Effect of dietary restriction on liver protein synthesis in rats

At 6 wk of age, male Fischer F344 rats were fed a purified, casein-based diet either ad libitum or in the amount of 60% of the diet consumed by the rats fed ad libitum (restricted diet). Hepatocytes were isolated from the rats between 2.5 and 19 mo of age. The protein content of the hepatocytes isolated from the rats fed the restricted amount of diet was significantly lower than that of hepatocytes isolated from rats fed ad libitum. The DNA and RNA content of the hepatocytes were similar for the rats fed the two dietary regimens. The absolute rate of protein synthesis for hepatocytes isolated from rats fed ad libitum decreased 55% between 2.5 and 19 mo of age. However, the rate of protein synthesis by hepatocytes from rats fed the restricted amount of diet decreased only slightly with increasing age. At 19 mo of age, the rate of protein synthesis by hepatocytes from the rats fed the restricted amount of diet was significantly higher than the rate of protein synthesis for hepatocytes from rats fed ad libitum. Therefore, dietary restriction retards the age-related decline in liver protein synthesis.     

Marginal dietary copper restriction induces cardiomyopathy in rats

Prior studies have provided evidence of marginal dietary copper restriction in humans. The present study was undertaken to examine in a rat model the effect of a long-term marginal dietary Cu deficiency on the heart. Male adult Sprague-Dawley rats were fed AIN-76 diet containing 6.0 (control), 3.0, or 1.5 mg Cu/kg starting at 11 wk of age. Groups of rats were killed at 6, 9, 12, 15, or 18 mo after initiation of feeding, and the same experiment was repeated once. The only systemic change induced by marginal dietary Cu restriction (P < 0.05) was depression of organ Cu concentrations in rats fed 1.5 mg Cu/kg diet. Cardiac pathological manifestations in rats fed lower Cu diets were evidenced by histopathological, ultrastructural, and functional alterations. Myocyte hypertrophy and excessive collagen deposition in the heart occurred in rats fed 1.5 mg Cu/kg diet. Ultrastructural changes, including increased number and volume of mitochondria along with disruption of cristae structure, diastolic and systolic dysfunction, and electrocardiograph alterations, occurred in rats fed 1.5 or 3.0 mg Cu/kg diet. These results demonstrate that, in the absence of most indications of systemic Cu deficiency, heart morphology and function are sensitive to marginal Cu deficiency.     

Effects of exposure to microwaves on cellular immunity and placental steroids in pregnant rats.

OBJECTIVES: Microwaves produce various detrimental changes based on actions of heat or non-specific stress, although the effects of microwaves on pregnant organisms has not been uniform. This study was designed to clarify the effect of exposure to microwaves during pregnancy on endocrine and immune functions. METHODS: Natural killer cell activity and natural killer cell subsets in the spleen were measured, as well as some endocrine indicators in blood--corticosterone and adrenocorticotrophic hormone (ACTH) as indices of the hypothalamic-pituitary-adrenal axis--beta-endorphin, oestradiol, and progesterone in six female virgin rats and six pregnant rats (nine to 11 days gestation) exposed to microwaves at 10 mW/cm2 incident power density at 2450 MHz for 90 minutes. The same measurements were performed in control rats (six virgin and six pregnant rats). RESULTS: Skin temperature in virgin and pregnant rats increased immediately after exposure to microwaves. Although splenic activity of natural killer cells and any of the subset populations identified by the monoclonal antibodies CD16 and CD57 did not differ in virgin rats with or without exposure to microwaves, pregnant rats exposed to microwaves showed a significant reduction of splenic activity of natural killer cells and CD16+CD57-. Although corticosterone and ACTH increased, and oestradiol decreased in exposed virgin and pregnant rats, microwaves produced significant increases in beta-endorphin and progesterone only in pregnant rats. CONCLUSIONS: Microwaves at the power of 10 mW/cm2 produced activation of the hypothalamic-pituitary-adrenal axis and increased oestradiol in both virgin and pregnant rats, suggesting that microwaves greatly stress pregnant organisms. These findings in pregnant rats suggest that--with exposure to microwaves--pregnancy induces immunosuppression, which could result in successful maintainance of pregnancy. This enhancement of adaptability to heat stress with pregnancy may be mediated by activation of placental progesterone and placental or pituitary beta-endorphin.     

