Iodothyronine deiodinase activity in methionine-deficient rats fed selenium-deficient or selenium-sufficient diets

We examined the effect of methionine deficiency on iodothyronine 5’-deiodinase activity in selenium-deficient rats or selenium-sufficient rats fed sodium selenate or selenomethionine. Forty-two weanling male Wistar rats were divided into six groups and pair fed the respective purifiedl-amino acid-based diets for 4 wk.l-methionine concentrations in the diet were 8.0 g/kg for sufficient rats, and 2.0 g/kg for deficient rats. Selenium concentrations in the diet were 0.5 mg/kg (as sodium selenate or selenomethionine) for selenium-sufficient rats and less than 0.005 mg/kg for selenium-deficient rats. Type I 5’-deiodinase activities were significantly lower in liver and higher in kidney of methionine-deficient rats than in those of methionine-sufficient rats fed either the selenium-sufficient or the selenium-deficient diets. The type I 5’-deiodinase activity in brain was significantly lower in the methionine-deficient rats than in the methionine-sufficient rats fed the selenium-deficient diet. Type II 5’-deiodinase activity in brain was significantly higher in the methionine-deficient rats than in the methionine-sufficient rats fed selenium-sufficient diet as sodium selenate. Both thyroxine and 3,3’,5-triiodothyronine concentrations in plasma were significantly higher in the methionine-deficient rats than in the methionine-sufficient rats. It is suggested that the methionine deficiency affects the 5’-deiodinase activity and thyroid hormones level in the rats.     

The effects of selenium depletion and repletion on the metabolism of thyroid hormones in the rat

Rats were fed selenium-deficient (less than 0.005 mg selenium/kg) or selenium-supplemented diets (0.1 mg selenium/kg, as Na2SeO2) for up to five wks from weaning to assess the effects of developing selenium deficiency on the metabolism of thyroid hormones. Within two wks 3:5,3'-triiodothyronine (T3) production from thyroxine (T4) in liver homogenates from selenium-deficient rats was significantly lower compared with the activity in liver homogenates from selenium-supplemented rats. This decreased activity was probably responsible, in part, for the higher T4 and lower T3 concentrations in plasma from the selenium-deficient rats after 3, 4, and 5 weeks of experiment. Repletion of selenium-deficient rats with single intra-peritoneal injections of 200 micrograms selenium/kg body wt. (as Na2SeO3) 5 days before sampling reversed the effects of the deficiency on thyroid hormone metabolism and significantly increased liver and plasma glutathione peroxidase activities. However a dose of 10 micrograms selenium/kg body wt given to rats of similar low selenium status had no effect on thyroid hormone metabolism or glutathione peroxidase activity but did reverse the increase in hepatic glutathione S-transferase activity characteristic of severe selenium deficiency. Imbalances in thyroid hormone metabolism are an early consequence of selenium deficiency and are probably not related to changes in hepatic xenobiotic metabolizing enzymes associated with severe deficiency.     

Zinc deficiency and the activities of lipoprotein lipase in plasma and tissues of rats force-fed diets with coconut oil or fish oil

The present study was performed to investigate the effect of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and tissues of rats fed diets containing either coconut oil or fish oil as dietary fat, using a bifactorial experimental design. To ensure an adequate food intake, all the rats were force-fed by gastric tube. Experimental diets contained either 0.8 mg zinc/kg (zinc-deficient diets) or 40 mg zinc/kg (zinc-adequate diets). The effects of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and postprandial triglyceride concentrations and distribution of apolipoproteins in serum lipoproteins depended on the type of dietary fat. Zinc-deficient rats fed the coconut oil diet exhibited a reduced activity of lipoprotein lipase in postheparin serum and adipose tissue, markedly increased concentrations of triglycerides in serum, and a markedly reduced content of apolipoprotein C in triglyceride-rich lipoproteins and high density lipoproteins compared with zinc-adequate rats fed coconut oil. By contrast, zinc-deficient rats fed the fish oil diet did not exhibit reduced activities of lipoprotein lipase in postheparin serum and adipose tissue and increased concentrations of serum lipids compared with zinc-adequate rats fed the fish oil diet. This study suggests that a reduced activity of lipoprotein lipase might contribute to increased postprandial concentrations of serum triglycerides observed in zinc-deficient animals. However, it also demonstrates that the effects of zinc deficiency on lipoprotein metabolism are influenced by dietary fatty acids.     

