The effect of milk diet on lead metabolism in rats

The effect of milk on lead absorption and retention was studied in four groups of 6-wk-old female rats after a single oral or intraperitoneal application of lead-203. The animals were fed different diets for 2 wk (1 wk prior and 1 wk after the radiolead application). All animals receiving milk diet or milk additives showed a higher intake of fats and proteins and a lower intake of carbohydrates, vitamin D, and iron than control rats fed on normal diet. The calcium, phosphate, and calorie intake was about the same in all groups.The body retention of the orally applied lead-203 was much higher in animals on milk diet (4 times higher in rats on normal diet and cow's milk; 57 in animals on cow's milk; 33 times in rats on powdered milk) than in controls. The milk diet had only a slight effect on the whole body retention of lead-203 after intraperitoneal application (1.3 and 1.2 times higher in rats on cow's and powdered milk, respectively).This indicates that milk causes considerable enhancement of lead retention in the body mainly by greatly increasing its absorption from the intestinal tract.     

膳食铁对饮食诱导肥胖大鼠代谢影响

目的研究轻度铁缺乏和轻度铁补充对饮食诱导肥胖大鼠代谢的影响。方法将雄性Wistar大鼠按血红蛋白值和体重随机分为4组，每组10只，分别为基础饲料A组（含铁50mg／kg），高脂0．5倍铁饲料B组（含铁25mg／kg），高脂正常铁饲料C组（含铁50mg／kg）和高脂1．5倍铁饲料D组（含铁75mg／kg）。饲料中添加铁剂为柠檬酸铁。于第11周末处死动物，取血测定血糖、血脂和各种激素水平，并测定血清铁蛋白、血清铁、血红蛋白和肝铁含量等铁指标。结果B组和C组血清铁和肝铁含量显著低于A组（P〈0．05）。与B、C组比较，D组血清铁和肝铁含量显著升高（P〈0．05），接近A组。与C组比较，B组体脂肪含量、甘油三酯水平显著升高（P〈0．05）．除瘦素外其他激素水平均有下降趋终，其中胰高血糖素显著下降（P〈0．05）。D组体脂肪含量、血糖和甘油三酯水平显著低于13组（P〈0．05），甘油三酯水平显著低下C组（P〈0．05）；游离四碘甲腺原氨酸（FT4）和生长激素显著高于B组（P〈0．05）。结论轻度铁缺乏可加重肥胖大鼠肥胖、血糖血脂和激素代谢紊乱的程度，而轻度铁补充对肥胖大鼠的肥胖、血糖血脂和激素代谢紊乱有一定程度的改善作用。     

Modification of vitamin A metabolism in rats fed a copper-deficient diet

The liver is the main storage site of vitamin A and copper. Inverse relationships between copper and vitamin A liver concentrations have been suggested. We have investigated the consequences of a copper-deficient diet on liver and blood vitamin A storage in Wistar rats. Animals were fed either a copper-deficient diet for 45 days from weaning, or an identical diet containing adequate amounts of copper. Concentrations of vitamin A were determined by isocratic high performance liquid chromatography using UV detection. We have observed in the liver of the rats fed a copper-deficient diet a significantly higher mean level of retinyl esters (148 +/- 37 micrograms/g of liver) and retinol (3.3 +/- 1.4 micrograms/g of liver) compared to the mean concentration of the retinyl esters (53 +/- 8.5 micrograms/g of liver) (p less than 0.01) and retinol (1.4 +/- 0.5 micrograms/g of liver) (p less than 0.01) in controls. Opposite results were observed in the serum of the group fed a copper-deficient diet as these rats had a significantly lower level of retinol (22 +/- 4 micrograms/100 ml) compared to the mean concentration in the controls (64 +/- 20 micrograms/100 ml) (p less than 0.01). These findings suggest that a copper-deficient diet may cause defective transport of vitamin A from liver to blood. This experimental model may be useful to further investigate unusual liver vitamin A and copper concentrations observed in children during various hepatobiliary diseases.     

Fructose-enriched diet modifies antioxidant status and lipid metabolism in spontaneously hypertensive rats

