Choice of diet impacts the incidence of stroke-related symptoms in the spontaneously hypertensive stroke-prone rat model

The spontaneously hypertensive stroke-prone (SHRSP) rat is a commonly used model of cerebrovascular disease and hypertension. SHRSP rats have been shown to develop stroke-related symptoms (SRS) by age 14 weeks when fed a purified diet, such as AIN-93G, supplemented with 1% NaCl. We conducted a pathology pilot study to compare the incidence of SRS in SHRSP rats fed either AIN-93G (with 1% NaCl in drinking water) or commercially available rat chow (with 4% NaCl in the diet), starting at 8 weeks of age. These results prompted us to analyze data from 5 earlier feeding trials using SHRSP rats. Overall, we found that SHRSP rats fed AIN-93G purified diet for 8 or 17 weeks did not demonstrate SRS (n?= 18), whereas all SHRSP rats fed lab chow exhibited SRS at age 15.1?± 0.6 weeks (n?= 23). In addition, SHRSP rats fed lab chow had decreased mass gain starting at age 13 weeks, as well as decreased feed efficiencies after the first 5 weeks of feeding (p?< 0.05). In conclusion, our data suggest that diet composition is a major contributor to the onset of stroke in SHRSP rats and that diet choice should be critically evaluated based on endpoint measures in the SHRSP model.     

Occurrence of pancreatic ductal cell dysplasia in rats fed with a high fat diet and ethanol

The effects of alcohol and diet on acute pancreatitis were studied in 192 male Wistar rats. The animals were fed with standard laboratory food up to three months of age and, after that, were divided into four groups of 48 animals, each group receiving a different diet: standard, fat-rich, protein-rich or carbohydrate-rich. In each diet group, 24 animals obtained 15% (v/v) ethanol in their drinking solution while the other 24 rats had water ad libitum. The diet period lasted for 12 weeks, after which acute experimental pancreatitis was induced under diethyl ether anesthesia by ductal injection of rat bile into the pancreatic ducts. Moderate or severe ductal cell dysplasia developed in three of the 15 survivors in the group fed with a high-fat diet and 15% ethanol in their drinking solution. Mild acute pancreatitis was histologically found in 13 rats and moderate pancreatitis in one rat in this group. One rat did not show any pancreatic parenchymal changes. Two of the rats with ductal cell dysplasia had mild pancreatitis and the pancreas of the third rat was normal in this respect. Dysplastic changes were not found in any other experimental group used in the study. The observation is statistically significant at p less than 0.025 level. The results indicate that alcohol and a high fat diet together might have a carcinogenic effect on pancreatic ductal epithelium in rats.     

Effect of dietary ghee – the anhydrous milk fat on lymphocytes in rats

Lymphocytes are important components of the immune system. Dietary lipids affect the functioning of the immune system. Changes in the lipid composition of the lymphocyte membrane is a case in point. Membrane structural changes are reflected in the altered function of the cell. Lymphocyte proliferation and lymphocyte rosetting are membrane associated phenomena. Ghee, is a clarified butter product, commonly used in the Indian diet. It is rich in saturated fatty acids and also contain oxysterols which are generated on prolonged heating of ghee. Male weanling rats were fed 2.5% (of the total fat levels) of fresh or thermally oxidized ghee for a period of 8 weeks. The control rats were fed groundnut oil. Lipid composition of lymphocytes in ghee fed rats showed changes. In vitro lipid peroxidation of lymphocyte membranes increased by 26% in oxidized ghee fed rats. Na⁺K⁺ ATPase activity was decreased in oxidized ghee fed rats (18%). Lymphocyte proliferation was reduced in ghee fed rats (32%), compared to the controls, irrespective of the mitogens used (ConA or PHA), or the tissue (splenocytes or peripheral blood lymphocytes). Oxysterols present in oxidized ghee are the likely agents inhibiting lymphoproliferation. Rosetting of lymphocytes decreased in the fresh ghee fed rats by 16% and in oxidized ghee fed rats by 25%. Membrane fluidity declined in the oxidized ghee fed rats. It is concluded that feeding ghee results in decreased proliferation of lymphocytes. Also, feeding oxidised ghee results in decreased proliferation of lymphocytes through alterations in the structure of the lymphocyte membranes in the rat.     