Zinc supplementation on serum levels and hepatic conversion of thyroid hormones in obese (ob/ob) mice

The supplemental effects of zinc on thyroid status in obese (ob/ob) mice were studied. Four-week-old obese mice and their lean controls were fed either a basal diet or a zinc-supplemented diet (200 mg/kg diet) for 8 wk. Following the 8-wk basal diet, obese mice had lower serum T4 values, as well as hepatic T4 and T3 values, than lean mice (p < 0.05). A significant decrease in hepatic 5′-deiodinase activity was also observed in obese mice. Dietary zinc supplementation significantly reduced serum T4 levels in both the obese and lean mice. However, the zinc-supplemented effects on diminishing hepatic T4 and T3 values, as well as on 5′-deiodinase activities, were found only in obese mice (p < 0.05). Furthermore, the 5′-deiodinase activities in hepatic microsomal pellets after incubation with various zinc concentrations (0.5, 1.0, and 2.5 mM) were also examined. The 5′-deiodinase activities, in hepatic samples from all mice, were significantly attenuated by zinc treatments. However, this effect was more predominant in obese mice following the addition of 0.5 mM zinc. This study suggests that a lower hepatic 5′-deiodinase activity, resulting from a higher zinc level, might be related to abnormal energy metabolism in theob/ob mice.     

Chromium (III) Propionate and dietary fructans supplementation stimulate erythrocyte glucose uptake and beta-oxidation in lymphocytes of rats

The study describes the effects of 10-wk dietary supplementation with fructans (inulin and oligofructose, 5% and 10%, respectively) as well as the biomimetic Cr(III) propionate complex (0.5 and 5 mg Cr/kg diet) on blood glucose, insulin, glucose transmembrane transport, and β-oxidation of fatty acids in healthy male rats. No significant differences in blood serum glucose concentrations were found. Rats fed diets supplemented with the biomimetic complex (5 mg Cr/kg diet) had markedly decreased serum insulin level by 15%, whereas the red blood cells (RBCs) glucose transmembrane transport and β-oxidation of fatty acids in white blood cells (WBCs) were elevated by 9% and 77%, respectively. These effects were accompanied by a slight decrease of the insulin-resistance index. Oligofructose and the high-fructan diet (10%) were more effective in increasing the RBCs glucose transmembrane transport vs inulin and lowfructan diet (5%). Also, β-oxidation of fatty acids in WBCs was increased by 37.5% in groups fed the high-fructan diet (10%). The results suggest that dietary fructans and the biomimetic Cr(III) complex exerted beneficial effects on glucose and lipid metabolism, increasing the efficiency of their utilization.     

Zinc status does not affect aluminum deposition in tissues of rats

To examine whether zinc deficiency would increase the toxicity of dietary aluminum, weanling, male Sprague-Dawley rats were fed purified diets containing either 2 or 30 mg Zn/kg diet, with or without 500 mg Al/kg diet for 28 d. Individually pair-fed rats were fed the 30 mg Zn/kg diet with or without added aluminum to control for inanition secondary to zinc deficiency. Rats fed the 2 μg Zn/kg diet showed evidence of zinc deficiency, including anorexia, growth retardation, and depressed concentrations of zinc in tibias and livers. Zinc deficiency did not significantly increase the concentrations of aluminum in the tibias, livers, kidneys, or regions of the brain examined (cerebrum, cerebellum, midbrain, and hippocampus). Inclusion of aluminum in the diet did not alter aluminum concentrations in the various tissues. Under the conditions of this study, zinc deficiency did not result in greater sensitivity to dietary aluminum exposure.     