饮食限制对小鼠学习记忆及抗氧化能力影响

目的探讨不同饮食限制(dietary restriction,DR)水平对小鼠学习记忆、抗氧化能力影响。方法120只ICR小鼠随机分为自由饮食(对照)组,20%,40%,60%DR组,连续25 d,进行力竭游泳及耐缺氧实验;39 d后,进行Y迷宫、水迷宫、脏器系数、超氧化物歧化酶(SOD)及丙二醛(MDA)含量的测定。结果Y迷宫结果表明,40%DR组记忆成绩(14.40±2.68)次,与自由饮食组比较差异有统计学意义(P0.05);水迷宫结果表明,40%DR组潜伏期(20.36±9.12)s,访问次数(1.5±0.5)次,游动距离(0.49±0.32)m。;60%DR组脑系数为(1.51±0.19)%,明显高于自由饮食组(1.12±0.09)%(P0.01);各饮食限制组小鼠脾脏、甲状腺系数及肾脏丙二醛(MDA)含量均有所下降;小鼠耐力及耐缺氧能力与限制水平成正比,雌鼠耐缺氧能力强于雄鼠。结论适当饮食限制可以提高机体对新环境适应能力,提高体内抗氧化系统活性。     

Effects of dietary protein, fat and restriction on body composition and energy balance in lactating rats

Isoenergetic diets formulated at three levels of dietary protein using 12,24 and 40% casein and at two levels of fat using 2.26 and 13.82% corn oil were fed at five levels of intake, ad libitum, 75, 62.5, 50 and 37.5% of average ad libitum intake, to 90 lactating rats from d 7 to 14 of lactation. Regression equations developed from lactating rats killed on d 7 of lactation were used to calculate initial body composition and energy of rats killed on d 14 of lactation. Changes in body weight and body water were significantly (P less than 0.05) affected by dietary fat and protein, but change in dry lean body mass was affected only by level of dietary fat, whereas body nitrogen and fat and lean body energy were not affected by level of dietary fat or protein. However, restricted intake significantly increased loss of all these. Likewise, restricted intake decreased milk production. Changes in weights of heart and liver were not affected by diet or intake, whereas intestinal weight decreased with intake restriction. Liver enzyme activities were markedly affected by intake restriction, whereas responses to dietary protein and fat were marginal.     

The effects of dietary energy restriction on overloaded skeletal muscle in rats

We evaluated the effects of three levels of energy intake, 73 % (CON73), 81 % (CON81) and 100 % (CON100) of the ad libitum intake of the control diet, on skeletal muscle growth induced by functional overload in male rats. Unlike most previous studies which have employed chronic or acute food restriction where all nutrients are reduced in the diet, the present study tested the effects of energy deprivation as a single factor without inducing other nutritional deficiencies. Muscular growth of plantaris and soleus muscles was induced by removal of synergist gastrocnemius muscles in one hindlimb; muscles in the other leg were used as sham-operated intra-animal controls. After 30 d, rats on the energy-restricted CON73 and CON81 diets gained less weight and had smaller livers, kidneys, hearts and fat pads (epididymal, retroperitoneal and omental) than CON100 rats They also had smaller sham-operated plantaris muscles (CON73 --13 %, CON81 --9 %) containing less total protein (CON73 --14 %; CON81 --10 %) than CON100 rats However, the same measurements in overloaded plantaris muscles were similar among groups. Soleus muscle mass and protein contents were not significantly affected by energy restriction in our study. Percentage distributions of myosin heavy-chain isoforms (types I, IIa, IIx and IIb) were similar among rats in CON100, CON81 and CON73 groups for both plantaris and soleus muscles. We conclude that the growth reduction of plantaris muscle induced by energy restriction at 73 % and 81 % for 30 d was prevented by functional overload in male rats.     

Influence of dietary phosphorus restriction on calcium and phosphorus metabolism in rats

The effect of dietary phosphorus (P) on calcium (Ca) and phosphorus metabolism was studied in young female rats. P levels in the semipurified diets ranged from 0.1 to 0.4% (w/w). A level of 0.4% P in the diet is recommended for rats. Kidney calcification was observed in rats fed the 0.4%-P diet whereas P restriction prevented this condition. Rats fed the diet containing 0.1% P, showed severe hypercalciuria, hypercalcemia, reduced growth and impaired bone mineralization. These effects did not occur when the diet contained 0.2 or 0.3% of P. This study suggests that in short-term studies P in the diet of female rats can be restricted to 0.2% so as to prevent nephrocalcinosis without affecting their development.     

