, remains to be established.

Acetates↗
PubMed1987

Dietary cottonseed protein and cholesterol metabolism.

Low-gossypol, glandless cottonseed protein may become a major product for human consumption. In this presentation, the influence of cottonseed protein on several aspects of cholesterol metabolism will be described. Studies with rabbits and rats have shown that dietary cottonseed protein very effectively lowers the concentration of plasma cholesterol when compared to the animal protein casein. No such effect has been found in hamsters, but cottonseed protein may slightly elevate the percentage of serum total cholesterol carried by the high density lipoproteins. There is suggestive evidence that in humans the replacement of animal proteins in the diet by cottonseed protein causes a small decrease in serum cholesterol levels, but more studies are required to substantiate this. In hamsters dietary cottonseed protein effectively suppresses the formation of gallstones when compared to casein. On diets containing cottonseed protein the concentrations of both cholesterol and phospholipids in bile fluid are significantly decreased. We tentatively suggest that the consumption of cottonseed protein will have a favorable effect on cholesterol metabolism.

Animals↗
PubMed1987

Type of dietary carbohydrate and liver cholesterol in rats.

Rats were fed semipurified diets containing either sucrose or corn starch (72% or 29% of their total calories). Carbohydrates were exchanged for corn oil in equicaloric amounts. After 28 days, dietary sucrose had caused significantly lower concentrations of liver cholesterol than had starch. The sucrose-induced lowering of liver cholesterol, compared to starch, was amplified by increasing the amount of fat in the diet, at the expense of the carbohydrate source.

Animals↗
PubMed1987

Dietary glycine and cholesterol metabolism in rats.

Generally, diets containing casein induce higher concentrations of serum cholesterol in rats than diets containing soybean protein. It has been suggested that at least part of this effect is due to the relatively low level of glycine in casein, when compared to soybean protein. We have tested this suggestion by adding glycine to a semipurified casein diet, so that the level of glycine was similar to that in a diet containing soy protein. The addition of glycine did not affect the casein-induced concentrations of cholesterol in serum and liver of rats. We conclude that the low proportion of glycine in casein does not play a role in casein-induced hypercholesterolemia.

Animals↗
PubMed1987

Lack of regression of preestablished gallstones in mice.

Feeding a high cholesterol, high cholic acid diet to mice for 28 days caused increased concentrations of plasma and liver cholesterol and formation of gallstones. Removal of cholesterol and cholic acid from the diet led to normalization of plasma and liver cholesterol within 28 days. Regression of the preestablished gallstones did not occur within 107 days.

Animals↗
PubMed1987

Cholesterol metabolism and sterol carrier protein-2 (non-specific lipid transfer protein).

Hepatic sterol carrier protein-2 significantly enhances the microsomal conversion of cholesterol to 7 alpha-hydroxy-cholesterol. In the present work we have attempted to correlate the hepatic content of sterol carrier protein-2 with bile acid formation. We have determined the amount of this protein in a variety of physiological and experimental conditions, in which the rate of bile acid synthesis varies over a wide range, viz. during fetal development, in inbred strains of rats with different rates of bile acid synthesis, and in rats fed diets containing drugs which modify the rate of bile acid synthesis. The outcome of these experiments does not support the idea that sterol carrier protein-2 has any association with bile acid synthesis. From our data we further conclude that hepatic sterol carrier protein-2 is an adaptable protein because its level increases during development from the fetal to the post-weaning stage of the rat and since it can be modulated by oral administration of certain drugs. Furthermore, it is demonstrated that the level of sterol carrier protein-2 varies between six inbred strains of rats.

Animals↗
PubMed1987

Esterases in inbred strains of mice with differential cholesterolemic responses to a high-cholesterol diet.