Effect of excitatory amino acids on serum TSH and thyroid hormone levels in freely moving rats

The actions of glutamate (L-Glu), and glutamate receptor agonists on serum thyroid hormones (T4 and T3) and TSH levels have been studied in conscious and freely moving adult male rats. The excitatory amino acids (EAA), L-Glu, N-methyl-D-aspartate (NMDA), kainic acid (KA) and domoic acid (Dom) were administered intraperitoneally. Blood samples were collected through a cannula implanted in the rats jugular 0--60 min after injection. Thyroid hormone concentrations were measured by enzyme immunoassay, and thyrotrophin (TSH) concentrations were determined by radioimmunoassay. The results showed that L-Glu (20 and 25 mg/kg) and NMDA (25 mg/kg) increased serum thyroxine (T4), triiodothyronine (T3) and TSH concentrations. Serum thyroid hormone levels increased 30 min after treatment, while serum TSH levels increased 5 min after i.p. administration, in both cases serum levels remained elevated during one hour. Injection of the non-NMDA glutamatergic agonists KA (30 mg/kg) and Dom (1 mg/kg) produced an increase in serum thyroid hormones and TSH levels. These results suggest the importance of EAAs in the regulation of hormone secretion from the pituitary-thyroid axis, as well as the importance of the NMDA and non-NMDA receptors in this stimulatory effect.     

Effects of copper, iron, and ascorbic acid on manganese availability to rats.

Four experiments were done to characterize the interactions of copper, iron, and ascorbic acid with manganese in rats. All experiments were factorially arranged Dietary Mn concentrations were less than 1 micrograms/g (Mn0) and 50 micrograms/g (Mn+). Dietary Cu was less than 1 mg/g (Cu0) and 5 micrograms/g (Cu+); dietary Fe was 10 micrograms/g (Fe10) and 140 micrograms/g (Fe140). Ascorbic acid (Asc) was not added to the diet or added at a concentration of 10 g/kg diet. Experiment 1 had two variables, Mn and Cu; in Experiment 2, the variables were Mn and Asc. In Experiment 3, the variables were Mn, Cu, and Asc; in Experiment 4, they were Mn, Cu, and Fe. Definite interactions between Mn and Cu were observed, but they tended to be less pronounced than interactions between Mn and Fe. Cu depressed absorption of 54Mn and accelerated its turnover. In addition, adequate Cu (Cu+), compared with Cu0, depressed liver, plasma, and whole blood Mn of rats. Absorption of 67Cu was higher in animals fed Mn0 diets than in those fed Mn+. Ascorbic acid depressed Mn superoxide dismutase activity and increased Cu superoxide dismutase activity in the heart. The addition of ascorbic acid to the diet did not affect Mn concentration in the liver or blood. Absorption of 54Mn was depressed in rats fed Fe140 compared with those fed Fe10. Interactions among Fe, Cu, and Mn resulted in a tendency for Mn superoxide dismutase activity to be lower in rats fed Fe140 than in rats fed Fe10. Within the physiologic range of dietary concentrations, Mn and Cu have opposite effects on many factors that tend to balance one another. The effects of ascorbic acid on Mn metabolism are much less pronounced than effects of dietary Cu, which in turn affects Mn metabolism less than does Fe.     

Serum superoxide dismutase 3 (extracellular superoxide dismutase) activity is a sensitive indicator of Cu status in rats