The effect of early caloric restriction on colonic cellular growth in rats

Although the inhibitory effect of caloric restriction on tumorigenesis is substantial and well known, the pertinent mechanisms remain to be determined. We recently suggested that the risk of cancer may be directly related to the total number of dividing cells within an affected organ. This study evaluates the effects of early caloric restriction on the cellular growth of the colon. The experiment began one day postpartum and ended six weeks later with the killing of all animals. It consisted of two consecutive periods: a) three weeks of suckling and b) three weeks postweaning. Animals whose food was restricted only during the suckling period showed normal colons when killed at six weeks. Caloric restriction (40%) for three weeks postweaning resulted in colons of lower weight with fewer cells (less total DNA) and reduced total DNA synthesis ([³H]thymidine uptake, dpm/colon) when compared with animals fed ad libitum postweaning. Conversely, only rats fed ad libitum from birth through the first three weeks after weaning demonstrated an increase (21%) in the rate of DNA synthesis (dpm/mg DNA) compared with other animals. In addition, the colonic crypts showed no differences in the number of cells or the number of dividing cells, as determined by autoradiography. By contrast, the total number of crypts (and/or the number of mucosal cells between crypts) are reduced, and hence the total number of colonic mucosal cells dividing at any given time are similarly decreased. The reduced number of dividing cells in the colons of these animals (i.e., those restricted postweaning) could explain previous data suggesting that they are resistant to the induction of colon cancer.     

The effect of early caloric restriction on colonic cellular growth in rats

Although the inhibitory effect of caloric restriction on tumorigenesis is substantial and well known, the pertinent mechanisms remain to be determined. We recently suggested that the risk of cancer may be directly related to the total number of dividing cells within an affected organ. This study evaluates the effects of early caloric restriction on the cellular growth of the colon. The experiment began one day postpartum and ended six weeks later with the killing of all animals. It consisted of two consecutive periods: a) three weeks of suckling and b) three weeks postweaning. Animals whose food was restricted only during the suckling period showed normal colons when killed at six weeks. Caloric restriction (40%) for three weeks postweaning resulted in colons of lower weight with fewer cells (less total DNA) and reduced total DNA synthesis [( 3H]thymidine uptake, dpm/colon) when compared with animals fed ad libitum postweaning. Conversely, only rats fed ad libitum from birth through the first three weeks after weaning demonstrated an increase (21%) in the rate of DNA synthesis (dpm/mg DNA) compared with other animals. In addition, the colonic crypts showed no differences in the number of cells or the number of dividing cells, as determined by autoradiography. By contrast, the total number of crypts (and/or the number of mucosal cells between crypts) are reduced, and hence the total number of colonic mucosal cells dividing at any given time are similarly decreased. The reduced number of dividing cells in the colons of these animals (i.e., those restricted postweaning) could explain previous data suggesting that they are resistant to the induction of colon cancer.     

Effects of age and dietary restriction on oxidative DNA damage, antioxidant protection and DNA repair in rats

Summary Background Experimentally imposed dietary restriction is known to extend the lifespan of rodents, perhaps by slowing the accumulation of oxidative damage that is thought to be one of the causes of aging. Aim of the study We examined the effects of restricted total food intake, and protein and calorie restriction, on DNA oxidation and related biomarkers in rats. Methods From 1 to 17 months, rats in group 1 received normal diet ad libitum. Group 2 received 70% of the quantity consumed by the first group. Group 3 had the same quantity as group 2, but with a reduction in protein (from 18% to 10% of the diet by weight), and group 4 were further restricted with a 30% decrease in calories. Lymphocytes were isolated from blood samples taken every two months. DNA breaks, oxidised pyrimidines, resistance to H₂O₂–induced damage, and strand break repair were measured with the comet assay. Organs were isolated from rats killed at 17 months, with 1 month–old rats for comparison; DNA oxidation and antioxidant enzyme activities were measured. Results DNA breaks in lymphocytes increased from 1 to 3 months but thereafter declined with age, except in ad libitum fed rats. Oxidised pyrimidines did not change significantly. Resistance to H₂O₂–induced damage was least at 3 months, and increased with age. Repair of DNA strand breaks was efficient at all ages. Diet had little effect on these endpoints. Diet had no influence on 8–oxo–7.8–dihydroguanine levels in DNA from liver, testis and brain of 17 monthold rats. Combining data from all four groups, the levels in brain and liver were significantly higher at 17 months compared with 1 month. Antioxidant enzyme activities tended to increase between 1 and 17 months; effects of diet were not so consistent. Conclusions While DNA damage shows a modest increase with age in some organs, antioxidant status and DNA strand break repair do not decline with age. Restricted diets (including protein and calorie restriction) have no effect on any of these markers of genetic stability.     