Effects of vitamin D supplementation on calcium balance and bone growth in young rats fed normal or low calcium diet

OBJECTIVE: We examined the effect of vitamin D supplementation on bone growth in young rats fed a normal or low calcium diet. METHODS: Fifty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into five groups with 10 rats in each group: baseline control, 0.5% (normal) or 0.1% (low) calcium diet, and 0.5 or 0.1% calcium diet + vitamin D (25 microg/100 g, food intake). Duration of the experiment was 10 weeks. RESULTS: Vitamin D supplementation stimulated intestinal calcium absorption and increased urinary calcium excretion in rats fed a low or normal calcium diet. Vitamin D supplementation prevented the reduction in periosteal bone gain but enhanced enlargement of the marrow cavity and reduced the maturation-related cancellous bone gain in rats fed a low calcium diet, and increased the maturation-related cancellous and cortical bone gains in rats fed a normal calcium diet. CONCLUSION: This study shows the differential effects of vitamin D supplementation on born growth in young rats fed a normal or low calcium diet.     

Effect of high- and low-protein diets on the regulation of rat liver tyrosine aminotransferase and tryptophan oxygenase activities by l-tyrosine and l-tryptophan

Induction of rat liver tyrosine aminotransferase by l-tyrosine and tryptophan oxygenase by l-tryptophan was studied in groups of rats fed on diets containing 18 or 5% protein. The basal activity of hepatic tyrosine aminotransferase of rats receiving 5% protein gradually increased with the age of the animals but that of rats receiving 18% protein did not. l-Tyrosine induced hepatic tyrosine aminotransferase in rats receiving 18% protein when tested at ages from 4 to 20 weeks. When induction by l-tyrosine was carried out in rats receiving the 5% protein diet, significant induction of tyrosine aminotransferase occurred only in 4- or 6-week-old rats. Induction by l-tryptophan of tryptophan oxygenase in liver or the basal activity of this enzyme in liver did not differ between the groups fed on 5 and 18% protein. On changing the diet from 0 to 18% protein, the above-mentioned effects on the induction of hepatic tyrosine aminotransferase were reversed.     

Postweaning low-calcium diet promotes later-life obesity induced by a high-fat diet

The aim of this study was to investigate the effects of a postweaning low-calcium diet on later obesity and explore the underlying mechanisms. Ninety-six male rats were weaned at 3 weeks of age, fed standard (STD: 0.50% calcium, n=48) and low-calcium (LC: 0.15% calcium, n=48) diets for 3 weeks, and then fed the standard diet for a 3-week washout period successively. Finally, the STD rats were divided into STD control and high-fat diet (HFD) groups, and the LC ones into LC control and LC+HFD (LCHF) groups. The STD and LC rats were fed the standard diet, while the HFD control and LCFD ones were fed a high-fat diet for 6 weeks to induce obesity. During the three feeding periods, adenosine-monophosphate-activated protein kinase (AMPK) and its responsive proteins phospho-acetyl-coA carboxylase, carnitine palmitoyltransferase 1 and uncoupling protein 3 were persistently down-regulated in the LC group (decreased by 18%, 24%, 18% and 20%, respectively) versus the STD group, and these effects were significantly more pronounced in the LCHFD group (decreased by 21%, 30%, 23% and 25%, respectively) than the HFD group by a later high-fat stimuli, causing more fat and body weight in adulthood. However, lipolysis enzymes, serum leptin, insulin and lipids were not significantly affected until the body weight and fat content changed at 15 weeks of age. The results suggest that the low-calcium diet after weaning promotes rat adult-onset obesity induced by high-fat diet, which might be achieved by programming expressions of genes involved in AMPK pathway.     