Sensitivity of the assay for Cu,Zn superoxide dismutase 3 (SOD3), the predominant form of SOD in serum, can be increased, and interferences caused by low-molecular-weight substances in the serum can be reduced by conducting the assay at pH 10 with xanthine/xanthine oxidase and acetylated cytochrome c (cyt c) as superoxide generator and detector, respectively. Serum SOD3 activity was assayed under these conditions in an experiment where weanling, male rats were fed diets for 6 weeks containing 3, 5 and 15 mg Zn/kg with dietary Cu set at 0.3, 1.5 and 5 mg Cu/kg at each level of dietary Zn. Serum SOD3 responded to changes in dietary Cu but not to changes in dietary Zn. A second experiment compared serum SOD3 activity to traditional indices of Cu status in weanling, male and female rats after they were fed diets containing, nominally, 0, 1, 1.5, 2, 2.5, 3 and 6 mg Cu/kg for 6 weeks. Serum SOD3 activity was significantly lower (P < .05) in male rats fed diets containing 0 and 1 mg Cu/kg and female rats fed diet containing 0 mg Cu/kg compared with rats fed diet containing 6 mg Cu/kg. These changes were similar to changes in liver Cu concentrations, liver cyt c oxidase (CCO) activity and plasma ceruloplasmin in males and females. Serum SOD3 activity was also strongly, positively correlated with liver Cu concentrations over the entire range of dietary Cu concentrations (R(2) = .942 in males, R(2) = .884 in females, P < .0001). Plots of serum SOD3 activity, liver Cu concentration, liver CCO activity and ceruloplasmin as functions of kidney Cu concentration all had two linear segments that intersected at similar kidney Cu concentrations (18-22 microg/g dry kidney in males, 15-17 microg/g dry kidney in females). These findings indicate that serum SOD3 activity is a sensitive index of Cu status.     

Goitres in rats fed polychlorinated biphenyls.

Rats fed a polychlorinated biphenyl (PCB) mixture in a high- or low-iodine diet (HID or LID respectively) for 15 days had thyroid enlargement, low serum thyroxine (T4), and high serum thyrotropin concentrations. Although binding of thyroid hormones to serum proteins was reduced in PCB-fed animals, the free T4 index (reflecting free T4 in serum) was less in these rats. Both serum triiodothyronine (T3) and the free T3 index were elevated in rats fed PCB in HID. LID-maintained rats elevated serum T3 concentrations but the free T3 index was similar to that in HID-fed rats, owing to enhanced binding of thyroid hormone to serum proteins. Addition of PCB to LID reduced serum T3 levels but did not alter the free T3 index because binding was less. In rats fed HID containing PCB, thyroid 131I uptake was increased.     

Oleuropein supplementation increases urinary noradrenaline and testicular testosterone levels and decreases plasma corticosterone level in rats fed high-protein diet

The effects of oleuropein, a phenolic compound in extra virgin olive oil, on protein metabolism were investigated by measuring testicular testosterone and plasma corticosterone levels in rats fed diets with different protein levels. In Experiment 1, rats were fed experimental diets with different protein levels (40, 25 and 10 g/100 g casein) with or without 0.1 g/100 g oleuropein. After 28 days of feeding, the testosterone level in the testis was significantly higher and the plasma corticosterone level was significantly lower in rats fed the 40% casein diet with oleuropein than in those fed the same diet without oleuropein. The urinary noradrenaline level, nitrogen balance and hepatic arginase activity were significantly higher in rats fed the 40% casein diet with oleuropein supplementation than in those fed the 40% casein diet without oleuropein supplementation. In Experiment 2, the effects of oleuropein aglycone (a major phenolic compound in extra virgin olive oil and the absorbed form of oleuropein ingested in the gastrointestinal tracts) on the secretion of luteinizing hormone (LH) from the pituitary gland, which regulates testosterone production in the testis, were investigated in anesthetized rats. Plasma LH level increased dose dependently after the administration of oleuropein aglycone (P<.001, r= 0.691). These findings suggest that dietary supplementation with 0.1 g/100 g oleuropein alters the levels of hormones associated with protein anabolism by increasing urinary noradrenaline and testicular testosterone levels and decreasing plasma corticosterone level in rats fed a high-protein diet.     

Effects of zinc and/or iron deficiency on rectal temperature in rats

O'Dell et al. reported that rectal temperature was decreased by zinc deficiency in rats. However, it is not known whether a combined deficiency of zinc and iron affects rectal temperature. Forty 4-wk-old male Sprague-Dawley rats were assigned into four dietary treatment groups of 10 rats each for the 4-wk study: zinc-deficient group (4.5 mg Zn and 35 mg Fe/kg diet; −Zn), iron-deficient group (30 mg Zn/kg diet, no supplemental iron; −Fe), zinc/iron-deficient group (4.5 mg Zn/kg diet, no supplemental iron; −Zn−Fe), and control group (AIN-93G; Cont). At d 24–27, the rectal temperature was determined. The rectal temperature of the −Zn group was significantly lower than the Cont group. The rectal temperature of the −Zn−Fe group was similar to that of the Cont group, although thyroid-stimulating hormone and total thyroxin concentrations were the lowest in the −Zn−Fe group among all groups. The pattern of the plasma nitrate/nitrite concentrations across groups was similar to rectal temperature. Although observation of the rectal temperature is not conclusive, the balance between zinc and iron intake seems to determine the body temperature set point. These results suggest that the thermogenic effect of thyroid hormones is not throught to influence the paradoxical maintenance of rectal temperature in combined deficiency of zinc and iron.     

