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ABSTRACT: Vitamin A deficiency produces anemia and altered iron status. In this study with rats we tested two hypotheses regarding vitamin A deficiency: (1) that it impairs erythropoiesis, leading to an increased red cell turnover, and (2) that it inhibits the glycosylation of transferrin. Erythropoietic activity was assessed indirectly by determining the myeloid:erythroid ratio in bone marrow smears, the number of erythroid colonies in the red pulp of spleen, the blood reticulocyte index, and zinc protoporphyrin and plasma transferrin receptor concentrations. Transferrin glycosylation was assessed by measuring the sialic acid content of transferrin. The effects of vitamin A deficiency were compared with those of iron deficiency. Iron deficiency produced anemia and low iron levels in organs. Vitamin A deficiency produced low levels of plasma and hepatic retinol, and it induced decreased plasma total iron-binding capacity and raised iron levels in tibia and spleen. Short- but not long-term iron deficiency reduced the number of erythroid colonies in spleen; vitamin A deficiency had no influence. Neither iron nor vitamin A deficiency influenced the myeloid:erythroid ratio in bone marrow smears and the blood reticulocyte production. Plasma transferrin receptor and erythrocyte zinc protoporphyrin concentrations were not affected by vitamin A deficiency but increased with iron deficiency. Vitamin A deficiency did not stimulate erythrocyte breakdown, as indicated by unaltered plasma lactate dehydrogenase activity and reduced plasma total bilirubin levels. Both vitamin A and iron deficiencies raised the proportion of multiple sialylated transferrins in plasma. Thus, we have not found evidence that vitamin A deficiency affects erythropoiesis and erythrocyte turnover. The iron accumulation in spleen and bone marrow may be related to reduced iron transport due to inhibition of transferrin synthesis rather than inhibition of transferrin sialylation.
The Journal of Nutritional Biochemistry 05/2000; 11(4):223-30. · 3.89 Impact Factor
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ABSTRACT: Studies with anaemic children and pregnant women from areas where vitamin A deficiency is endemic have shown a beneficial effect on Fe status of supplemental vitamin A in addition to Fe supplementation. This suggests a relationship between vitamin A and Fe status, which we attempted to mimic in rats with anaemia and chronic vitamin A deficiency. Male rats were fed on Fe-adequate diets (35 mg Fe/kg) containing different levels of vitamin A (1200, 450, 150, 75 and 0 retinol equivalent (RE)/kg feed) until they were 5 weeks old. These diets were identical to the diets fed to their mothers. Then the young male rats were transferred to diets containing the same levels of vitamin A but no added Fe. After another 2 weeks the rats were repleted with Fe (35 mg/kg feed) without or with vitamin A to a level of 1200 RE/kg feed. Increased vitamin A intake by the groups previously fed on diets with either 0 or 75 RE/kg produced a reduction in blood haemoglobin concentration, packed cell volume and erythrocyte count. In the group which had been fed on the diet without vitamin A, supplemental vitamin A raised mean cell volume, plasma Fe concentration and total Fe-binding capacity. Vitamin A supplementation during the period of Fe repletion produced a decrease in splenic and tibia Fe concentration, the effect being greater with increasing severity of previous vitamin A deficiency. The paradoxical effect of supplemental vitamin A on haemoglobin, packed cell volume and erythrocyte count can be explained by a decrease in the degree of haemoconcentration. Thus, the positive effect of supplemental vitamin A seen in humans is also observed with rats under controlled experimental conditions. We speculate that supplemental vitamin A during Fe repletion contributes to optimum erythropoiesis and Fe mobilization when baseline vitamin A status is impaired.
British Journal Of Nutrition 05/1996; 75(4):623-36. · 3.01 Impact Factor
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ABSTRACT: In order to induce a range of vitamin A-deficient states in young growing rats and to study the effect of vitamin A deficiency on Fe status, we designed the following two-generation experiment. Dams were fed on diets with one of five vitamin A levels from 2 weeks before and throughout pregnancy and lactation. The pups received the same diets as their mothers both before and after weaning. The five dietary levels of vitamin A were 1200, 450, 150, 75 and 0 retinol equivalents/kg feed. Vitamin A intake did not affect reproduction outcome, nor were body and liver weights of the pups affected when they were 3.5 weeks old. Male pups with normal vitamin A status had higher plasma retinol levels than female pups. Vitamin A status of the offspring was affected from 3.5 weeks onwards. Body and liver weights were decreased in the male pups given the lowest dietary vitamin A levels from week 6.5 onwards but not in the female pups. Fe status was marginally affected. Haemoglobin levels were increased and total Fe-binding capacity was decreased in the groups given no dietary vitamin A at week 9.5. Splenic Fe was increased only in the male pups given the lowest levels of dietary vitamin A. However, as a whole, Fe status was only mildly affected and subject to considerable variation. We conclude that the two-generation rat model described here is not suitable for studying effects of vitamin A deficiency on Fe metabolism.
