AIN-93M Diet Research Articles

Does gender influence cardiovascular remodeling in C57BL/6J mice fed a high-fat, high-sucrose and high-salt diet?

Animal models are widely used to study the physiopathology of human diseases. However, the influence of gender on modern society diet style-induced cardiovascular disease has not thus far been explored in these models. Thus, this study investigated cardiovascular remodelling in C57BL/6J mice fed a diet rich in saturated fat, sucrose and salt, evaluating gender effect on this process. Male and female C57BL/6J mice were fed AIN93M diet or a modified AIN93M rich in fat, sucrose and salt (HFSS) for 12weeks. Body mass, water and food intake and cardiovascular remodelling were assessed. The HFSS diet did not lead to body mass gain or glucose metabolism disturbance as assessed by serum glucose, insulin and oral glucose tolerance test. However, female mice on a HFSS diet had increased visceral and subcutaneous adiposity. Only male mice displayed heart hypertrophy. The left ventricle was not hypertrophied in either male or female mice, but its lumen was dilated. Intramyocardial arteries and the thoracic aorta showed media thickening in male mice, but in the female it was only observed in the thoracic aorta. Finally, intramyocardial artery dilation was present in both genders, but not in the aorta. Therefore changes in LV dimensions and arterial remodelling were influenced by both gender and the HFSS diet. In conclusion, male and female C57BL/6J mice suffered cardiovascular remodelling after 12weeks of HFSS feeding, although they did not develop obesity or diabetes. Sexual dimorphism occurred in response to diet for body adiposity, heart hypertrophy and intramyocardial artery remodelling.

Yacon (Smallanthus sonchifolius)-based product increases fecal short-chain fatty acids and enhances regulatory T cells by downregulating RORγt in the colon of BALB/c mice

Abstract Although yacon (Smallanthus sonchifolius) is a known source of prebiotics (fructooligosaccharides (FOS) and inulin) and phenolic compounds beneficial to gut microbiota and intestinal immune response modulation, its regulatory mechanisms still remain unclear. Therefore, we investigated whether the consumption of a yacon-based product (PBY) modulates the population of intestinal lymphocytes as well as transcription factors that drive host adaptive immune responses. For this purpose, BALB/c male mice were fed either a standard AIN-93M diet or AIN-93M diet supplemented with PBY (6.0% FOS + Inulin) for 8 weeks. We found that PBY consumption in mice reduced food intake, improved fecal humidity and viscosity, intensified fecal short-chain fatty acid production, increased the number of regulatory T cells, and downregulated the expression of RORγt transcription factor in the colon. Thus, it can be inferred from the findings that PBY consumption improves satiety and mucosal integrity, and possibly favors anti-inflammatory immune responses in the colon.

Chromium(III) Glycinate Complex Supplementation Improves the Blood Glucose Level and Attenuates the Tissular Copper to Zinc Ratio in Rats with Mild Hyperglycaemia

The aim of the study was to evaluate the hypoglycaemic potential of supplementary Cr in the form of chromium(III) glycinate (CrGly) in the diabetic model of rats. The experiment was conducted on 40 male Wistar rats, of which 30 were made diabetic by injection of a single dose of streptozotocin (55 mg/kg b.m.), while the remaining 10 rats served as the healthy control. After inducing hyperglycaemia, 2 groups of diabetic rats (10 rats each) were supplemented with Cr either as CrGly or chromium(III) picolinate (CrPic) given orally at a dose of 10 mg/kg diet (about 0.75 mg Cr/kg b.m.) with adequate AIN-93M diet for 7 weeks. At the termination of experiment, all animals were sacrificed to collect blood and internal organs for biochemical assays. Blood biochemical indices and tissular trace element contents (Fe, Zn, Cu, Cr) were measured and compared with the values of the untreated groups. It was found that CrGly significantly decreased blood glucose, total cholesterol, HDL cholesterol and triacylglycerol levels more efficiently than CrPic. Furthermore, both Cr compounds normalized disturbed the serum, renal and cardiac molar Cu/Zn ratio, as well as restored the kidney Zn and Cu levels in rats with hyperglycaemia. Supplementary Cr did not increase the tissular Cr levels in diabetic rats. The study confirmed the hypoglycaemic potential of CrGly in the diabetic model of rats.

Comparative analysis of the influence of a high-fat/high-carbohydrate diet on the level of anxiety and neuromotor and cognitive functions in Wistar and DAT-KO rats.