Dietary daidzein,but not genistein,has a hypocholesterolemic effect in non-ovariectomized and ovariectomized female Sprague-Dawley rats on a cholesterol-free diet

We compared the effects of two major isoflavones, daidzein and genistein, on lipid metabolism in rats. Daidzein (150 mg/kg diet), genistein (150 mg/kg diet), daidzein and genistein (1:1, 300 mg/kg diet), or control diets were fed to 4 groups of 6-week-old ovariectomized (Ovx) and non-Ovx Sprague Dawley rats for 4 weeks. Dietary daidzein, but not genistein, reduced serum and hepatic total cholesterol levels significantly relative to that by the control group, regardless of whether the rats had undergone ovariectomy. Genistein did not exhibit any physiological effects on lipid levels, but did affect genes involved in cholesterol metabolism. These results indicate that daidzein and genistein may influence lipid regulation via differing modes of action.     

The effects of marginal maternal vitamin A status on penta‐brominated diphenyl ether mixture‐induced alterations in maternal and conceptal vitamin A and fetal development in the Sprague Dawley rat

BACKGROUND: Polybrominated diphenyl ether (PBDE) toxicity in rodents can be associated with disruptions in endocrine signaling. We previously reported that the penta‐BDE mixture, DE‐71, disrupts thyroid hormones and vitamin A metabolism in rats during lactation, and that this disruption is amplified in animals fed diets marginal in vitamin A. The ability of the DE‐71 to disrupt vitamin A metabolism during the prenatal period has not been evaluated. While penta‐BDE mixtures are not strong teratogens in pregnant animals fed standard commercial laboratory diets, we hypothesized that they could be teratogenic under conditions of marginal vitamin A status. METHODS : rats were fed diets containing 0.4 retinyl equivalents (RE, marginal) or 4.0 RE (adequate) of vitamin A per gram of diet. Pregnant animals were exposed to DE‐71 (0, 6, 18, 60, or 120 mg/kg) from gestation days (GD) 6–11.5, or on GD 6–19.5. RESULTS : DE‐71 treatment resulted in dose‐responsive reductions in maternal thyroid hormone and markers of vitamin A metabolism, with the latter reduction amplified in marginal vitamin A dams. Fetuses from marginal vitamin A, DE‐71‐exposed dams exhibited a dose‐responsive increase in liver retinol binding protein levels. DE‐71 treatment did not result in gross malformations; however, consistent with our hypothesis, GD 20 fetal weights were lower, and skeletal ossification was less when DE‐71 exposure occurred concomitant with a marginal vitamin A status. For several endpoints, observable effects were evident at the lowest dose tested, consistent with a dose‐response trend. CONCLUSIONS : The results of this study support the concept that marginal vitamin A status enhances the disruptive effects of DE‐71 during prenatal development. Birth Defects Research (Part B) 86:48‐57, 2009. © 2009 Wiley‐Liss, Inc.     