British Journal Of Nutrition 12/1995; 74(5):689-700. · 3.01 Impact Factor
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ABSTRACT: 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.
British Journal Of Nutrition 07/1994; 71(6):887-95. · 3.01 Impact Factor
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ABSTRACT: 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.
British Journal Of Nutrition 06/1994; 71(5):687-99. · 3.01 Impact Factor
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ABSTRACT: Severe vitamin A deficiency in rats is known to cause anaemia associated with growth retardation and impaired water retention. However, study of the effect of marginal vitamin A intake is of more interest because such intake may mirror the situation in humans in many developing countries. Therefore, in two experiments, the effect of marginal vitamin A deficiency on Fe status was investigated in male rats. After 28 d of feeding either low- or high-vitamin A diets (0 or 120 v. 1200 retinol equivalents/kg feed), body weight and feed intake were not influenced by the level of vitamin A in the diet. Liver weight was lowered by vitamin A deficiency. Water intake was not influenced in rats fed on a low-vitamin A diet. Plasma retinol concentrations were decreased in rats fed on diets low in vitamin A. Marginal vitamin A deficiency produced slightly lower blood haemoglobin concentrations; it did not systematically affect packed cell volume. The concentration of Fe in liver was significantly higher when diets low in vitamin A were fed, but hepatic Fe mass was not affected. Significantly lower Fe levels were observed in femurs of rats with vitamin A deficiency. The effects on liver and femur Fe concentrations were seen with diets adequate in Fe but not with diets deficient in Fe. The efficiency of apparent Fe absorption was significantly increased by low intakes of vitamin A, provided that the dietary Fe concentration was adequate. It is speculated that depressed uptake of Fe by bone marrow is the primary feature of altered Fe status in rats with marginal vitamin A deficiency.
British Journal Of Nutrition 12/1993; 70(3):777-85. · 3.01 Impact Factor
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ABSTRACT: The effect of vitamin A deficiency or the lentogenic La Sota strain of Newcastle disease virus (NDV) infection, or both, on immunoglobulin (IgA and IgM) levels in bile and plasma were investigated. In addition, tissue distribution of IgA-, IgG- and IgM-containing cells was studied to establish the source of these Ig. Chickens (1-d-old) with limited vitamin A reserves were fed ad lib. on diets containing either marginal or adequate levels of vitamin A. At 4 weeks of age, half the chickens in each group were infected with NDV. The number of IgA- and IgM-containing cells was not significantly affected by vitamin A deficiency, demonstrating that neither class-switching nor homing of Ig-containing cells is influenced by vitamin A deficiency. Although bile IgM levels were not significantly different in vitamin A-deficient chickens compared with normal chickens, IgA levels were significantly lower. This decrease was even more pronounced in deficient NDV-infected chickens, despite the higher number of IgA-containing cells found in these birds. These results, together with the slightly increased levels of IgA in plasma of vitamin A-deficient chickens, suggest that the hepatobiliary transport of IgA is impaired by vitamin A deficiency and possibly also by NDV infection, although disturbed secretion by IgA-containing cells cannot be excluded.
British Journal Of Nutrition 12/1992; 68(3):753-63. · 3.01 Impact Factor
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ABSTRACT: The effect of vitamin A deficiency on iron status was investigated in rats. After 28 d of feeding either low or high vitamin A diets (0 vs 4000 IU of vitamin A per kg feed), the final body weight was slightly but significantly lowered by the low vitamin A diet. Plasma retinol concentrations were decreased in rats fed diets low in vitamin A. Marginal vitamin A deficiency produced slightly, but significantly lower blood hemoglobin concentrations; it did not clearly affect hematocrit. The concentration of iron in liver was significantly higher when diets low in vitamin A were fed while significantly lower levels were observed in femur.