We compared anxiety, neuromotor, and cognitive functions in mutant rats with different allelic variants of dopamine transporter DAT knockout receiving balanced or excess in fat and fructose diet. The experiments were performed in DAT−/− homozygotes, DAT+/− heterozygotes, and DAT+/+ wild type rats. The genotype of DAT‐KO rats was confirmed by restriction analysis of DAT gene compared to behavioral responses in the open field test (OF). Animals in the first groups of each strain were fed a balanced AIN93M diet; and those in the second groups with a high‐fat/high‐fructose diet. Neuromotor function was studied as grip strength, and behavioral responses were assessed in the elevated plus maze and conditioned passive avoidance response tests. The mass of the internal organs and white and brown fat, as well as selected lipid and nitrogen metabolism parameters in blood plasma were determined at the end of the experiment. DAT−/− had the highest specific grip strength, and showed an increase in initial exploratory activity in comparison with DAT+/− and DAT +/+. The exploratory activity was significantly reduced in the second test compared to the first one in DAT−/− and DAT+/− of first but not second group. Anxiety decreased with age in the second groups of DAT+/− and DAT+/+ (but not in DAT−/−) and was higher in DAT+/+ than in DAT+/− and DAT−/−. Excess fat and fructose resulted in the deterioration of short‐term memory in DAT+/+. Lipidomic indices of blood plasma were less responsive to diet in DAT−/− and DAT−/+ in comparison to DAT+/+. The increased AsAT/AlAT activity ratio in DAT−/− compared with those in DAT+/+ suggests the activation of catabolism activity in the mutants. The consumption of excess fat and fructose significantly modified the effects produced by DAT gene allelic variants presumably due to the influence on the processes of dopamine metabolism.

Dietary Daidzein Supplementation During Pregnancy Facilitates Fetal Growth in Rats.

Daidzein, a natural isoflavone with estrogen-like activity, has been implicated in the regulation of reproductive performance in mammals. However, little is known about the molecular mechanisms involved. Here, the effects and potential mechanisms of daidzein supplementation on fetal growth in rats have been explored. Thirty-six pregnant Sprague-Dawley rats are assigned to receive either an AIN-93M diet or an AIN-93M diet supplemented with 50mgkg-1 daidzein. Blood, placental, and fetus samples were collected on day 15 of gestation. It is shown that daidzein significantly improves the rat reproductive performance, which is associated with a higher fetus number, and the weight of the fetus and placenta (p<0.05). Daidzein also increases the maternal serum estrogen and leptin concentrations, and the activity of superoxide dismutase (SOD) (p<0.05). Notably, the isobaric tags for relative and absolute quantification (iTRAQ)-based proteomics analysis identifies 43 differentially expressed (DE) proteins in the placenta upon daidzein supplementation (p<0.05). Interestingly, critical proteins involved in amino acid transport and metabolism, embryonic development, ubiquitination processes, and immune responses are upregulated in the daidzein group (p<0.05). These results not only indicate a beneficial effect of daidzein supplementation on reproductive performance but also offer potential mechanisms behind daidzein-facilitated fetal growth in rats.

Montmorency tart cherry protects against age-related bone loss in female C57BL/6 mice and demonstrates some anabolic effects

Age-related bone loss is a consequence of endocrine and immune changes that disrupt bone remodeling. Functional foods (e.g., tart cherries) with antioxidant, anti-inflammatory and prebiotic activity can potentially counter this age-related phenomenon. The aim of this study was to determine if Montmorency tart cherry protects against early age-related bone loss and the culpable alterations in bone metabolism. Female, 5-month-old, C57BL/6 mice were assigned to baseline or treatment groups: AIN-93M diet supplemented with 0, 1, 5, or 10% tart cherry for 90 days. Bone mineral density (BMD) and trabecular and cortical bone microarchitecture were assessed. Treatment effects on bone metabolism and regulators of bone formation, resorption and mineralization were determined. Mice consuming the 5% and 10% doses had higher vertebral and tibial BMD (p < 0.05) compared to controls. The age-related decrease in trabecular bone volume (BV/TV) of the distal femur was prevented with these doses. Vertebral trabecular BV/TV and cortical bone thickness of the femur mid-diaphysis were greater (p < 0.05) in the groups receiving the 5% and 10% cherry than the control diet. Notably, these improvements were significantly greater than the baseline controls, consistent with an anabolic response. Although no differences in systemic biomarkers of bone formation or resorption were detected at 90days, local increases in Phex and decreases in Ppar-γ suggest a bone environment that supports increased mineralization. These findings demonstrate that cherry supplementation (5% and 10%) improves BMD and some indices of trabecular and cortical bone microarchitecture; these effects are likely attributed to increased bone mineralization.

