Astaxanthin alleviates renal damage of rats on high fructose diet through modulating NFκB/SIRT1 pathway and mitigating oxidative stress.

This study was conducted to determine the effect of astaxanthin (ASX) treatment on alleviation of renal damage in high fructose induced nephrotoxicity in rats. Treatments were arranged in a 2 × 2 factorial fashion: administrations of fructose (30%, via drinking water) and ASX (1 mg/kg/day, within 0.2 ml olive oil) for 8 weeks. Data were analyzed by two-way ANOVA. The ASX treatment decreased serum urea (p < .01) and blood urea-N concentrations (p < .02) at a lower extent in rats receiving fructose than those not receiving fructose. Moreover, the ASX treatment reversed the increases in malondialdehyde (MDA) (p < .0001) and nuclear factor kappa B (NF-κB) (p < .0003) levels and the decreases in superoxide dismutase (SOD) activity (p < .0001) and sirtuin-1 (SIRT1) level (p < .0004), in the kidney upon high fructose consumption. The data suggest that ASX supplementation alleviates renal damage induced by high fructose consumption through modulating NF-κB/SIRT1 pathway and mitigating oxidative stress.

Effects of dietary supplementation of arginine-silicate-inositol complex on absorption and metabolism of calcium of laying hens.

The effects of supplementation of arginine-silicate-inositol complex (ASI; 49.5-8.2-25 g/kg, respectively) to laying hens were investigated with respect to eggshell quality, calcium (Ca) balance, and expression of duodenal proteins related to Ca metabolism (calbindin and tight junction proteins). A total of 360 laying hens, 25 weeks old, were divided into 3 groups consisting of 6 replicate of cages, 20 birds per cage. The groups were fed a basal diet and the basal diet supplemented with 500 or 1000 mg ASI complex per kilogram for 90 days. Data were analyzed by ANCOVA using data during the first week of the adaptation period as covariates. As the ASI complex supplementation level increased, there were increases in feed intake (P < 0.0001), egg production (P < 0.001), egg weight (P < 0.0001) and eggshell weight (P < 0.001) weight, and shell thickness (P < 0.001) and decreases in feed conversion ratio and cracked egg percentage (P < 0.0001 for both). Concentrations of serum osteocalcin (P < 0.0001), vitamin D (P < 0.0001), calcium (P < 0.001), phosphorus (P < 0.001), and alkaline phosphatase (P < 0.008) as well as amounts of calcium retention (P < 0.0001) and eggshell calcium deposition (P < 0.001), and Ca balance (P < 0.0001) increased, whereas amount of calcium excretion (P < 0.001) decreased linearly in a dose-dependent manner. The ASI complex supplementation increased expressions of calcium transporters (calbindin-D28k, N sodium-calcium exchanger, plasma membrane calcium ATPase, and vitamin D receptor) and tight junction proteins (zonula occludens-1 and occludin) in the duodenum in a linear fashion (P < 0.0001 for all). In conclusion, provision of dietary ASI complex to laying hens during the peak laying period improved eggshell quality through improving calcium utilization as reflected by upregulation of genes related to the calcium metabolism. Further studies are needed to elucidate the contribution of each of the ASI complex ingredients.

Protective effects of resveratrol against streptozotocin-induced diabetes in rats by modulation of visfatin/sirtuin-1 pathway and glucose transporters.

This experiment was aimed at elucidating the protective effect of resveratrol against diabetes. Forty male Wistar albino rats were allocated into four groups: the control and streptozotocin (STZ)-induced diabetes groups were treated either with placebo (1 ml/kg, i.p.) or resveratrol (20 mg/kg, i.p.) for 8 weeks. Body weight, blood glucose and serum malondialdehyde (MDA) concentrations were monitored. At the end of the experimental period, expression levels of visfatin, sirtuin-1 (SIRT1) and glucose transporters (GLUTs, 2 and 4) were measured in skeletal muscle and pancreas by Western blotting. The resveratrol treatment partially compensated for body weight loss and alleviated hyperglycaemia and returned serum MDA concentrations to the control group levels. Data suggest that supplementation may reduce the severity of diabetes and its complications through suppressing oxidative stress and increasing potential to internalise glucose by extrahepatic tissues.