Dietary low linolenic acid compared with docosahexaenoic acid alter synaptic plasma membrane phospholipid fatty acid composition and sodium-potassium ATPase kinetics in developing rats

The objective of this study was to investigate if maternal dietary 20:4n-6 arachidonic acid (AA) and 22:6n-3 compared with adequate or low levels of 18:3n-3 linolenic acid (LNA) increases synaptic plasma membrane (SPM) cholesterol and phospholipid content, phospholipid 20:4n-6 and 22:6n-3 content, and Na,K-ATPase kinetics in rat pups at two and five weeks of age. At parturition, Sprague-Dawley rats were fed semi-purified diets containing either AA + docosahexaenoic acid (DHA), adequate LNA (control; 18:2n-6 : 18:3n-3 ratio of 7.1 : 1) or low LNA (18:2n-6 : 18:3n-39 ratio of 835 : 1). During the first two weeks of life, the rat pups received only their dams' milk. After weaning, pups received the same diet as their respective dams to five weeks of age. No significant difference was observed among rat pups fed the diet treatments for SPM cholesterol or total and individual phospholipid content at two and five weeks of age. Fatty acid analysis revealed that maternal dietary AA + DHA, compared with feeding the dams the control diet or the low LNA diet, increased 20:4n-6 in phosphatidylserine and 22:6n-3 content of SPM phospholipids. Rats fed dietary AA + DHA or the control diet exhibited a significantly increased Vmax for SPM Na,K-ATPase. Diet treatment did not alter the Km (affinity) of SPM Na,K-ATPase in rat pups at two and five weeks of age. It is concluded that dietary AA + DHA does not alter SPM cholesterol and phospholipid content but increases the 22:6n-3 content of SPM phospholipids modulating activity of Na,K-ATPase.     

高脂饲料诱导的肥胖大鼠肠道内硫酸盐还原菌的定量检测

目的 检测高脂饲料诱导大鼠肥胖过程中,大鼠肠道内硫酸盐还原菌( sulfate-reducing bacteria,SRB)的数量变化,为研究SRB与肥胖的关系提供参考.方法 20只Wistar大鼠随机分为2组(每组10只),一组饲喂高脂饲料(HFD组)18周,另一组饲喂正常饲料(NCD组,即对照组)18周.以编码腺苷酰硫酸还原酶α亚基的基因(aprA)作为分子标记,通过荧光定量PCR的方法检测两组大鼠在0、8和18周,肠道内SRB的数量变化;同时,以16S rRNA基因作为标记基因定量大鼠肠道内总菌的数量,以计算肠道内SRB在总菌中的比例变化.结果 分组饲喂8周后,高脂饲料饲喂组大鼠的体重与正常饲料组相比显著升高.对SRB的定量结果显示,饲喂8周和18周,高脂饲料组大鼠肠道内SRB的数量和含量与正常饲料组相比显著升高.结论 大鼠肠道中的硫酸盐还原菌与饮食诱导的肥胖密切相关,为进一步研究SRB在肥胖及其相关代谢疾病的发生发展中的作用提供了依据.     

Preventive Effects of Supplemental Selenium and Selenium Plus Iodine on Bone and Cartilage Development in Rats Fed with Diet from Kashin–Beck Disease Endemic Area

The purpose of this study was to investigate the effects of supplemental selenium and selenium plus iodine on bone and growth plate cartilage histology and serum biochemistic parameters in rats. Ninety-six Wistar rats were randomly divided into the following four groups: group A, the rats fed with normal diet; group B, fed with diet from Kashin–Beck disease (KBD) endemic area; group C, fed with diet from KBD endemic area supplemented with selenium; and group D, fed with diet from KBD endemic area supplemented with selenium and iodine. After 4, 8, and 12 weeks, bone and cartilage samples were collected from the rats and were examined for morphological changes in the tibial growth zone and for changes in the plate cartilage and metaphysic. Compared to the rats fed with diet from the KBD endemic area, the rats fed with the supplemental selenium or selenium plus iodine exhibited diminished necrosis of the chondrocytes in the growth plate. In the groups of rats receiving supplemental selenium and selenium plus iodine, the bone volume/tissue volume ratio (BV/TV), the trabecular thickness (Tb.Th), and the trabecular number were increased, while the trabecular separation was decreased. In the 12th week of the experiment, BV/TV and Tb.Th were significantly increased in the selenium plus iodine group compared to the selenium group. It is concluded that feeding the diet from the KBD endemic area caused necrosis of chondrocytes and dysfunctions of bone development similar to the pathological changes that are seen in KBD. Selenium and iodine protected chondrocytes in growth plate and promoted the formation of trabecular bone. The effects of selenium plus iodine on bone formation were more obvious than those of selenium alone     

Viability and plasma vitamin K levels in the common bile duct-ligated rats.