Specific esterase isoenzyme patterns in plasma may be associated with responsiveness of serum cholesterol to dietary cholesterol. In rabbits and rats the presence and absence of a high-mobility, anodal esterase band on electrophoresis have been shown to be associated with hypo- and hyperresponsiveness, respectively. We fed for 28 days male mice of 7 inbred strains either a low-cholesterol, commercial diet or a diet containing 2% (w/w) cholesterol, 0.5% cholic acid and 5% olive oil. Feeding the high-cholesterol diet revealed marked inter-strain differences in the responses of plasma and liver cholesterol; the increases ranged from 21 to 129% and from 10 to 80-fold, respectively. There was no association between esterase isoenzyme patterns in plasma and the sensitivity to the high-cholesterol diet. The mean baseline plasma total esterase activity tended to be positively associated with the absolute response of plasma cholesterol to the high-cholesterol diet (r = 0.56; n = 7), but the positive relationship between the baseline concentration of the ES-1 component in plasma and the cholesterolemic response was stronger (r = 0.84; n = 7; P less than 0.05). The high-cholesterol diet caused a significant increase in plasma total esterase activities in 6 out of the 7 strains. Evidence is presented that the increase in plasma total esterase activity, which was associated with an increase in the activity and concentration of the so-called ES-2 isoenzyme, is the result of an enhanced release of esterases from the intestine, rather than from the liver. A significant, positive correlation was found between the baseline intestinal esterase activity and the cholesterolemic response after cholesterol feeding (r = 0.83; n = 7; P less than 0.05).

Alanine Transaminase↗
PubMed1987

Cholesterol metabolism and esterases in four strains of rats with differential cholesterolemic responses to a high-cholesterol, high-cholate diet.

The increase in serum cholesterol after feeding a diet containing 2% (w/w) of cholesterol and 0.5% of cholate for 13 days was 200 and 800% in two hypo- and two hyper-responsive inbred strains of rats, respectively. While remaining on the high-cholesterol, high-cholate diet for longer periods, the level of serum cholesterol dropped in the hyper-responsive strains, and after 8 weeks on the diet one hyper-responsive strain had similar serum cholesterol concentrations as the two hypo-responsive strains. The feeding of a semipurified diet, containing 1% (w/w) of cholesterol and 20% of fat, did not discriminate between the two hypo- and hyper-responsive strains with respect to the response of serum cholesterol. The activities in plasma of the indicators for liver function, aspartate amino transferase and alkaline phosphatase, were significantly increased in all strains after feeding the high-cholesterol, high-cholate diet. Only alkaline phosphatase was increased by the semipurified diet. Evidence is presented that in the four inbred strains of rats the differential cholesterolemic response to the high-cholesterol, high-cholate diet is not related to the baseline serum lipoprotein profile, liver cholesterol accumulation, fecal bile acid excretion, and the total activities and patterns of esterases in serum, liver and small intestine.

Animals↗
PubMed1987

Hypo- and hyperresponders: individual differences in the response of serum cholesterol concentration to changes in diet.

The feeding of cholesterol-rich diets to random-bred animals results in marked interindividual differences in the response of serum cholesterol. Certain animals show only small responses (hyporesponders), whereas others develop high degrees of hypercholesterolemia (hyperresponders). Inbred strains of rabbits, rats, and mice differing in their sensitivity to dietary cholesterol are available. In these animals, and also in monkeys, the responsiveness to high-cholesterol diets has a strong genetic basis. The existence of hyper- and hyporesponders also holds in humans, though not as pronounced as in laboratory animals. Repeated trials with the same subjects have shown that persons exist with a consistently low or high response to increased intakes of cholesterol. However, "spontaneous," diet-independent within-person variations in the level of serum cholesterol markedly inflate the between-person variation in the response of serum cholesterol; both variations are of the same order of magnitude. Hypo- and hyperresponsiveness to dietary cholesterol extends to other hypercholesterolemic components of the diet. In humans and rabbits hyperresponsiveness to dietary cholesterol is associated with responsiveness to dietary saturated fatty acids. The mechanisms underlying hypo- and hyperresponsiveness to dietary cholesterol have not yet been unraveled. On the basis of available data, we propose that in hyperresponders, compared with hyporesponders, there is a higher hepatic efflux of cholesterol in low-density lipoproteins (LDL), or its precursors, after cholesterol consumption. This may be caused by insufficient inhibition of cholesterol biosynthesis and/or the high capacity of cholesterol absorption in the hyperresponders. The stimulation of LDL production accounts for the increase in LDL cholesterol in serum. The number of hepatic LDL receptors, which may be already decreased in hyperresponders, will decrease further through down-regulation. The receptor-mediated LDL clearance decreases, but the absolute amount of LDL cholesterol taken up by the cells via the receptor and by the receptor-independent pathway increases because of the increased level of LDL cholesterol. In this way a new equilibrium is reached in which LDL production equals LDL catabolism. The phenomenon of hypo- and hyperresponsiveness may have implications for counseling subjects who attempt to lower their serum cholesterol by diet. However, identification of true hyper- and hyporesponders is greatly hampered by within-person fluctuations of the level of serum cholesterol. No simple test is available to discriminate hypo- from hyperresponders.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