Biological Trace Element Research 11/1992; 35(1):81-4. · 1.92 Impact Factor
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ABSTRACT: Marginally vitamin A-deficient 1-d-old chickens capable of remaining healthy for at least 6 weeks were produced using a two-generation model. In this model, hens fed on diets with a limited vitamin A content were used to obtain 1-d-old chickens which were marginally deficient in vitamin A. Only hens with a narrow range of plasma retinol values (0.60-0.85 mumol/l) were satisfactory for this purpose. Above this range the 1-d-old chickens were not marginally vitamin A deficient. Below this range egg production and hatchability were affected to some extent depending on the degree of vitamin A deficiency. Even when egg production and hatchability remained at a high level in such birds, the 1-d-old chickens produced were not sufficiently strong to survive the first weeks of life. The advantages of the two-generation model for producing marginally vitamin A-deficient chickens are the increased uniformity and predictability of the chickens with respect to body-weight, general health and vitamin A status. However, it does take about 3 months to produce such chickens.
British Journal Of Nutrition 08/1992; 68(1):283-91. · 3.01 Impact Factor
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ABSTRACT: The effect of infection with infectious bronchitis virus (IBV) and reovirus (RV) on vitamin A status was investigated in chickens with a normal or marginal intake of vitamin A. At the age of 4 wk, chickens were infected with either IBV or RV, primarily affecting the respiratory or intestinal tract, respectively. Both viruses lowered plasma retinol levels significantly. The effect was more pronounced in chickens fed a diet marginally deficient in vitamin A than in those fed a diet adequate in vitamin A. Concentrations of retinol-binding protein, transthyretin and albumin in RV-infected chickens were also significantly lower than in noninfected chickens fed the same diets; in chickens infected with IBV, there was no effect. These results suggest that the reduced vitamin A status of IBV-infected chickens could be attributed to increased rate of utilization by tissues. In RV infection, this mechanism could be involved but impaired absorption of nutrients (including vitamin A) and direct loss of nutrients via the intestinal tract could also be important.
Journal of Nutrition 03/1992; 122(2):333-9. · 3.92 Impact Factor
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ABSTRACT: The effect of vitamin A deficiency and Newcastle disease virus (NDV)-infection on peripheral blood lymphocytes (PBL) was studied by differential cell counting and flow cytometry. Day-old chickens were fed purified diets containing either marginal or adequate levels of vitamin A and at 26 days of age half of the chickens in each group were infected with NDV. The absolute numbers of PBL and their subpopulations were studied until 10 days after infection. Vitamin A deficiency resulted in significantly lower numbers of PBL throughout the experiment. NDV-infection produced lymphopenia during the first 3 days, followed by a strong increase in PBL numbers after 6 days. Both changes in PBL were less pronounced in vitamin A-deficient birds. For flow cytometric analysis monoclonal antibodies reacting specifically with B-cells or a subpopulation of T-cells were used. Vitamin A-induced lymphopenia could be attributed to a decreased number of PBL, negative for both antibodies, and to the absence of an increase in B-cells which normally occurs at this age. The negative cells are suggested to represent, at least partially, cytotoxic T-cells, which may explain the impaired cytotoxic T-cell-activity found in earlier studies. NDV-induced lymphopenia and subsequent increase of PBL could be attributed to all cell types investigated. However, in vitamin A-deficient birds negative cells did not show these reactions. Therefore, it can be concluded that vitamin A deficiency has a detrimental effect on PBL, negative for both antibodies used, and on the normal growth of the number of B-cells at this age.
Veterinary Immunology and Immunopathology 03/1992; 31(1-2):155-66. · 2.08 Impact Factor
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Proceedings of The Nutrition Society 09/1991; 50(2):251-62. · 2.77 Impact Factor
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ABSTRACT: The effect of vitamin A deficiency on the activity of peritoneal macrophages (PM) was investigated in noninfected and Newcastle disease virus (NDV)-infected chickens. Day-old chickens with limited vitamin A reserves were fed diets containing either marginal (120 retinol equivalents (RE)/kg) or adequate (1200 RE/kg) levels of vitamin A. At 4 weeks of age, half of the chickens in each group were infected with the La Sota strain of NDV and PM were isolated 11 or 12 days later. These were used for counting the uptake of fluorescein isothiocyanate-labeled yeast cells as an indicator of phagocytic activity and for measuring the reduction of nitroblue tetrazolium (NBT), which provides an estimate of oxygen-dependent killing of microorganisms. Vitamin A deficiency impaired NBT reduction and, to a lesser extent, phagocytosis in both infected and noninfected chickens. NDV infection increased phagocytosis and NBT reduction in normal and, to a lesser extent, in vitamin A-deficient chickens.
