Increased Stress Reactivity as a Possible Factor of Early Degenerative Changes in OXYS Rats

After stress (immobilization in cages) plasma corticosterone level in prematurely aging OXYS rats was higher, while the content of NO metabolites was much lower than in Wistar rats. Stress increased blood pressure in OXYS and Wistar rats, the maximum values were observed in control and stressed OXYS rats. The concentration of reduced glutathione in the brain of OXYS rats was lower than in Wistar rats. After immobilization the concentration of reduced glutathione decreased in animals of both strains. The concentration of oxidized protein increased by 1.5 times only in OXYS rats. SOD activity remained unchanged, but in OXYS rats this parameter was higher than in Wistar rats. It can be hypothesized that high blood pressure, low NO content, high corticosterone concentration, and stress-induced deficiency of the antioxidant system (or combined effects of these factors) contribute to the development of neurodegenerative changes in the brain of OXYS rats.__________Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 139, No. 4, pp. 387–390, April, 2005     

The Turnover of 85Zn in Rats Fed a Zinc-Deficient Diet

The fresh weight zinc concentration in spleen is unchanged, the concentrations in serum, kidney, pancreas, liver and heart are reduced moderately and those in incisors and four bone samples are reduced markedly in rats fed a zinc-deficient diet (7.2 fig Zn/g) for six weeks compared to those in rats pair-fed the same diet and given a 200 fig zinc supplement daily. The ash weight zinc concentrations in mineralized tissue samples from both groups decrease rapidly and, after three weeks on the diet, assume relatively stable levels. The retention of ⁸⁵Zn in the serum, heart and viscera is higher in rats not given the supplement. The pattern is consistent with decreased turnover of zinc due to reduced intake and excretion. The ⁶⁵Zn retention data from the bones and teeth were analyzed using the Bauer, Carlsson, Lindquist equation. Reduced zinc intake causes a decrease in bones of the rate at which zinc is “accreted”, most likely as a result of decreased accretion of bone as well as decreased availability of zinc. The slowly exchanging zinc in incisors and cortical bone is markedly reduced while the rapidly exchanging zinc in bones is less affected.     

Heat-killed Lactobacillus Reuteri GMNL-263 Prevents Epididymal Fat Accumulation and Cardiac Injury in High-Calorie Diet-Fed Rats

High-calorie diet-induced obesity leads to cardiomyocyte dysfunction and apoptosis. Impaired regulation of epididymal fat content in obese patients has been known to increase the risk of cardiac injury. In our study, a lactic acid bacteria, Lactobacillus reuteri GMNL-263, was evaluated for its potential to reduce body weight and body fat ratio and to prevent heart injury in rats with high-fat diet-induced obesity. Lactic acid bacteria supplementation restored the cardiac function and decreased the physiological changes in the heart of the obese rats. In addition, the Fas/Fas-associated protein pathway-induced caspase 3/e Poly polymerase mediated apoptosis in the cardiomyocytes of the obese rats was reversed in the Lr263-treated rats. These results reveal that fed with Lr-263 reduces body fat ratio, inhibits caspase 3-mediated apoptosis and restores cardiac function in obese rats through recovery of ejection fraction and fractional shortening. Our results indicated that the administration of Lr263 lactic acid bacteria can significantly down-regulate body fat and prevent cardiomyocyte injury in obese rats.     

Interaction of Diet and Training on Endurance Performance in Rats

We determined the interaction of diet and training on metabolic adaptations in skeletal muscle and liver, and the consequences of these adaptations for endurance. Eighty rats performed a baseline treadmill run to exhaustion at 16 m min(-1) (RUN1) and were then divided into two groups and given one of two diets: high carbohydrate (CHO) or high fat (FAT). Each dietary group was then divided into one of four subgroups: sedentary control that performed no training (NT); low-intensity running (8 m min(-1); LOW) and two groups who trained at their maximal voluntary running speed without electrical stimulation (28 m min(-1); VMAX). Training volume was identical for LOW and VMAX (1000 m session(-1)) and animals ran 4 days week(-1) for 8 weeks. To assess the interaction of the higher intensity exercise with diet, a second endurance test (RUN2) was undertaken after 6 weeks at either 16 m min(-1) or 28 m min(-1). The NT group ran for a longer duration (increase of 77 %) after FAT than CHO (239 +/- 28 vs. 135 +/- 30 min, P < 0.05) at 16 m min(-1). There were no differences in RUN2 for the LOW group when rats ran at 16 m min(-1) (454 +/- 86 vs. 427 +/- 75 min for CHO and FAT groups, respectively), but rats in the VMAX group fed FAT ran longer than rats fed CHO at 28 m min(-1) (100 +/- 28 vs. 58 +/- 11 min, respectively, P < 0.05). FAT increased the activities of the enzymes citrate synthase, beta-hydroxyacyl-CoA dehydrogenase and carnitine palmitoyl-transferase compared to CHO (P < 0.01), but there was no systematic effect of training. We conclude: (1) there was no additive effect of a high-fat diet on endurance performance when rats performed low-intensity training; (2) running performance at 28 m min(-1) was only enhanced by a high-fat diet after more intense training; (3) diet-induced and training-induced adaptations that increase exercise capacity may be under independent control. Experimental Physiology (2001) 86.4, 499-508.     

Growth of Trichinella Spiralis Larvae in Rats Receiving Folic-Acid-Deficient Diet

A study of the effect of growth of Trichinella spiralis in rats fed a folic-acid-deficient diet is described. Trichinella spiralis larvae encysted in the diaphragms of two groups—rats fed a folic acid-deficient diet and rats fed a complete (normal) diet—were examined. In rats fed a folic-acid-deficient diet, the number of the encysted larvae was larger than that in the controls. However, the encysted larvae were substantially longer in the control group of rats fed complete (normal) diets.     