Fat metabolism is regulated by altered gene expression of lipogenic enzymes and regulatory factors in liver and adipose tissue but not in semimembranosus muscle of pigs during the fattening period

It has been shown previously that lipid metabolism is regulated by fatty acids (FA) and that thyroid hormones are important regulators of energy metabolism. The effects of weight, dietary fat level and dietary FA profile on thyroid hormone levels and expression of lipogenic genes and tissue FA composition were studied. Sixty-one crossbred gilts weighing 62 ± 5.2 kg BW average were either slaughtered at the beginning of the trial (n = 5) or fed one of seven diets (n = 8 pigs per diet): a semi-synthetic diet formulated to contain a very low level of fat (NF) and six diets based on barley-soybean meal supplemented with approximately 10% fat of different origin and slaughtered at 100 kg BW. The supplemental fats were tallow, high-oleic sunflower oil, sunflower oil (SFO), linseed oil, fat blend (55% tallow, 35% sunflower oil, 10% linseed oil) and fish oil blend (40% fish oil, 60% linseed oil). In general, the dietary FA profiles altered the FA composition of liver, semimembranosus muscle and adipose tissues. Pigs fed the NF diet had the highest free and total triiodothyronine (T3) values followed by pigs fed SFO. Total T3 levels were higher in pigs at 60 kg than in pigs at 100 kg. Correlations between thyroid hormones and genes encoding enzymes of fat synthesis in adipose tissue (acetyl CoA carboxylase (ACACA), fatty acid synthase and stearoyl CoA desaturase (SCD)) and the large differences in expression of lipogenic genes at different weights (60 and 100 kg BW), suggest a role for thyroid hormones and for T3, in particular, in regulating whole animal fat metabolism, with effects brought about by altered expression of lipogenic genes. Liver sterol receptor element binding protein-1 (SREBP1) mRNA content was affected by dietary treatment (P < 0.001) and was correlated with ACACA and SCD, whereas adipose tissue SREBP1 was not correlated with the mRNA abundance of any lipogenic enzyme. Weight and tissue factors showed greater influence on mRNA abundance of genes related with lipid metabolism than diet and tissue FA composition. In the pig, FA synthesis appear to be of greater magnitude in adipose tissue than in the liver as suggested by the higher expression of lipogenic genes in adipose tissue.     

High intakes of tin lower iron status in rats

The effects of relatively low (1, 10, and 50 mg/kg) and high (100 and 200 mg/kg) dietary concentrations of tin (added as stannous chloride) on iron status of rats were determined. After feeding the diets for 28 d, feed intake and body weights were not significantly affected. Iron concentrations in plasma, spleen, and tibia as well as percentage transferrin saturation were decreased in rats fed the diets supplemented with 100 or 200 mg tin/kg. In rats fed the diet containing 200 mg tin/kg, group mean hemoglobin, hematocrit, and red blood cell count were slightly lowered but total iron binding capacity was not affected. Iron status was not influenced by dietary tin concentrations lower than 100 mg/kg. If these results can be extrapolated to humans, then it may be concluded that tin concentrations in the human diet, which range from 2 to 76 mg/kg dry diet, do not influence iron status in humans.     

Fusarium toxin residues in physiological samples of piglets

Physiological samples of 100 piglets fed diets containing 0.01, 0.06, 0.15, 0.22 and 0.42 mg ZON and 0.2, 0.8, 1.0, 1.9 and 3.9 mg DON per kg over a period of 35±1.5 days were investigated for concentrations of deoxynivalenol (DON) and zearalenone (ZON) and their metabolites. DON was detected in serum, bile and urine in increasing concentrations corresponding to the diet contamination. The metabolite de-epoxy-DON was detected only in urine. The DON contamination of the diet was closely reflected by the serum concentrations of the piglets. ZON and its metabolite α-zearalenol were detected in bile fluid, liver and urine, while β-zearalenol was only detected in bile fluid. In serum neither ZON nor its metabolites were found. The total concentration of ZON plus its metabolites in the bile fluid corresponded well with the dietary contamination. For all analyses it has to be noted that toxin residues were detectable even in individual samples of piglets fed the control diet containing 0.01 mg ZON/kg and 0.2 mg DON/kg. Presented at the 25^th Mykotoxin Workshop in Giessen, Germany, May 19–21, 2003     

Zinc deficiency decreases the activity of calmodulin regulated cyclic nucleotide phosphodiesterases in vivo in selected rat tissues