The common bile duct-ligated (CBDL) rat, which is widely used as a model of human cirrhosis, rapidly develops secondary biliary cirrhosis (SBC) within 4 weeks. The CBDL rat shows poor viability, however, a detailed examination of the causes of its death has not been made. In this study, we investigated the outcome of bile duct ligation in detail and attempted to extend the life span of this model by feeding the animals a diet supplemented with nutrients. Survival rate, blood chemistry, blood cell counts, plasma levels of K vitamins and liver histology were compared among CBDL rats fed a standard diet and an enriched diet. Sham-operated rats were used as a control. Six out of 18 CBDL rats fed the standard diet died within 32 days of operation. The cause of death was massive internal hemorrhage in various organs or body cavities. All CBDL rats fed the enriched diet survived more than 31 days, but the viability of CBDL rats was not significant between those fed the standard diet and the enriched diet. The degree of anemia correlated significantly with the prolongation of prothrombin time. Plasma vitamin K1 levels in CBDL rats were significantly lower than those in sham-operated rats, but vitamin K2 levels were similar. We suggest that massive hemorrhage, which was the direct cause of death, is caused by the impairment of hemostasis resulting from vitamin K deficiency. The enriched diet with vitamin K nutritional supplements seemed to contribute to the prolongation of the life span of CBDL rats.     

Gene expression profile in bone of diabetes-prone BB/OK rats fed a high-fat diet

A high-fat diet (HFD) has been recognized as a risk factor for diseases such as dyslipidemia, atherosclerosis, obesity, and osteoporosis. However, studies analyzing gene expression after HFD in bone are rare. That prompted us to analyze the expression of selected genes in bone of 4-week-old diabetes-prone B(io)B(reeding) rats. Two breeding pairs were fed a HFD (+10 % tallow) or were fed a normal diet (ND; Ssniff R-Z) before mating and afterward during pregnancy. After the birth of progeny, parents continued to be given HFD or ND until the progeny was weaned (3 weeks). Thereafter, offspring were weaned and were fed the same food as their parents up to an age of 4 weeks. Body weight was measured at an age of 4 weeks, and subsequently 13 HFD rats and 13 ND rats were killed and the tibial bone was harvested to analyze the expression of 53 genes in bone. All rats fed HFD were significantly heavier than rats fed ND after 3 and 4 weeks. The diet also influenced the expression of genes in bone. There were significant differences in 20 out of 53 genes studied between rats fed HFD compared with rats fed ND. Four out of 20 had a lower and 17 out of 20 genes a higher expression in HFD rats, but differences in gene expression showed obvious differences between males and females. There were only two genes that were similarly different between males and females: Bmp4 and Atf4. Two genes, Foxg1 and Npy, were inversely expressed in males and females. It seems that the gene expression is differently regulated by diet during pregnancy and later in life between males and females. Nevertheless, it cannot be excluded that HFD also acts as an epigenetic factor in the development of offspring in utero.     

Effects of vitamin K2 administration on calcium balance and bone mass in young rats fed normal or low calcium diet

