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Biomedical subjects

A C Beynen

Publications and source records attributed to A C Beynen.

At least 181 records · Page 10Linked to original sources

Dietary medium-chain fatty acids raise and (n-3) polyunsaturated fatty acids lower hepatic triacylglycerol synthesis in rats.

The hypothesis tested was that dietary medium-chain or (n-3) polyunsaturated fatty acids, when compared with (n-6) polyunsaturated fatty acids, alter plasma triacylglycerol levels by affecting hepatic triacylglycerol synthesis as reflected by the activities of acetyl-CoA carboxylase, fatty acid synthase and diacylglycerol acyltransferase in liver. In two separate experiments rats were fed purified diets containing (n-6) polyunsaturated fatty acids in the form of corn oil and either (n-3) polyunsaturated fatty acids in the form of fish oil or medium-chain triacylglycerols (MCT). Consumption of MCT significantly raised plasma triacylglycerol concentrations, whereas fish oil feeding had a lowering effect compared with the corn oil-fed group. In individual rats, the hepatic triacylglycerol concentration was directly correlated with the plasma triacylglycerol concentration (r = 0.60, P < 0.001). The MCT oil diet vs. the corn oil diet markedly raised the activities of hepatic acetyl-CoA carboxylase, fatty acid synthase and diacylglycerol acyltransferase. In the rats fed fish oil, the activities of fatty acid synthase and diacylglycerol acyltransferase were significantly reduced, whereas the activity of acetyl-CoA carboxylase was not affected relative to activities in rats fed corn oil. The activities of the three enzymes were directly correlated with plasma triacylglycerol concentrations in individual rats (r = 0.60-0.75, P < 0.001). The type of fat in the diet probably affects the rate of hepatic triacylglycerol synthesis which is an important determinant of plasma triacylglycerol concentrations.

Acetyl-CoA Carboxylase↗

Increasing phosphorus intake reduces urinary concentrations of magnesium and calcium in adult ovariectomized cats fed purified diets.

We assessed the phosphorus requirement of adult cats and the relationship between phosphorus intake and the fecal and urinary excretion of calcium, magnesium and phosphorus. Female cats (ovariectomized at the onset of sexual maturity) were fed purified diets containing 4.6, 9.2, 18.4 or 27.7 mmol phosphorus/MJ in a 4 x 4-wk crossover study. During the experiment, balance studies were performed and blood samples were taken. A dietary level of 4.6 mmol phosphorus/MJ was found to be sufficient to maintain phosphorus balance and normal plasma concentrations of phosphorus in the adult ovariectomized cats. Increasing levels of dietary phosphorus in the form of NaH2PO4.2H2O caused lower urinary pH values, lower urinary concentrations of calcium and magnesium, and higher urinary concentrations of phosphorus. When dietary levels of phosphorus were raised, the percentage of apparent absorption of magnesium was lower, whereas that of phosphorus was higher. Although it could be predicted that dietary phosphorus levels higher than the National Research Council recommendation of 9.2 mmol/MJ markedly reduced urinary struvite saturation, these higher levels are discouraged because they are associated with lower plasma phosphorus concentrations and creatinine clearance.

Absorption↗

Cholesterol consumption alters hepatic sphingomyelin metabolism in rats.

The hypothesis that cholesterol consumption alters hepatic sphingomyelin homeostasis was tested. Rats were fed a purified diet with or without added cholesterol (1 g/100 g) for up to 21 d. In accordance with previous work, cholesterol consumption significantly increased hepatic, whole plasma and VLDL cholesterol concentrations. Dietary cholesterol also raised the amount of sphingomyelin in the VLDL fraction, which was associated with a decrease in hepatic sphingomyelin concentrations. We suggest that the increase in hepatic VLDL secretion after cholesterol consumption imposed an increase in the demand for sphingomyelin in the liver because this phospholipid is a structural component of VLDL. Determination of the activity of two key enzymes of sphingomyelin homeostasis revealed that cholesterol consumption reduced the activity of acid sphingomyelinase in the liver but did not affect that of serine palmitoyltransferase. These enzyme data indicate that the extra sphingomyelin needed after cholesterol loading results from a decrease in the rate of its catabolism in the liver.

Acyltransferases↗

Coffee oil consumption does not affect serum cholesterol in rhesus and cebus monkeys.