OBJECTIVE: High-fructose consumption in industrial countries has been shown to induce metabolic abnormalities or syndrome X. Changes in antioxidant defense are unknown in hypertension associated with metabolic disorders induced by high-fructose feeding. METHODS: Twenty spontaneously hypertensive rats were assigned to one of two groups; one received a fructose-enriched diet (60% fructose) and the other a starch diet. After a 13-wk diet period, total antioxidant status was assessed in the blood and liver by monitoring the rate of free radical-induced red blood cell hemolysis. Antioxidants (enzymes and vitamins) were determined in blood and liver. Gene expression of antioxidant enzymes (copper/zinc superoxide dismutase and glutathione peroxidase) were also investigated in hepatic tissue. RESULTS: Fructose-fed rats showed blood pressure values similar to that of control rats but had increased glycemia and insulinemia. The antioxidant capacity in the blood of the fructose-fed group represented by copper/zinc superoxide dismutase and glutathione peroxidase activities and ascorbic acid was lower. However, the fructose diet enhanced the total antioxidant capacity of liver correlated with increased antioxidant enzyme activities and retinol concentrations. Gutathione peroxidase mRNA expression was decreased in livers of spontaneously hypertensive rats fed the fructose diet. CONCLUSION: Fructose feeding negatively affects antioxidant capacity in the blood of hypertensive rats but improves this capacity in the liver.     

Influence of intestinal resection and type of diet on digestive utilization and metabolism of magnesium in rats.

The influence of intestinal resection and type of diet on nutritive utilization of magnesium was studied in rats in which 50% of the distal small intestine was removed and in sham-operated controls. Nutritive parameters were analyzed after feeding the rats different diets for one or three months after surgery. Loss of 50% of the distal small intestine reduced digestive utilization of Mg as reflected in the mineral content of bone, however digestive and metabolic utilization of Mg were seen to recover by three months postsurgery. When dietary fat was supplied as equal parts of medium chain triglycerides, sunflower seed oil and olive oil instead of 100% olive oil, Mg absorption and retention were enhanced in resected rats after one month with the beneficial effects on Mg metabolism becoming even more marked after three months. One month after resection, dietary supplementation with vitamin D3 clearly stimulated digestive utilization of Mg. Although this effect was less notable at three months, nutritive utilization of Mg remained higher than in resected rats fed a diet lacking vitamin D3 supplementation. Dietary levels of vitamin D3 favored the deposition of Mg in bone tissue.     

Age-related alteration of vitamin D metabolism in response to low-phosphate diet in rats

The responses of renal vitamin D metabolism to its major stimuli alter with age. Previous studies showed that the increase in circulating 1,25-dihydroxyvitamin D (1,25(OH)2D3) as well as renal 25-hydroxyvitamin D3 1-alpha hydroxylase (1-OHase) activity in response to dietary Ca or P restriction reduced with age in rats. We hypothesized that the mechanism involved in increasing circulating 1,25(OH)2D3 in response to mineral deficiency alters with age. In the present study, we tested the hypothesis by studying the expression of genes involved in renal vitamin D metabolism (renal 1-OHase, 25-hydroxyvitamin D 24-hydroxylase (24-OHase) and vitamin D receptor (VDR)) in young (1-month-old) and adult (6-month-old) rats in response to low-phosphate diet (LPD). As expected, serum 1,25(OH)2D3 increased in both young and adult rats upon LPD treatment and the increase was much higher in younger rats. In young rats, LPD treatment decreased renal 24-OHase (days 1-7, P<0.01) and increased renal 1-OHase mRNA expression (days 1-5, P<0.01). LPD treatment failed to increase renal 1-OHase but did suppress 24-OHase mRNA expression (P<0.01) within 7 d of LPD treatment in adult rats. Renal expression of VDR mRNA decreased with age (P<0.001) and was suppressed by LPD treatment in both age groups (P<0.05). Feeding of adult rats with 10 d of LPD increased 1-OHase (P<0.05) and suppressed 24-OHase (P<0.001) as well as VDR (P<0.05) mRNA expression. These results indicate that the increase in serum 1,25(OH)2D3 level in adult rats during short-term LPD treatment is likely to be mediated by a decrease in metabolic clearance via the down-regulation of both renal 24-OHase and VDR expression. The induction of renal 1-OHase mRNA expression in adult rats requires longer duration of LPD treatment than in younger rats.     

Effects of high protein diet and sodium bicarbonate supplementation on calcium metabolism in rats

This study was conducted to determine the effect of a high protein diet on calcium metabolism in rat. Wistar strain male rats (50 days old) were divided into 5 groups (day 0): control diet (18% casein); high protein diet (18% casein +20% lactalbumin); high protein and 0.1% sodium bicarbonate diet; high protein and 0.2% sodium bicarbonate diet; and high protein and 0.4% sodium bicarbonate diet. On days 0, 1, 3, 5, 7, 9, urine samples were collected and, at the same time, feces were collected from half of the animals in each group. Urinary titratable acidity (TA-HCO3-), ammonium ion (NH4+), and net acid excretion (NAE) were measured as an index of acid-base balance in rat body. Urinary volume was rapidly increased and the increase of urinary volume continued throughout the study in rats fed the high protein diet. Urinary excretions of calcium and phosphorus were increased after day 3 and day 1, respectively, in rats fed the high protein diet. The high protein diet depressed calcium absorption and elevated phosphorus absorption from the digestive tract in rats fed the high protein diet. The high protein diet decreased TA-HCO3-, which was closely correlated with the decrease of NAE. Sodium bicarbonate supplementation to the high protein diet had little effect on urinary calcium excretion and NAE. This study suggested that there was no relationship between metabolic acidosis and hypercalciuria in rats fed the high protein diet.     