Taurine ameliorates neuropathy via regulating NF-κB and Nrf2/HO-1 signaling cascades in diabetic rats.

Diabetic neuropathy is one of common complications of diabetes mellitus. Hyperglycemia induced oxidative stress involves in the development of diabetic neuropathy, which could be reversed by supplementation of taurine, an endogenous antioxidant. This experiment was conducted to evaluate alterations in the expressions of transcription factors [nuclear factor kappa B (NF-κB), nuclear factor-E2-related factor-2 (Nrf2), and heme oxygenase 1 (HO-1)] and glucose transporters and glucose metabolism in the brain of diabetic rats. In a 2×2 factorially arranged groups, taurine (2%) or water was administered per orally to healthy and streptozotocin (STZ)-induced diabetic rats (n=10 per group) for 8 weeks. Diabetes was associated with weight loss, hyperglycemia, and oxidative stress as reflected by increased serum malondialdehyde (MDA) concentrations. Diabetic rat brains had increased the NF-κB expression and decreased the Nrf2, HO-1, GLUT1,3 expressions as compared to healthy rat brains. Supplemental taurine did not alter body weight and blood glucose concentration, but partially reduced serum MDA concentration in the diabetic rats. Taurine also partially alleviated neuroinflammation as reflected by suppressed the NF-κB expression and enhanced the Nrf2, HO-1, GLUT1,3 expressions in the diabetic rats. In conclusion, taurine reduces the severity of oxidative stress through activating antioxidative defense signaling pathway in diabetic rat brain.

Berberis vulgaris root extract alleviates the adverse effects of heat stress via modulating hepatic nuclear transcription factors in quails.

To evaluate the action mode of Berberis vulgaris root extract in the alleviation of oxidative stress, female Japanese quails (n 180, aged 5 weeks) were reared, either at 22°C for 24 h/d (thermoneutral, TN) or 34°C for 8 h/d (heat stress, HS), and fed one of three diets: diets containing 0, 100 or 200 mg of B. vulgaris root extract per kg for 12 weeks. Exposure to HS depressed feed intake by 8·5% and egg production by 12·1%, increased hepatic malondialdehyde (MDA) level by 98·0% and decreased hepatic superoxide dismutase, catalase and glutathione peroxidase activities by 23·5, 35·4 and 55·7%, respectively (P<0·001 for all). There were also aggravations in expressions of hepatic NF-κB and heat-shock protein 70 (HSP70) by 42 and 43%, respectively and suppressions in expressions of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and haeme-oxygenase 1 (HO-1) by 57 and 61%, respectively, in heat-stressed quails (P<0·001 for all). As supplemental B. vulgaris extract increased, there were linear increases in performance parameters, activities of antioxidant enzymes and hepatic Nrf2 and HO-1 expressions (P<0·001 for all) and linear decreases in hepatic MDA level and NF-κB and HSP70 expressions at a greater extent in quails reared under TN condition and those reared under HS condition. In conclusion, dietary supplementation of B. vulgaris root extract to quails reduces the detrimental effects of oxidative stress and lipid peroxidation resulting from HS via activating the host defence system at the cellular level.

The effects of chromium picolinate and chromium histidinate administration on NF-κB and Nrf2/HO-1 pathway in the brain of diabetic rats.

The objective of this experiment was to investigate the effects of supplemental chromium picolinate (CrPic) and chromium histidinate (CrHis) on nuclear factor-kappa B (NF-κB p65) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathway in diabetic rat brain. Nondiabetic (n = 45) and diabetic (n = 45) male Wistar rats were either not supplemented or supplemented with CrPic or CrHis via drinking water to consume 8 µg elemental chromium (Cr) per day for 12 weeks. Diabetes was induced by streptozotocin injection (40 mg/kg i.p., for 2 weeks) and maintained by high-fat feeding (40 %). Diabetes was associated with increases in cerebral NF-κB and 4-hydroxynonenal (4-HNE) protein adducts and decreased in cerebral nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IκBα) and Nrf2 levels. Both Cr chelates were effective to decrease levels of NF-κB and 4-HNE protein adducts and to increase levels of IκBα and Nrf2 in the brain of diabetic rats. However, responses of these increases and decreases were more notable when Cr was supplemented as CrHis than as CrPic. In conclusion, Cr may play a protective role in cerebral antioxidant defense system in diabetic subjects via the Nrf2 pathway by reducing inflammation through NF-κB p65 inhibition. Histidinate form of Cr was superior to picolinate form of Cr in reducing NF-κB expression and increasing Nrf2 expression in the brain of diabetic rats.