Oil from coffee beans contains the diterpenes cafestol and kahweol, which greatly elevate cholesterol in humans. Consumption of 0.03 g coffee oil (0.86 mg cafestol and 1.04 mg kahweol)/kg body wt raised serum cholesterol by 1.27 mmol/L in volunteers. We fed coffee oil from this same batch to cebus and rhesus monkeys. Two groups of eight cebus monkeys were fed a purified diet containing 0.5% coffee oil or placebo oil (sunflower plus palm oil, 3:2, wt/wt) for 2 x seven and a half weeks in a crossover design. The daily intake of the coffee oil was 0.18 g (5.13 mg cafestol and 6.21 mg kahweol)/kg body wt, or sixfold that in the human study. Coffee oil did not affect plasma cholesterol or triglyceride concentrations compared with the placebo oil. Two groups of three rhesus monkeys were fed a commercial diet containing either 0.5% coffee oil or 0.5% placebo oil for 2 x 6 wk in a crossover design. The daily intake of coffee oil was 0.20 g (5.70 mg cafestol and 6.90 mg kahweol)/kg body wt. Again, there was no effect of coffee oil on plasma cholesterol or triglyceride concentrations. Contrary to the findings in human studies, coffee oil had no impact on plasma alanine aminotransferase activity in nonhuman primates. The cholesterol-raising effect of diterpenes from coffee oil, present in boiled coffee, seems to be specific for human primates.

Alanine Transaminase↗

Spleen pigmentation in young C57BL mice is caused by accumulation of melanin.

It has been previously reported that in 2 C57BL mouse sublines a dark pigmentation of the cranial part of the spleen occurs in up to 30% of the animals within the populations. It was not clear whether this discoloration is caused by melanosis, lipofuscinosis or haemosiderosis. With the use of light and electron microscopy of stained spleen sections, we identified the pigment in 14 out of 60 C57BL mice aged 8-10 wks. In the mice with pigmented spleens there was accumulation of melanin, predominantly in melanophores. Literature data indicate that apart from melanin, lipofuscin and haemosiderin can be observed in splenic macrophages provided that the mice are older than those studied by us. We conclude that melanin is the principal pigment causing spleen discoloration in young C57BL mice. Splenic melanosis displays inter-individual variation, but its relevance from a pathophysiological point of view remains obscure.

Animals↗

Absorption and retention studies of trace elements and minerals in rats using radiotracers and whole-body counting.

A description is given of a whole-body counting technique using radiotracers, permitting the determination of true absorption and endogenous excretion of trace elements and minerals in the rat in vivo. This non-invasive counting method involves oral and intraperitoneal administration of tracer doses of a radioisotope in a cross-over fashion and subsequent measurement of the whole-body retention in a whole-body counter. Thus, true absorption can be determined in one animal which contributes to the reduction of animal use. To study the variations in counting response due to radioisotope distribution, to size or shape of the animal body, the influence of the position of a point source and distribution over different phantoms to simulate various body sizes are experimentally evaluated for 64Cu, 65Zn, 59Fe and 28Mg. Results from 2 studies, with 64Cu and 28Mg, as an example for a trace element and a mineral respectively, are presented and illustrate that absorption as measured by apparent absorption does not necessarily reflect true absorption. True absorption as determined by the whole-body retention method using radioisotopes corrects for faecal losses of endogenous origin.

Absorption↗

Time trends of plasma lipids and enzymes synthesizing hepatic triacylglycerol during postpartum development of fatty liver in dairy cows.

We studied development of fatty liver in high producing dairy cows with free access to feed during the dry period and thus showed the combined effects of parturition and prepartum overfeeding. Postpartum liver triacylglycerol concentrations at 1 wk postpartum, as measured in liver biopsies, had increased more than 6-fold, which was preceded or accompanied by an increase in plasma NEFA concentrations. Concentrations of hepatic phospholipid changed only slightly. The amounts of total lipids in serum, very low density lipoproteins, and high density lipoproteins significantly decreased by .5 wk after parturition, and concentrations of high density lipoproteins rose steadily. The pattern was similar for concentrations of total cholesterol and phospholipid in serum. Total lipid concentrations in low density lipoproteins were not altered after parturition. The activity of microsomal phosphatidate phosphohydrolase in the liver showed a transient increase at .5 wk after calving, but activity of microsomal glycerolphosphate acyltransferase remained relatively constant. The activities of diacylglycerol acyltransferase had increased about twice at 1 wk after calving and remained at this high level until at least 4 wk after parturition. The rise in activity of diacyglycerol acyltransferase was probably a response to the extra influx of fatty acids to channel them into triacylglycerol. Activities of microsomal cholinephosphate cytidylyltransferase initially increased after calving and then decreased slightly. Activities of hepatic choline kinase had increased after calving. This study indicates that hepatic triacylglycerol accumulates because of the increased hepatic uptake of NEFA and the simultaneous increase in activity of diacylglycerol acyltransferase.