Effects of a high protein diet on bone formation and calcium metabolism in rats

The effects of a high protein diet on bone formation and calcium (Ca) metabolism were evaluated in rats using an ectopic endochondral bone induction model. A control diet (18% casein) or a high protein diet (18% casein + 20% lactalbumin) was given to 50-day-old rats. Ten days after the feeding of the experimental diet, rats were intramuscularly implanted with demineralized bone powder (day 0). On day 14 and day 21, the implanted bone powder was harvested, and blood and urine samples were also obtained. Urinary Ca excretion was not increased on day 12-14; however, it was elevated on day 19-21 in rats fed the high protein diet compared with rats fed the control diet. The high protein diet remarkably stimulated urinary sulfate excretion in both sampling periods, which reflected dietary sulfur-containing amino acids contents. Also, rats fed the high protein diet exhibited a decrease in serum Ca concentrations. There was little difference in Ca contents and the activities of alkaline phosphatase and acid phosphatase in the implants between control group and high protein diet group on day 14 and day 21. Histological examination in the implanted demineralized bone powder on day 14 indicated only cartilage in rats fed the high protein diet in contrast to the occurrences of osteogenesis and remodeling in those fed the control diet. Retarded bone formation in rats fed the high protein diet might be owing to, in part at least, a restricted amount of Ca utilized at the stage of cartilage calcification.     

Studies dealing with hepatic RNA metabolism in rats force-fed a threonine-devoid diet

Young rats were force-fed for 3 days a purified diet devoid of threonine and a number of aspects relating to RNA metabolism in the livers were studied. The findings in the livers of rats force-fed the threonine-devoid diet in comparison with those force-fed the complete diet were as follows: a) poly(A)-mRNA was increased in nuclei and in polyribosomes; b) DNA-dependent RNA polymerases I and II activities were increased; c) in vitro release of 14C-orotic acid labeled RNA from nuclei revealed that transport was unchanged and nucleoside triphosphatase activity of nuclear envelopes was unchanged; d) polyribosomes (total, free and membrane-bound) shifted toward heavier aggregation and in vitro 14C-leucine incorporation into protein was increased; e) RNase activities (at pH 5.4, 7.6, 9.5) were essentially unaltered; and f) in vivo 14C-choline incorporation into microsomal membranes was increased. By administering selected inhibitors of RNA and protein synthesis, such as actinomycin D, alpha-amanitin or cycloheximide, prior to killing the rats force-fed the threonine-devoid or complete diet for 3 days, it was demonstrated that the stimulatory effect on hepatic polyribosomes and protein synthesis in the experimental group was dependent upon new synthesis of poly(A)mRNA and of protein.     

Effect of palatable hyperlipidic diet on lipid metabolism of sedentary and exercised rats

OBJECTIVE: The present study was designed to examine 1) whether continuous feeding with a palatable hyperlipidic diet and cycling this diet with chow diet would affect lipid and carbohydrate metabolism in a similar way; and 2) whether the effect of chronic exercise on lipid and carbohydrate metabolism would be modified by these diet regimens. METHODS: Male 25-d-old Wistar rats were assigned to one of six groups: sedentary rats fed with chow diet; exercised (swimming 90 min/d, 5 d/wk) rats fed with chow diet; sedentary rats fed with a palatable hyperlipidic diet; exercised rats fed with the palatable hyperlipidic diet; sedentary rats fed with food cycles (four cycles alternating the chow and hyperlipidic diets weekly); and exercised rats fed with food cycles. After 8 wk of treatment, the animals were killed 24 h after the last exercise session. RESULTS: The hyperlipidic diet and food cycles schedules caused similar increases in body weight gain, carcass lipogenesis rate and adiposity, lipid content of the liver and gastrocnemius muscle, and serum total lipid, triacylglycerol, insulin, and leptin levels. The exercise attenuated body weight gain, adipose tissue mass, and serum triacylglycerol, insulin, and leptin levels similarly in the hyperlipidic and food cycles groups. Carcass lipogenesis rate was not affected by exercise in any of the three groups. CONCLUSIONS: The data showed that the continuous intake of a hyperlipidic palatable diet for 8 wk and the alternation of the high-fat intake with periods of chow intake cause obesity and affected lipid metabolism in a similar way. Chronic exercise attenuated body weight gain and adiposity and improved serum lipid concentrations in both high-fat feeding regimens.