The effect of zinc deficiency on calmodulin function was investigated by assessing the in vivo activity of two calmodulin regulated enzymes, adenosine 3′,5′-monophosphate (c-AMP) and guanosine 3′,5′-monophosphate (c-GMP) phosphodiesterase (PDE) in several rat tissues. Enzymatic activities in brain, heart, and testis of rats fed a zinc deficient diet were compared with activities in these tissues from pair fed, zinc supplemented rats. In testis, a tissue in which zinc concentration decreased with zinc deficient diet, enzyme activities were significantly decreased over those in rats who were pair fed zinc supplemented diets. In brain and heart, tissues in which zinc concentrations did not change with either diet, enzymatic activities between the groups were not different. These results indicate that zinc deficiency influences the activity of calmodulin-regulated phosphodiesterases in vivo supporting the hypothesis that zinc plays a role in calmodulin function in vivo in zinc sensitive tissues.     

Calcium exacerbates the inhibitory effects of phytic acid on zinc bioavailability in rats

BackgroundComplementary feeding of breastfed infants with foods high in bioavailable zinc (Zn) can help meet physiological requirements for Zn. Some infant cereals contain high concentrations of phytic acid (PA) and calcium (Ca) that may reduce absorbable Zn.ObjectivesThis study measured PA, Zn and Ca concentrations in selected infant cereals sold in Canada and investigated the effects of dietary PA and Ca at concentrations present in infant cereals on Zn bioavailability in rats.Methods and resultsMale Sprague-Dawley rats (36-day old) were fed a control diet containing normal Zn (29.1 mg/kg) and Ca (4.95 g/kg) or six test diets (n = 12/diet group). Test diets were low in Zn (8.91–9.74 mg/kg) and contained low (2.16–2.17 g/kg), normal (5.00–5.11 g/kg) or high (14.6–14.9 g/kg) Ca without or with added PA (8 g/kg). After 2 weeks, rats were killed and Zn status of the rats was assessed. PA, Zn and Ca concentrations in infant cereals (n = 20) differed widely. PA concentrations ranged from undetectable to 16.0 g/kg. Zn and Ca concentrations ranged from 7.0–29.1 mg/kg and 0.8–13.4 g/kg, respectively. The [PA]/[Zn] and [PA × Ca]/[Zn] molar ratios in infants cereals with detectable PA (16 of 20 cereals) ranged from 22–75 and 0.9–14.9 mol/kg, respectively, predicting low Zn bioavailability. Body weight, body composition (lean and fat mass), right femur weight and length measurements and Zn concentrations in serum and femur indicated that diets higher in Ca had a more pronounced negative effect on Zn status of rats fed a PA-supplemented diet. Addition of PA to the diet had a greater negative effect on Zn status when Ca concentration in the diet was higher.ConclusionThese results show that, in rats, higher concentrations of dietary Ca and PA interact to potentiate a decrease in bioavailable Zn and may suggest lower Zn bioavailability in infant cereals with higher PA and Ca concentrations.     

Effect of dietary fiber of “Rihane” barley grains and azoxymethane on serum and liver lipid variables in Wistar rats

The aim of the present study is to evaluate the effects of diet enriched with dietary fiber of barley variety “Rihane” and azoxymethane on serum and liver lipid variables in male rats. Forty male rats were divided into four groups and fed on control diet or experimental diet that contained control enriched with dietary fiber of barley variety “Rihane”. Animals were injected with saline (controls) or azoxymethane (20 mg/kg body weight s.c.) at 7 and 8 weeks of age. The experimental diet significantly decreased cholesterol level compared with the control diet. Rats fed with BR diet significantly increased the serum high-density lipoprotein (HDL) cholesterol and significantly decreased low-density lipoprotein (LDL) cholesterol concentrations. The experimental diet decreased the atherogenic index (p < 0.05) compared with the control diet. Whereas the azoxymethane induced a significant increase of liver lipid, serum LDL and triglyceride concentrations, but it caused a significant reduction of HDL. Consequently, the ratio of HDL/TC decreased significantly compared with the control (p < 0.05). Accordingly, these results indicated that the diet enriched with dietary fiber of barley variety “Rihane” could be effective in decreasing the atherogenic risk factors in rats whereas the use of the azoxymethane as colon-specific carcinogen substance altered the lipid metabolism.