Acyltransferases↗

Dietary cholesterol--the role of eggs in the prudent diet.

The recommendation that not more than 300 mg cholesterol be consumed daily to prevent high serum cholesterol levels and coronary heart disease is often used to justify a restriction of egg intake to three or four per week. One egg contains about 200 mg of cholesterol, but eggs are also excellent and relatively inexpensive sources of essential amino acids and certain vitamins. In this paper, the place of eggs in a prudent, cholesterol-lowering diet as a substitute for other animal products, is scrutinised. The extra cholesterol, where considered as the only variable, will increase serum cholesterol levels, but the effect is relatively small. The exclusion of eggs from the diet should be weighed against deprivation of essential nutrients especially in vulnerable groups. While restriction of egg intake in westernised populations seems justifiable, the upper limit of three or four per week may not always be applicable, depending on the overall diet and lipid profile of the individual.

Cholesterol↗

Influence of dietary retrograded starch on the metabolism of neutral steroids and bile acids in rats.

Diets enriched in retrograded amylose (RS3) have been shown to lower serum cholesterol concentrations in rats. The possibility was tested that this hypocholesterolaemic effect of RS3 is caused by an increase in excretion of neutral steroids and/or bile acids. Six groups of ten rats were fed on purified diets containing either 12 or 140 g RS3/kg solid ingredients with and without added cholesterol (5g/kg). Low-RS3 diets, with and without added cholesterol, to which the bile-acid-binding resin cholestyramine (20 g/kg) was added, were used as reference. The high-RS3 diets v. the low-RS3 diets tended to reduce the increase in the total serum cholesterol concentration during the course of the experiment (P = 0.067), decreased serum triacylglycerol concentrations, raised total neutral steroids and total bile acids in caecal contents and faecal excretion of total bile acids, but lowered faecal excretion of neutral steroids. In addition, the serum concentration of total 3 alpha-bile acids was markedly raised by the high-RS3 diets. The high-RS3 diets raised the faecal excretion of lithocholic and muricholic acids, but lowered that of hyodeoxycholic acid, and increased the caecal amounts of lithocholic, ursodeoxycholic, beta-muricholic and omega-muricholic acids. Apart from the stimulation of faecal bile acids excretion, the effects of cholestyramine on bile acid metabolism differed at various points from those of RS3. Cholesterol feeding had predictable effects on cholesterol metabolism and led to greater elevating effects of RS3 on the faecal and caecal amounts of muricholic acids. The results suggest that the serum-cholesterol-lowering effect of high-RS3 diets may be explained by an increased influx of neutral steroids and bile acids into the caecum, and increased faecal excretion of bile acids, and/or by an altered intestinal bile acid profile.

Amylose↗

[Neurodegenerative disorders of the central nervous system in horses].

The most important neurodegenerative diseases of the horse are reviewed. In addition to the literature, neurodegenerative diseases occurring in patients (horses, Mongolian Przewalski-horses, and two zebras) referred to the Utrecht Veterinary Faculty are mentioned. Neurodegenerative diseases described are: I. ataxia associated with: A/ static stenosis, B/ dynamic stenosis, C/ lesions at various locations in the central nervous system, D/ equine herpesvirus infections, E/ equine degenerative myelo-encephalopathy, or F/ cerebellar abiotrophy; II. equine motor neuron disease; III. grass sickness or equine dysautonomia; IV. postanaesthetic myelomalacia; and V. equine leuko-encephalomalacia. The patient descriptions show, that mixed forms of some of the differentiated diseases can be diagnosed. Little is known with certainty about the aetiology of the neurodegenerative lesions found. In some patients vitamin E may play a role, possibly in combination with other factors. A mycotoxin known to interfere with myelin metabolism is involved in leuko-encephalomalacia.

Animals↗

Thyroid function and deiodinase activities in rats with marginal iodine deficiency.