OBJECTIVE: The purpose of this study was to examine the effects of vitamin K2 administration on calcium balance and bone mass in young rats fed a normal or low calcium diet. METHODS: Forty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into four groups with 10 rats in each group: 0.5% (normal) calcium diet, 0.1% (low) calcium diet, 0.5% calcium diet + vitamin K2 (menatetrenone, 30 mg/100 g chow diet), and 0.1% calcium diet + vitamin K2. After 10 weeks of feeding, serum calcium and calciotropic hormone levels were measured, and intestinal calcium absorption and renal calcium reabsorption were evaluated. Bone histomorphometric analyses were performed on cortical bone of the tibial shaft and cancellous bone of the proximal tibia. RESULTS: Feeding a low calcium diet induced hypocalcemia, increased serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D] levels with decreased serum 25-hydrovyvitamin D [25(OH)D] level, stimulated intestinal calcium absorption and renal calcium reabsorption, and reduced cortical bone mass as a result of decreased periosteal bone gain and enlarged marrow cavity, but did not significantly influence cancellous bone mass. Vitamin K2 administration in rats fed a low calcium diet stimulated renal calcium reabsorption, retarded the abnormal elevation of serum PTH level, increased cancellous bone mass, and retarded cortical bone loss, while vitamin K2 administration in rats fed a normal calcium diet stimulated intestinal calcium absorption by increasing serum 1,25(OH)2D level, and increased cortical bone mass. CONCLUSION: This study clearly shows the differential response of calcium balance and bone mass to vitamin K2 administration in rats fed a normal or low calcium diet.     

Zinc Deficiency Enhances the Induction of Micronuclei and 8-Hydroxy-2′-Deoxyguanosine Via Superoxide Radical in Bone Marrow of Zinc-Deficient Rats

The aim of the present study was to examine whether zinc (Zn) deficiency augmented the frequency of micronuclei, an indicator of chromosome aberration, and the induction of 8-hydroxy-2′-deoxyguanosine (8-OHdG), a marker of cellular DNA damage derived from oxidative stress, in rat bone marrow cells or not. Both the frequency of micronuclei and the induction of 8-OHdG were significantly increased in rats fed with a Zn-deficient versus a standard diet for 6 weeks (p?<?0.005). The supplementation of Zn with a standard diet for 4 weeks to rats fed with a Zn-deficient diet for 6 weeks restored the enhanced induction of micronuclei and 8-OHdG to levels comparable to those seen in rats fed with a standard diet for 10 weeks, indicating that the shortage of Zn in the body is involved in the induction of micronuclei and 8-OHdG. Again, the membrane-permeable superoxide dismutase mimetic superoxide scavenger, 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl, treatment (100 μmol/kg, twice a day) for 10 days prior to the termination of dietary treatment reduced the induction of micronuclei and 8-OHdG in rats fed with a Zn-deficient diet for 6 weeks to levels comparable to those in rats fed with a standard diet for 6 weeks, indicating that superoxide radical participates in the induction of micronuclei and 8-OHdG. In fact, the endogenous superoxide scavenger, Cu/Zn superoxide dismutase, was significantly reduced in the bone marrow cells of rats fed with a Zn-deficient diet for 6 weeks when compared to those of rats fed with a standard diet for 6 weeks (p?<?0.005). These observations demonstrate that Zn deficiency elevates the frequency of micronuclei and the induction of 8-OHdG through an increase in the biological action of the superoxide radical. This suggests an increase in carcinogenic initiation resulting from Zn deficiency-induced oxidative stress.     

Effects of a high soy protein diet on intestinal polyamines and ornithine decarboxylase activity in rats

This study was performed to determine whether intestinal luminal polyamine concentrations are affected by a high soy protein diet when compared with a high casein diet or a normoprotein casein diet. We also determined the effects of these diets, with differences in polyamines content, on mucosal polyamines and ornithine decarboxylase (ODC) activity to assess cell proliferation. Three groups of eight male Wistar rats were fed either a 50% soy protein diet, a 50% casein diet, or an 18% casein diet as a control. After 4 weeks of feeding, both intestinal content and mucosa were recovered. Polyamines were assayed by high performance liquid chromatography. ODC activity was measured by the release of (14)CO(2) from (14)C-L-ornithine. Luminal putrescine and cadaverine concentrations were higher in the jejunum than in the ileum, suggesting an absorptive process. The highest concentrations of intestinal polyamines were observed in rats fed the soy protein diet (P < 0.05). Only minor differences were observed in mucosal polyamines according to the diets. ODC activity was also higher in the intestinal mucosa of rats fed the high soy protein diet (P < 0.05). These results suggest that intestinal luminal polyamine concentrations and ODC activity are modulated by the dietary protein source.     