Veterinary Immunology and Immunopathology 04/1991; 28(1):17-27. · 2.08 Impact Factor
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ABSTRACT: The effect of vitamin A deficiency in the presence or absence of Newcastle disease virus infection (NDV, La Sota strain) on weight of lymphoid organs and on the number and type of circulating white blood cells (WBC) was investigated in chickens. Day-old chickens with limited vitamin A reserves were fed purified diets containing either marginal (ad libitum) or adequate (pair-fed) levels of vitamin A and at 21-28 days of age; half the chickens in each group were infected with NDV. Vitamin A deficiency resulted only in significantly lower absolute and relative weights of bursa of Fabricius and after infection both weights of bursa and thymus were significantly lower. Relative weight of spleen was significantly higher after infection irrespective of vitamin A status. Liver weights were not affected by vitamin A status and/or NDV infection. Both vitamin A deficiency and NDV infection resulted in lymphopenia, while the lowest number of WBC were observed in vitamin A-deficient chickens during the acute phase of NDV (5 days after infection). Subsequent to lymphopenia due to NDV infection, a marked lymphocytosis was observed in controls and to a lesser extent in vitamin A-deficient birds. These results indicate that vitamin A deficiency, which is aggravated by concomitant NDV infection, affects lymphoid cell systems.
Developmental & Comparative Immunology 02/1991; 15(4):349-56. · 3.27 Impact Factor
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ABSTRACT: The effect of vitamin A deficiency on cytotoxic T lymphocyte (CTL) activity was investigated during the acute phase of disease 7 days after primary inoculation and 1 day after secondary inoculation in chickens with or without Newcastle disease virus (NDV, La Sota strain) infection. Day-old chickens with limited vitamin A reserves were fed purified diets containing either marginal (ad libitum) or adequate (pair-fed) levels of vitamin A, and at 3 weeks of age half of the chickens in each group were infected with NDV. Cytotoxic activity was investigated during the acute phase of disease (7 days after primary inoculation) and 1 day after secondary inoculation, in an assay system with either peripheral blood lymphocytes (PBL) or nonadherent splenocytes as effector cells and adherent splenocytes from the same animal as target cells. After primary inoculation, cytotoxic activity could only be demonstrated in nonadherent splenocytes. Vitamin A deficiency resulted in significantly reduced CTL activity at all effector/target cell ratios tested. After reinfection CTL activity could also be demonstrated in PBL, but only from chickens fed the control diet, suggesting a diminished pool of CTL in vitamin A deficiency. The results of this study indicate that vitamin A deficiency impairs CTL activity - a part of the cell-mediated defense system - and this may have important implications for recovery from viral infection.
Veterinary Immunology and Immunopathology 11/1990; 26(2):191-201. · 2.08 Impact Factor
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ABSTRACT: The effect in rabbits of giving isonitrogenous purified diets containing casein, ovalbumin, fish protein, milk-whey protein and soya-bean protein were compared. The diets were balanced for cholesterol and for the amount and type of fat. When incorporated into low-cholesterol diets (0.08 g cholesterol/kg), casein, ovalbumin and soya-bean protein produced similar levels of serum cholesterol. With a high background of dietary cholesterol (1.5 g/kg), serum cholesterol concentrations increased with soya-bean protein, whey protein, casein and fish protein, in that order. Thus, the hypercholesterolaemic effect of casein in carefully balanced diets was only seen against a high-cholesterol background. The development of hypercholesterolaemia produced by giving fish protein was different from that produced by casein. First, less cholesterol accumulated in the very-low-density-lipoprotein fractions and more in the lipoproteins of higher density with fish protein than with casein. Second, fish protein, unlike casein, did not increase liver cholesterol. Third, transfer of rabbits from a diet containing soya-bean protein to one containing casein resulted in an immediate marked depression in neutral steroid and bile acid excretion in faeces. However, when rabbits were fed on the diet with fish protein after the diet with soya-bean protein, there was no significant depression in neutral steroid output and the depression in bile acid output was delayed. The present study suggests that different animal proteins cause hypercholesterolaemia by different mechanisms.