Fish diet and male reproductive hormones in albino rats

BackgroundFish, a widely claimed healthy food for humans, could also pose problems to health due to accumulation of pollutants, especially heavy metals and pesticides. Since the world’s fish stocks are limited due to overfishing, degraded freshwater, and pollution from various sources, the government proposed farmed fish which is one of the fastest growing food production sectors as an alternative.The objective of this study was to investigate the effects of tilapia or Mugil cephalus fish diets obtained from polluted areas on male reproductive hormones and prolactin. A total of 80 male Wister albino rats having an average weight of 130–150 g at the beginning of the experiment were used. They were divided into control group and seven treated groups which received the following doses that increased monthly according to the increase in rat body weight (b.w.). The treated groups received 200 g/70 kg human b.w. which is equivalent to 0.4 g/140 g rat b.w., 0.63 g/220 g rat b.w., and 0.83 g/291 g rat b.w. of tilapia fish (wild and farmed freshwater and brackish water) or Mugil cephalus fish (farmed freshwater and brackish water and wild marine water) daily for 3 months then were left on AIN-93M diet and purified water ad libitum.ResultsThe present results demonstrated that tilapia and Mugil cephalus fish diets caused decrease in serum total testosterone, follicle-stimulating hormone, luteinizing hormone, and sperm count, while sperm abnormalities significantly increased. Also, significant elevation of serum prolactin was observed in male rats fed with the same diets except wild brackish water tilapia fish and farmed freshwater and brackish water Mugil cephalus fish diets which showed a decrease. However, tilapia and Mugil cephalus fish diets had no effect on serum 17β-estradiol. The histopathological studies confirmed biochemical data as less dense packing of spermatogenic cell of the seminiferous tubules with reduction in the number of sperms in lumen of the epididymal tubules.ConclusionsThese results may indicate that consumption of tilapia and Mugil cephalus fish diets from polluted areas has adverse effects on male reproductive hormones and prolactin in male albino rats.

Quinoa whole grain diet compromises the changes of gut microbiota and colonic colitis induced by dextran Sulfate sodium in C57BL/6 mice

A plethora of evidence highlights that the dysbiosis of gut microbiota is a critical factor for inflammatory bowel disease (IBD). Both in vivo and in vitro studies have demonstrated that quinoa possesses potential prebiotic effects. The present study aims to examine the potential in using quinoa to ameliorate the dysbiosis and colitis induced by dextran sodium sulfate (DSS). A total of 40 C57BL/6 mice were fed either an AIN-93M diet or a quinoa-based diet, separately. Colitis was induced for 10 animals/dietary group with a 5-days exposure to 2.5% DSS. The clinical symptoms were monitored every other day, and the gut microbiota was characterized by 16S rRNA gene sequencing. The results indicated that consumption of quinoa lessened clinical symptoms as indicated by the reduced disease activity index and the degree of histological damage (P < 0.05). As expected, the DSS treatment induced significant dysbiosis of gut microbiota in mice on an AIN-93M diet. However, compared to mice fed the AIN-93M diet, the consumption of quinoa alleviated the DSS-induced dysbiosis remarkably, as indicated by increased species richness and diversity, decreased abnormal expansion of phylum Proteobacteria, and decreased overgrowth of genera Escherichia/Shigella and Peptoclostridium (P < 0.05). The relative abundances of Firmicutes and Bacteroidetes were less altered in mice fed with quinoa comparing to those mice fed the AIN-93M diet. In summary, the consumption of quinoa suppressed the dysbiosis of gut microbiota and alleviated clinical symptoms induced by DSS, indicating the potential to utilize quinoa as a dietary approach to improve intestinal health.

Mango leaf tea promotes hepatoprotective effects in obese rats

As mango leaf tea contains mangiferin and other bioactive compounds, this study investigated its anti-inflammatory, antioxidant and hepatoprotective effects on rats with high-fat induced obesity. Three groups were established: a control group (AIN93M diet), an obese group (high-fat diet HFD) and a treatment group (HFD with mango leaf tea for 8 weeks). Mango leaf tea increased antioxidant enzymes, total antioxidant capacity, AdipoR2 and PPAR-α mRNA and proteins expressions and, it also inhibited the NF-κB p65 and SREBP1c genes expressions in the liver. This beverage also leads to Cpt1 overexpression and a significant decrease in the accumulation of fat droplets, improving the hepatic steatosis. Molecular docking suggested a positive interaction between mangiferin, the main bioactive compound of mango leaf tea, and PPAR-α. Mango leaf tea exhibited a hepatoprotective effect through activating PPARα and decreasing the NF-κB p65 expressions, reducing oxidative stress and steatosis, and improving the lipid metabolism.