Effect of dietary polyunsaturated fat and 7,12-dimethylbenz(a)-anthracene on rat splenic natural killer cells and prostaglandin E synthesis

Summary Dietary polyunsaturated fat has been shown to stimulate mammary tumorigenesis induced in rats by 7,12-dimethylbenz(a)anthracene (DMBA). Studies were undertaken to investigate the effect of polyunsaturated fat and DMBA on splenic natural killer (NK) activity and prostaglandin E (PGE) synthesis. In a first experiment, splenic NK activity at 33, 55, 75, and 110 days of age was measured in Sprague-Dawley rats fed 0.5% low fat (LF), 5% normal fat (NF), or 20% high fat (HF) corn oil diets from 23 days of age. At 55 days of age, half of the rats from the 75 and 110 day age groups were given 5 mg DMBA. Ten days after the initiation of the diets splenic NK activity against YAC-1 lymphoma was decreased from 50% cytotoxicity in rats fed NF diet to 21% cytotoxicity in rats fed HF diet, but was not affected by LF feeding. No difference in NK activity was observed among the groups at the later time periods. DMBA had no effect on NK activity at 20 or 55 days after its administration. In a second experiment, where DMBA (15 mg/rat) was given to half of the rats at 50 days of age and NF or HF diets were started 3 days later, NK activity was 35% in rats fed NF diet and 21% in rats fed HF diet, 5 days after the diets were started. No difference in NK activity in rats fed either diet was observed at later time periods. DMBA decreased both NK activity and spleen cellularity transiently. In both experiments, PGE synthesis by spleen cells cultured for 18 h was not affected by dietary fat intake, but was slightly increased 3 days after DMBA administration. Results from these experiments suggest that the stimulation of DMBA-induced mammary tumorigenesis by polyunsaturated fat and by DMBA itself may possibly be mediated by a transient decrease in splenic NK cell activity.This work was supported by grants CA-35641, CA-33240, CA-13038 and Core Grant CA-24538 from the National Cancer Institute     

Effect of polaprezinc on taste disorders in zinc-deficient rats

The effect of polaprezinc, a chelate compound consisting of zinc ion and L-carnosine, on abnormalities of taste sensation induced by feeding a zinc-deficient diet to rats was examined by using the two-bottle preference test (quinine hydrochloride as a bitter taste and sodium chloride as a salty taste). Rats were fed either a zinc-deficient or a zinc-sufficient diet. The zinc-deficient diet increased the preference for both taste solutions, while polaprezinc (at doses of 3 and 10 mg/kg) restored the altered taste preferences. We also evaluated the proliferation of taste bud cells using 5-bromo-2'-deoxyuridine (BrdU). The BrdU incorporation into taste bud cells was significantly reduced in rats fed a zinc-deficient diet compared with rats fed a zinc-sufficient diet (from 50.8% to 45.0%, p<0.05) and this reduction was reversed by polaprezinc at doses of 1, 3, and 10 mg/kg, increasing to 50.2%, 53.5%, and 52.5%, respectively. These findings indicate that zinc deficiency induces the delayed of proliferation of taste bud cells, while polaprezinc improves cell proliferation. In conclusion, polaprezinc had a therapeutic effect in a rat model of abnormal taste sensation. Its mechanism of action was suggested to involve improvement of the decrease in taste bud cell proliferation caused by zinc deficiency.     