Histomorphometric Study of Alveolar Bone Healing in Rats Fed a Boron‐Deficient Diet

Bone healing after tooth extraction in rats is a suitable experimental model to study bone formation. Thus, we performed a study to determine the effects of boron (B) deficiency on bone healing by using this model. The first lower right molar of weanling Wistar rats was extracted under anesthesia. The animals were divided into two groups: +B (adequate; 3 mg B/kg diet), and ?B (boron‐deficient; 0.07 mg/kg diet). The animals in both groups were killed in groups of 10 at 7 and 14 days after surgery. The guidelines of the NIH for the care and use of laboratory animals were observed. The mandibles were resected, fixed, decalcified, and embedded in paraffin. Buccolingually oriented sections were obtained at the level of the mesial alveolus and used for histometric evaluations. Total alveolar volume (TAV) and trabecular bone volume per total volume (BV/TV) in the apical third of the alveolus were determined. Percentages of osteoblast surface (ObS), eroded surface (ES), and quiescent surface (QS) were determined. No statistical significant differences in food intake and body weight were observed. Histomorphometric evaluation found ?B rats had 36% and 63% reductions in BV/TV at 7 and 14 days, respectively. When compared with +B rats, ?B rats had significant reductions (57% and 87%) in ObS concomitantly with increases (120% and 126%) in QS at 7 and 14 days, respectively. The findings show that boron deficiency results in altered bone healing because of a marked reduction in osteogenesis. Anat Rec, 291:441–447, 2008. © 2008 Wiley‐Liss, Inc.     

Insomnia as a Health Risk Factor

This article reviewed insomnia epidemiological research, identifying areas where insomnia was a risk factor and isolating areas deserving of further investigation. Insomnia was consistently predictive of depression, anxiety disorders, other psychological disorders, alcohol abuse or dependence, drug abuse or dependence, and suicide, indicating insomnia is a risk factor for these difficulties. Additionally, insomnia was related to decreased immune functioning. The data were inconclusive regarding insomnia as a risk factor for cardiovascular disease and mortality, but sleep medication use was predictive of mortality. These results must be tempered with the knowledge that significant weaknesses existed in the studies reviewed. The main weaknesses were inadequate definition of insomnia and inadequate control for alternative explanations. Despite these limitations, this review suggests that insomnia is a risk factor for poor mental and physical health.     

Diet as a risk factor for atopy and asthma

It has been hypothesized that decreasing antioxidant (fruit and vegetables), increased n-6 polyunsaturated fatty acid (PUFA; (margarine, vegetable oil), and decreased n-3 PUFA (oily fish) intakes have contributed to the recent increases in asthma and atopic disease. Epidemiologic studies in adults and children have reported beneficial associations between dietary antioxidants and lipids and parameters of asthma and atopic disease. The associations with n-6 and n-3 PUFA appear to be very complex and might differ between asthma and atopic dermatitis. Dietary antioxidants are probably exerting antioxidant and nonantioxidant immunomodulatory effects. Dietary lipids exert numerous complex effects on proinflammatory and immunologic pathways. It has also been suggested that atopic dermatitis is associated with an enzyme defect in lipid metabolism. In spite of this, the results of interventional supplementation studies in established disease have been disappointing, and there is now increasing interest in the possibility that dietary antioxidant and lipid intakes might be important in determining expression of disease during pregnancy and early childhood and that dietary interventions should be targeted at these groups. It also seems likely that there is individual variation in the responses of individuals to lipid, and probably antioxidant, supplementation. Further research to determine whether dietary intervention can reduce the risk of asthma and atopic disease is justified.     

小檗碱改善高脂饮食大鼠的胰岛素抵抗

目的:观察小檗碱是否能改善高脂饮食诱导的胰岛素抵抗,以探讨小檗碱干预糖耐量受损(IGT)的可能性。方法:8周龄雄性SD大鼠29只,分为正常组(NC,n=9)和高脂组(HF,n=20)。高脂饲料喂养14周后高脂组分为二组,10只大鼠继续喂养高脂饮食,另一小檗碱组(HF B,n=10)每天灌胃小檗碱150mg/kg体重,治疗6周后进行口服葡萄糖耐量试验和胰岛素耐量试验(ITT),评估小檗碱对胰岛素敏感性的影响。结果:HF组大鼠体重、肝重和附睾脂肪重量均明显高于HF B和NC组(均P<0.01),HF B组空腹血糖和葡萄糖负荷后2h血糖明显低于HF组(分别为5.70±0.52mmol/Lvs6.66±0.51mmol/L和7.88±0.46mmol/Lvs8.85±1.01mmol/L),空腹和葡萄糖负荷后2h胰岛素HF B组也显著低于HF组(分别为0.63±0.25ng/mlvs1.64±0.68ng/ml和1.20±0.21ng/mlvs3.60±0.36ng/ml)。各时间点血糖和胰岛素HF组均显著高于NC组(均P<0.01)。Homa胰岛素抵抗指数HF组明显高于HF B组(P<0.01)。ITT腹腔注射胰岛素后各时间点血糖下降幅度HF B组均高于HF组,15min时HF B组血糖下降23%,而HF组仅下降7%。结论:长期高脂饮食可导致大鼠胰岛素抵抗,小檗碱明显降低高脂大鼠的高胰岛素血症,改善胰岛素抵抗,因此适合于IGT的干预。