Effect of dietary energy restriction on bone mineral content of mature rats

Male adult 16 months old Fischer-344 rats (7 per group) were feda control diet ad libitum and energy modified diets restricted to 80% (R-80) and to 60% (R-60) of the control intake, while mineral and protein intakes were held constant at adequate levels. The control diet contained Ca, P, Mg & protein at 0.7, 0.4, 0.05 & 18.8%, respectively, and the two restricted diets contained higher levels of these nutrients to provide quantities equal to control diet when restricted to the respective energy level. After 16 weeks of feeding, significantly lower content in ash of the right femur (p<-0.03) accompanied by lower content in Ca, P and Mg were observed in R-60 rats as compared to the control rats (p<-0.02). Similar observations were made on tibia and fibula. Thus, the present study suggests that adequate energy intake is essential for the maintenance of normal bone mineral content, and consequently the requirement of Ca, P and Mg could increase when dietary energy consumption is restricted.     

The effects of dietary lead content and food restriction on lead retention in rats

The effects of restricted food intake and of various dietary lead contents on lead retention¹ were studied in young rats. In three experiments the rats were given either unrestricted or restricted access to diets providing 200 or 400 mg lead/kg for 3 or 6 weeks. At the end of the experiments a sample of blood was taken and the rats were ashed. Lead was determined in blood and ash from the carcass. Food restriction always increased the retention of lead but not always the lead content of blood or carcass. The retention of lead was similar when the diet was supplemented with 50, 200 or 400 mg lead/kg. Lead supplementation at 200 or 400 mg/kg reduced food intake and growth but did not affect food conversion ratios. Blood lead was related to the rate of ingestion of lead. The effect of food restriction in reducing lead retention should be taken into account in interpreting the effects of lead exposure accompanied by dietary conditions which reduce appetite or food supply.     

Hyperhomocysteinaemia induced by dietary folate restriction causes kidney oxidative stress in rats

Diet is the most common cause of mild hyperhomocysteinaemia (HHcy), which occurs in approximately 5-7 % of the general population. Since HHcy causes endothelial damage by oxidative stress in different organs, the present study was designed to examine whether HHcy might be involved in renal oxidative stress. Twenty-five male Wistar rats were randomly divided into two groups: one (n 13) was fed ad libitum a folate-free diet (FF) and the other (n 12) was fed the same diet supplemented with folic acid (control, CO). After 8 weeks the animals were killed and kidneys removed. Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured in plasma and kidney homogenates. Renal tissue sections were analysed by indirect immunostaining with the primary antibody against oxidatively modified LDL receptor (LOX-1). A marked HHcy was confirmed in the FF group. As compared with CO animals, MDA levels in plasma and kidney homogenate were significantly higher in FF rats (P < 0.05). Similarly, renal GPx and SOD activities were significantly higher in the FF group (P < 0.001). No differences were found in LOX-1 immunohistochemical expression, which in the two groups was displayed in tubular cells. The present study provides evidence that HHcy does produce renal oxidative stress mediated by lipid peroxidation, and that the increased kidney MDA displayed by FF animals may enhance kidney antioxidant activity and thereby attenuate both kidney damage and expression of LOX-1.     

膳食纤维对大鼠排锰效果及微量元素影响

目的 探讨膳食纤维的排锰效果及对其他微量元素的影响.方法 将48只3周龄雄性SD大鼠随机分为对照组、膳食纤维组、单纯染锰组(50 mg/kg)、染锰+高、中、低剂量膳食纤维组(分别在饲料中参入16%,8%和4%的膳食纤维);1个月后处死大鼠,测定大鼠体重、24 h粪锰以及脑、肝组织和血液中锰、铜、铁、锌含量.结果 染锰+高、中剂量膳食纤维组24 h粪锰排出率分别为29.44%,28.49%高于单纯染锰组的20.87%(P<0.05);染锰+高、中、低剂量膳食纤维组脑、锰含量分别为1.37,1.62,2.24,2.57μg/g肝组织和锰含量分别为1.78,2.73,2.54,2.70μg/g,明显低于单纯染锰组(P<0.01);脑、肝组织和血液中Cu、Fe、Zn含量在各组之间差异均无统计学意义(P>0.05).结论 膳食纤维能通过增加锰的排出以减少锰的蓄积.     