Wnt/beta-catenin 信号通路在高脂血症中的激活

目的:建立大鼠高脂血症模型,观察活体内高脂刺激下血管平滑肌细胞内wnt/-catenin信号通路的激活及血管平滑肌细胞增殖情况,探讨活体内wnt/-catenin信号通路的激活与血管平滑肌细胞增殖的关系。方法:以雄性SD大鼠为研究对象,体重200~250g。通过饲以高脂饲料建立高脂血症模型。12周后处死大鼠,获取主动脉。苏丹III染色检测血管壁粥样硬化病变,HE染色、透射电镜检测血管平滑肌细胞增殖及表型变化,实时定量RT-PCR及Western Blot检测β-catenin、T cell factor 4(TCF-4)、cyclin D1的变化。结果:通过3个月的高脂饮食饲养,成功建立大鼠高脂血症模型,但大鼠主动脉壁粥样硬化病变不明显。高脂刺激下,mRNA及蛋白水平的β-catenin、TCF-4、cyclin D1表达均增加;同时血管壁内平滑肌细胞增殖增加、表型由收缩型向合成型变化。结论:高脂饮食可以成功建立大鼠高脂血症模型,但由于大鼠本身的代谢特点,不容易出现动脉粥样硬化斑块。Wnt/-catenin信号通路在高脂情况下被激活,同时平滑肌细胞增殖增加、表型改变,提示wnt/-catenin信号通路的激活与平滑肌细胞增殖之间存在联系。     

Modifying effects of fermented brown rice on fecal microbiota in rats

Brown rice fermented by Aspergillus oryzae (FBRA) is a fiber-rich food. Effects of dietary administration of FBRA on rat fecal microbiota composition were examined. Male Wistar rats were fed a basal diet or a 5% FBRA- or 10% FBRA-containing diet, and fecal microbiota was analyzed by culture and terminal-restriction fragment length polymorphism (T-RFLP) analysis. The viable cell number of lactobacilli significantly increased after feeding 10% FBRA diet for 3 weeks compared with that in the basal diet group and that in the same group at the beginning of the experiment (day 0). An increase in the viable cell number of lactobacilli was also observed after feeding 10% FBRA for 12 weeks compared with the effect of a basal diet. T-RFLP analysis showed an increase in the percentage of lactobacilli cells in feces of rats fed 10% FBRA for 14 weeks. Lactobacilli strains isolated from rat feces were divided into six types based on their randomly amplified polymorphic DNA (RAPD) patterns, and they were identified as Lactobacillus reuteri, L. intestinalis and lactobacilli species based on homology of the partial sequence of 16S rDNA. FBRA contains lactic acid bacteria, but their RAPD patterns and identified species were different from those in rat feces. These results indicated that dietary FBRA increases the number of lactobacilli species already resident in the rat intestine.     

Effect of a chronic suboptimal intake of magnesium on magnesium and calcium content of bone and on bone strength of the rat.

Sprague-Dawley rats were kept at 28 degrees C from 21 to 517 days age and fed one of the two following diets: a semi-purified diet containing 502 p.p.m. of Mg (control) or the same diet containing only 120 p.p.m. (mg/kg) (low-Mg). The chronic suboptimal intake of Mg by rats fed the low-Mg diet did not result in overt signs of Mg deficiency even when Mg levels were greatly reduced in carcass, plasma, and tibia, but it significantly decreased bone strength. It is suggested that Mg deficiency in man could be a factor in the weakening of bone, commonly observed in old age, even when there are no visible signs of Mg deficiency. Studies of the human situation would be of interest.     

Citrus limonoids obacunone and limonin inhibit azoxymethane-induced colon carcinogenesis in rats

Obacunone and limonin are bitter limonoids in citrus. Their modifying effects on the development of aberrant crypt foci (ACF), the activity of detoxification enzymes, glutathione S-transferase (GST) and quinone reductase (QR), and cell proliferation activity were investigated in male F344 rats treated with azoxymethane (AOM). Obacunone and limonin were administered in the diet, during the initiation (for 4 weeks) or postinitiation phase (for 4 weeks) of AOM-induced tumorigenesis. Feeding of obacunone and limonin (0.02% or 0.05%) caused significant reduction (55-65% by "initiation" feeding and 28-42% by "postinitiation" feeding) in the yield of ACF. The ability to reduce the proliferating cell nuclear antigen-labeling index in crypts and correlated well with the prevention of ACF. In a subsequent long-term experiment (38 weeks), in which rats were initiated with AOM and fed 0.05% obacunone or 0.05% limonin during the initiation or post-initiation phase, both compounds in diet caused significant reduction (65%-92% inhibition) in the incidence of colonic adenocarcinoma. Thus, citrus bitter limonoids obacunone and limonin possess chemopreventive effects on chemically induced rat colon carcinogenesis.