The hypothesis tested was whether marginal iodine deficiency for a period of 6 wk affects iodothyronine deiodinase activities in liver and brain of rats. Male rats were fed purified diets either deficient or sufficient in iodine; the diets were fed on a restricted basis (60% of ad libitum intake). Body weight gain of the two groups was comparable. Iodine deficiency was evidenced by increased thyroid weight (26%), reduced urinary iodine excretion (80%), and reduced plasma T4 concentrations (22%). Activities of liver type I and brain type III deiodinase were unchanged, but the activity of type II deiodinase in brain was increased (28%) in the iodine-deficient rats. Food restriction per se significantly lowered T3 (30%) and T4 (22%) concentrations in plasma and decreased type III deiodinase activity in brain (30%). These results indicate that in marginal iodine deficiency the activities of hepatic type I deiodinase and brain type III deiodinase are unchanged, whereas that of brain type II deiodinase is increased.

Animals↗

The combined effect of high iron and zinc intake on copper status in rats.

The interactions between copper, zinc, and iron intake in rats were investigated with regard to copper status. Weanling male rats were fed purified diets containing two levels of each of the three elements in a 2(3) factorial design. The added amounts of copper, zinc, and iron in the diets were 5, 12, and 35 mg/kg feed or were 10 times as high. After feeding on the experimental diets for 4 wk, the rats were killed and copper concentrations in plasma and organs measured. Plasma copper concentration was lowered by high zinc and iron intakes but this was seen only in the rats fed the normal-copper instead of the high-copper diets. In essence, the effects of zinc and iron were additive. Neither in rats fed the normal-copper diets nor in those fed the high-copper diets did extra iron or zinc intake alter copper concentrations in liver, spleen, kidney, and tibia.

Analysis of Variance↗

Dietary fructose v. glucose in rats raises urinary excretion, true absorption and ileal solubility of magnesium but decreases magnesium retention.

Apparent Mg absorption, that is Mg intake minus faecal excretion, was found to be greater in rats fed on diets containing fructose instead of glucose. This effect of fructose was accompanied by enhanced urinary excretion and diminished retention of Mg. True Mg absorption was then determined with the use of oral and intraperitoneal administration of tracer doses of 28 Mg. True Mg absorption was significantly greater in rats fed on fructose. There was no significant effect of fructose v. glucose on faecal excretion of endogenous Mg. It was hypothesized that fructose enhances the solubility of Mg in the ileal lumen and thereby facilitates its absorption. The distribution of Mg between the solid and liquid phases of the ileum was determined in rats fed on either glucose or fructose. Fructose reduced the amount of Mg in the solid phase but raised both the amount and the concentration of Mg in the liquid phase. We conclude that the dietary-fructose-induced stimulation of Mg absorption in rats is caused by a raised solubility of ileal Mg, but the mechanism by which fructose exerts this effect and why it was not associated with a decrease in faecal excretion of endogenous Mg remain unknown. Dietary fructose v. glucose did not systematically affect the apparent absorption of Ca and P.

Animals↗

Iron, copper and zinc status in rats fed on diets containing various concentrations of tin.

The effects of various dietary concentrations of Sn (1, 10, 50, 100 and 200 mg/kg; added as SnCl2) on Fe, Cu and Zn status of rats were determined. After feeding the diets for 28 d body weight was not significantly affected, but there was a linear inverse response of feed intake. Plasma, kidney, spleen and tibia Fe concentrations as well as blood haemoglobin concentration and percentage transferrin saturation decreased in a linear dose-response manner as the level of dietary Sn increased. The addition of Sn to the diet depressed Cu status, as indicated by a significant inverse response of plasma, liver, kidney, spleen and tibia Cu levels. Plasma, kidney and tibia Zn concentrations were decreased by increasing levels of dietary Sn, but spleen and liver Zn concentrations were not significantly influenced. Fe, Cu and Zn status was influenced by dietary Sn concentrations lower than 50 mg/kg. If the results can be extrapolated to man it would follow that a high v. low Sn concentration in the human diet, which can be as distinct as 75 v. 2 mg/kg dry diet, may decrease plasma and tissue concentrations of Fe, Cu and Zn by up to 15%.

Animals↗

Comparison between time-dependent changes in iron metabolism of rats as induced by marginal deficiency of either vitamin A or iron.