烹调油烟冷凝物对小鼠细胞免疫及免疫监视功能的影响

昆明种雌性小鼠皮下注射经动式染毒装置制备的豆油、菜籽油以及精炼色拉油油烟冷凝物。发现当皮下注射菜籽油油烟冷凝物后,与溶剂对照组相比,低剂量（１．１３ｇ／ｋｇ）菜籽油油烟冷凝物使动物迟发型变态反应明显下降。高剂量使小鼠迟发型变态反应和自然杀伤细胞活性明显下降。皮下注射高剂量（２．２６ｇ／ｋｇ）豆油油烟冷凝物后,小鼠迟发型变态反应、自然杀伤细胞活性和钙调素水平下降,并均具有显著性意义。动物在皮下注射低剂量色拉油油烟冷凝物后,与对照相比动物迟发型变态反应和自然杀伤细胞活性明显下降。本文结果表明,皮下注射一定剂量的烹调油烟冷凝物对小鼠细胞免疫及免疫监视功能会造成一定的损伤     

Effects of dietary carbohydrate on hepatic gluconeogenesis in BHE rats

The effects of feeding different carbohydrates on hepatic gluconeogenesis in BHE rats was studied. Three experiments were conducted that differed only in the aspects of gluconeogenesis examined. In experiment 1, gluconeogenesis and ketogenesis by hepatocytes isolated from 48-h starved rats were determined. In experiment 2, the activities of selected gluconeogenic enzymes were determined in starved and nonstarved rats. In experiment 3, the levels of the various metabolites of glycolysis and the citric acid cycle were determined in nonstarved rats. Rats were fed diets containing starch, maltose, glucose, sucrose or an equimolar mixture of glucose and fructose. In starved rats, gluconeogenesis was less in starch-fed rats than in rats fed any of the sugar diets. These same diet differences, with few exceptions, were also observed in ketogenesis. Glucose 6-phosphatase activity was lower in nonstarved rats fed starch and maltose than in rats fed glucose, sucrose, or glucose and fructose. These same nonstarved rats also had lower phosphoenolpyruvate carboxykinase and higher glutamate pyruvate transaminase activities than rats fed the other diets. In the starved rats, the diet differences were erased. Starved rats had lower activities of these gluconeogenic enzymes than nonstarved rats. Diet differences in the levels of the different metabolites in nonstarved rats were observed. The results show that dietary carbohydrate can influence gluconeogenesis. However, the mechanism of their effect is as yet unknown.     

Effects of dietary polychlorinated biphenyls on cholesterol catabolism in rats

Dietary polychlorinated biphenyls (PCBs) caused hypercholesterolaemia in rats. The concentration and output of biliary cholesterol was significantly lower than that of the control group. Biliary output of total bile acids was significantly decreased in rats given the PCB-supplemented diet. Faecal excretion of total steroids (sum of neutral steroids and acidic steroids) was not significantly changed in rats given the PCB-supplemented diet. The present results indicate that dietary PCBs cause hypercholesterolaemia without modifying the faecal total steroids excretion. These results suggest that PCBs produce hypercholesterolaemia accompanied by changes in biliary or faecal excretion of bile acids and neutral steroids in addition to an increase in hepatic cholesterol synthesis.     

Effects of dietary fiber on intestinal ion fluxes in rats

The effect of short-term fiber ingestion on jejunal ion fluxes was evaluated in rats using a standard Ussing chamber technique. Ingestion of cellulose and pectin decreased the mucosal to serosal fluxes of both Na and Cl but did not significantly alter serosal to mucosal fluxes; net fluxes of both Na and Cl were significantly lower in the group supplemented with dietary fiber as compared to those animals fed a fiber-free diet. Both potential difference and short-circuit current were higher in the fiber-free group than in the group supplemented with dietary fiber; tissue conductance, however, was unaffected by fiber ingestion. The residual flux of all three groups was virtually identical suggesting that electrical alterations observed after cellulose and pectin ingestion are not the result of ion fluxes other than Na and Cl. These data, coupled with previous observations that short-term fiber supplementation impairs glucose and leucine absorption, suggest that fiber ingestion alters the intestinal membrane, specifically sites of active transport.