The effects of chromium complex and level on glucose metabolism and memory acquisition in rats fed high-fat diet.

Conditions in which glucose metabolism is impaired due to insulin resistance are associated with memory impairment. It was hypothesized that supplemental chromium (Cr) may alleviate insulin resistance in type 2 diabetes and consequently improve memory acquisition, depending upon its source and level. In a complete randomized design experiment, male Wistar rats (n=60; weighing 200-220 g) were fed either normal (8%, normal diet (ND)) or high-fat (40%, high-fat diet (HFD)) diet and supplemented with Cr as either chromium-glycinate (CrGly) or chromium-acetate (CrAc) at doses of 0, 40, or 80 µg/kg body weight (BW) via drinking water from 8 to 20 weeks of age. Feeding HFD induced type 2 diabetes, as reflected by greater glucose/insulin ratio (2.98 vs. 2.74) comparing to feeding ND. Moreover, HFD rats had greater BW (314 vs. 279 g) and less serum (53 vs. 68 µg/L) and brain (14 vs. 24 ng/g) Cr concentrations than ND rats. High-fat diet caused a 32% reduction in expressions of glucose transporters 1 and 3 (GLUTs) in brain tissue and a 27% reduction in mean percentage time spent in the target quadrant and a 38% increase in spatial memory acquisition phase (SMAP) compared with ND. Compared with supplemental Cr as CrAc, CrGly was more effective to ameliorate response variables (i.e., restoration of tissue Cr concentration, enhancement of cerebral GLUTs expressions, and reduction of the glucose/insulin ratio and SMAP) in a dose-response manner, especially in rats fed HFD. Supplemental Cr as CrGly may have therapeutic potential to enhance insulin action and alleviate memory acquisition in a dose-dependent manner, through restoring tissue Cr reserve and enhancing cerebral GLUTs expressions.

Impacts of calcium addition and different oil types and levels on in vitro rumen fermentation and digestibility.

This in vitro study was designed to investigate the effects of calcium addition to substrates differing in source and level of oil on fermentation, gas production, and digestibility parameters. Substrates were made from basal mixtures containing three levels of calcium salt (0, 1, and 2% CaCl2) to contain three levels (3, 6, and 9%) of two types (sunflower and soy) of oil. After collecting from two Holstein bulls and mixing with buffer, rumen fluid was used to incubate the resulting 18 mixtures in duplicate. Ionizable calcium, pH and NH3-N concentration were measured during incubation. Gas production was measured at 6, 12, 24, and 48 h after incubation. Kinetics parameters of gas production and in vitro dry matter digestibility (IVDMD) were calculated from regression coefficients of an exponential equation and a linear equation, respectively. Data were analysed using 3-way ANOVA with repeated measure option in which the parameter time was a subplot. Oil type did not affect pH and ionizable calcium concentration. There were linear increases and decreases in pH and ionizable calcium concentration in response to increasing oil and calcium levels, respectively. However, with increasing oil levels there were no interactions between calcium addition and oil level on pH and ionizable calcium concentration. None of the treatments affected NH3-N concentration. The amount of gas produced from substrates containing sunflower oil was greater than soy oil (41.7 vs. 40.5 ml). Cumulative gas production and amount of gas production from insoluble but slowly fermentable portion of the supplemental mixtures linearly decreased and linearly increased as oil and calcium levels increased in the substrates, respectively. However, interactions of calcium addition and oil level on gas production and kinetics of gas production were lacking. Oil type did not affect IVDMD. Despite lacking main effects, interaction of calcium addition and oil level indicated that increasing calcium level alleviated depression in IVDMD resulting from increasing oil level. In conclusion, increasing oil level depressed, whereas calcium addition stimulated ruminal fermentation. Improvement in IVDMD may partially support that calcium addition alleviates the adverse effects of oil and that more calcium is needed when diets are supplemented with increasing amounts of oil.