To compare the changes in Fe metabolism during the development of vitamin A and Fe deficiencies, rats were given either a control diet with sufficient Fe (35 mg added Fe/kg feed) and retinol (1200 retinol equivalents/kg feed), a diet without added vitamin A or a diet with sufficient vitamin A but only 3.5 mg added Fe/kg feed. During a period of 10 weeks, indicators of vitamin A and Fe status were monitored. Neither vitamin A nor Fe deficiency produced clinical signs. Fe deficiency induced an immediate fall in blood haemoglobin concentration. Vitamin A deficiency produced a mild anaemia as the first change in Fe metabolism, pointing to impaired erythropoiesis. This effect was followed by a rise in Fe absorption and an increased amount of Fe in the spleen. By the end of the study, blood haemoglobin, packed cell volume, plasma Fe and Fe content in kidney and femur had increased above control levels, while total Fe-binding capacity had decreased. We speculate that the initial anaemia was masked later by haemoconcentration. The decrease in Fe mobilization, shown by lower total Fe-binding capacity, and the increase in Fe absorption may have caused the observed continuous rise in tissue Fe concentration in rats with vitamin A deficiency. In the rats with Fe deficiency, low tissue Fe levels coincided with high Fe absorption and high total Fe-binding capacity. Thus, changes in Fe metabolism with vitamin A deficiency differed from those with Fe deficiency.

Anemia, Hypochromic↗

Dietary ascorbic acid lowers the concentration of soluble copper in the small intestinal lumen of rats.

We tested the hypothesis that ascorbic acid in the diet of rats lowers the concentration of soluble Cu in the small intestine, causing a decrease in apparent Cu absorption. Male rats were fed on diets adequate in Cu (5 mg Cu/kg) without or with 10 g ascorbic acid/kg. The diet with ascorbic acid was fed for either 6 or 42 d. Ascorbic acid depressed tissue Cu concentrations after a feeding period of 42, but not after 6 d. Dietary ascorbic acid lowered apparent Cu absorption after 6, but not after 42 d. The lowering of tissue Cu concentrations after long-term ascorbic acid feeding may have increased the efficiency of Cu absorption, and thus counteracted the inhibitory effect of ascorbic acid. Dietary ascorbic acid caused a significant decrease in the Cu concentrations in the liquid phase of both the proximal and distal parts of the small intestinal lumen. This effect was due to both a decrease in the amount of Cu in the liquid digesta and an increase in the volume of the liquid phase; only the latter effect for the distal intestine was statistically significant. We conclude that ascorbic acid supplementation lowers Cu absorption by decreasing the concentration of soluble Cu in the small intestine.

Animals↗

Increasing intakes of iron reduce status, absorption and biliary excretion of copper in rats.

High intakes of Fe may impair Cu status, but the underlying mechanism is not known. Male rats, aged 7 weeks, were given purified diets adequate in Cu (8 mg Cu/kg) and containing either 7, 40 or 389 mg Fe/kg. After 6 weeks the concentrations of Fe in liver and spleen were positively related with dietary Fe level and those of Cu were negatively related with dietary Fe level. Increasing Fe intakes reduced apparent absorption and biliary excretion of Cu in a dose-dependent fashion. In individual rats, biliary Cu excretion showed a significant, positive correlation with liver Cu concentration. It is concluded that increased Fe intakes depress Cu absorption which produces a decrease in plasma and organ Cu concentrations. As a result, biliary Cu excretion is lowered which contributes to achieving Cu balance at high Fe intakes. Because the concentrations of Cu in plasma and bile, and also plasma ceruloplasmin (EC 1.16.3.1) activities, showed much greater percentage reductions with increasing Fe intake than did the concentrations of Cu in organs, it is possible that increased Fe status interferes with the mobilization of Cu stores.

Animals↗

Substitution of dietary calcium chloride for calcium carbonate reduces urinary ph and urinary phosphorus excretion in adult cats.

In a 4x4-wk cross-over study, eight adult cats were given four moist diets containing identical amounts of calcium (13.9 mmol/MJ) but with different ratios of calcium carbonate to calcium chloride, the calcium salts providing half of the total dietary calcium. Increasing amounts of calcium chloride were substituted for equimolar amounts of calcium carbonate. Higher intakes of calcium chloride caused significantly lower pH values in postprandial and 24-h urine samples. The urinary excretion of ammonium and titratable acid rose with increasing calcium chloride intake. The urinary concentrations of calcium and magnesium were not affected by the type of calcium salt, but the urinary excretion and concentration of phosphorus were significantly depressed when the amount of calcium chloride in the diet was increased. The results are discussed in the context of dietary prevention of and therapy for struvite urolithiasis in cats.

Animals↗