British Journal Of Nutrition 10/1990; 64(2):473-85. · 3.01 Impact Factor
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ABSTRACT: Swine fitted with re-entrant ileo-cecal cannulas were fed purified diets containing either casein or soybean protein to study possible relations between cholesterol metabolism, digestion of dietary constituents and postprandial patterns of various serum components. Compared with soybean protein, dietary casein produced an increase in serum total cholesterol in which the excess cholesterol was located in the low density lipoprotein fraction. Ileal and fecal excretion of neutral steroids was diminished in pigs fed casein, suggesting that cholesterol absorption was stimulated. The apparent ileal absorption of protein was increased in pigs fed casein. The enhanced absorption of cholesterol and protein was associated with a reduced rate of flow of chyme through the ileum. The output of bile acids in the feces of pigs fed casein was decreased, whereas the ileal output was not significantly affected. This could be attributed to increased uptake of bile acids from the cecum and/or colon, which may in part be related to the indirectly observed decreased formation of secondary bile acids. Postprandial serum concentrations of insulin and glucose were temporarily increased in pigs fed casein, whereas those of triglycerides were decreased. We suggest that the decreased excretion of cholesterol and bile acids is the major determinant of casein-induced hypercholesterolemia in swine.
Journal of Nutrition 06/1990; 120(5):422-30. · 3.92 Impact Factor
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ABSTRACT: One day old pullets derived from marginally vitamin A deficient laying hens were fed diets containing either adequate or marginal amounts of vitamin A. At the age of 34 days, animals fed the diet low in vitamin A had group mean plasma concentrations of retinol which were one tenth the mean plasma concentrations of controls. When compared with their controls, the deficient animals displayed body weights which were on average 16% less. Of 20 pullets per dietary group one control animal and 9 deficient animals died by the age of 34 days. At the age of 29 days, control (n = 16) and deficient chickens (n = 11) were examined clinically by assigning scores to a number of parameters. Three assessors carried out the examination independently. The birds were presented for examination at random and their treatment groups were not disclosed to the assessors. Out of 26 parameters assessed quantitatively per individual animal, only three parameters discriminated between control and deficient chickens. Deficient animals grew poorly, had a hunched up posture and increased fluid content in faeces. Classical signs of chronic vitamin A deficiency in domestic fowl such as bone deformities, keratinization of the tongue and decreased transparency of the cornea were not observed.
Laboratory Animals 11/1989; 23(4):307-12. · 1.21 Impact Factor
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ABSTRACT: Adult male rabbits were fed on semi-purified diets containing soya-bean protein isolate, casein or formaldehyde-treated casein as the protein source and 1 g cholesterol and 5 g of the non-absorbable marker chronic oxide/kg diet. The concentration of cholesterol in serum and in liver was increased on both the casein and formaldehyde-treated-casein diets. Excretion of bile acids and their concentration in faeces were lower in rabbits fed on casein or formaldehyde-treated casein when compared with rabbits fed on soya-bean protein. Apparent digestibility of nitrogen was lowest when formaldehyde-treated casein was fed, and highest on the casein diet. In rabbits fed on casein treated with formaldehyde, higher proportions of N were found in the water-soluble and trichloroacetic acid-insoluble protein fractions of the gastrointestinal tract contents compared with rabbits on the other two diets. Absorption of phosphate from the gastrointestinal tract was higher in rabbits fed on casein than in rabbits fed on soya-bean protein or formaldehyde-treated casein. The results indicate that, in rabbits, protein digestibility may not be an important determinant of serum cholesterol.
British Journal Of Nutrition 10/1989; 62(2):331-42. · 3.01 Impact Factor
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ABSTRACT: Treatment of casein with formaldehyde changes its tertiary structure and decreases its hypercholesterolemic properties in rabbits. To investigate whether formaldehyde-treated casein exerts this hypocholesterolemic effect in the same manner as soybean protein, rabbits were fed high or low cholesterol diets containing soybean protein, casein, formaldehyde-treated casein or a mixture of casein and formaldehyde-treated casein. Formaldehyde-treated casein was hypocholesterolemic when fed in a low, but not in a high, cholesterol diet. The hypocholesterolemic effect of soybean protein was independent of the amount of cholesterol included in the diet. In contrast to rabbits fed soybean protein, steroid absorption in those fed formaldehyde-treated casein did not differ from that in rabbits fed native casein. Furthermore, the absorption of phosphorus and nitrogen was lower in rabbits fed formaldehyde-treated casein than in those fed native casein, whereas the absorption found in rabbits fed soybean protein resembled that of their casein-fed counterparts. The diets containing soybean protein and formaldehyde-treated casein produced a comparable ratio of lysine to arginine in serum. The results presented in this paper indicate that the hypocholesterolemic action of dietary formaldehyde-treated casein does not resemble that of soybean protein.
Journal of Nutrition 07/1989; 119(6):843-56. · 3.92 Impact Factor