Increased Ratio of Non-mercaptalbumin-1 Among Total Plasma Albumin Demonstrates Potential Protein Undernutrition in Adult Rats.

The redox state of plasma albumin shifts in response to dietary protein intake in growing rats, and the shift is more sensitive than that of plasma albumin level, a classical marker of protein nutritional status. While it has been suggested that plasma albumin redox state could be useful as a novel marker of protein nutritional status, the above animal model is highly sensitive to dietary protein intake and the observation may not be extrapolated widely to humans. This study aimed to investigate whether albumin redox state also reflects protein nutritional status in adult rats, which have a lower dietary protein requirement and are less responsive to protein intake. Male adult rats were placed on AIN-93M diet (14% casein), or AIN-93M-based low protein diets (10 or 5% casein) ad libitum for 24 weeks. Whereas there was no significant difference in body weight between the groups at the end of the experimental period, the 5% casein diet group had the smallest gastrocnemius muscle weight among the groups, which was significantly lower than that of the 10% casein diet group. Plasma albumin level was also lower in the 5% casein diet group compared with the other groups, but the differences were limited and inconsistent during the experimental period. Among the albumin redox isoforms such as mercaptalbumin, non-mercaptalbumin-1, and non-mercaptalbumin-2, the ratio of non-mercaptalbumin-1 among total albumin was significantly higher in the 5% casein diet group, and the increase remained constant throughout the experimental period. Increased non-mercaptalbumin-1 ratio would thus demonstrate the presence of potential protein undernutrition in adult rats, as manifested only by a decreased gain in a specific type of skeletal muscle; non-mercaptalbumin-1 among total albumin ratio could be useful as a robust marker of protein nutritional status, contributing to prevention of protein undernutrition-related diseases such as frailty and sarcopenia.

Abstract 270: Effect of dietary methylseleninic acid and Se-methylselenocysteine on carcinogen-induced, androgen-promoted prostate carcinogenesis in rats

Abstract Selenomethionine (SeMet) did not inhibit development of prostate cancer in the SELECT trial and in preclinical rat models. However, we and others have shown that oral intake of next-generation selenium (Se) forms, especially methylseleninic acid (MSeA) and Se-methylselenocysteine (MSeC), inhibits prostate carcinogenesis in the TRAMP mouse model and growth of human prostate cancer cells xenografted in immunodeficient mice. We recently showed that MSeA suppresses progression of high-grade prostatic intraepithelial neoplasia to adenocarcinoma in pten-deficient mice (Cancer Prev Res 2016;9:35-42). To determine whether next-generation Se forms inhibit prostate carcinogenesis in models driven by a different etiology, we tested the in vivo effect of different Se forms fed to rats undergoing chemically induced androgen-promoted prostate carcinogenesis. We previously established that SeMet was not inhibitory in this model (Cancer Prev Res 2010;3:381-92). Wistar-Unilever (WU) rats (10-12 wks) were sequentially treated with androgen receptor blocker flutamide for 21 days (10 mg/kg/day by gavage), followed by testosterone propionate (TP, 10 mg/kg, s.c) on day 22. Three days after TP, the carcinogen methylnitrosourea (MNU, 30 mg/kg/bw) was administered by i.p. injection. One week later, the rats received slow-release Silastic implants containing testosterone. Rats were then randomized to one of three groups fed the AIN-93M diet supplemented with 3 ppm of Se as MSeA or MSeC or control AIN-93M diet. Moribund animals were euthanized and the study was terminated 400 days after MNU injection. Mean survival (days ± SEM) after MNU was 344±11 in controls (n=31), 354±8 in MSeA fed rats (n=30), and 363±10 in rats given MSeC (n=29). These differences were not statistically significant, which was confirmed by survival analysis using the logrank test. Overall tumor incidence in all accessory sex glands combined (dorsolateral and anterior prostate plus seminal vesicle) was 68% in controls, 83% in MSeA rats, and 72% in MSeC rats. The incidence of large tumors of uncertain origin was 42% in controls, 40% in MSeA rats, and 41% in MSeC rats. The incidence of smaller tumors clearly confined to dorsolateral and/or anterior prostate was 19% in controls, 20% in MSeA rats, and 38% in MSeC rats (some rats had more than one tumor). None of these differences was statistically significant and there were no shifts from large to small tumor or small to large tumors. Thus, MSeA and MSeC were not preventive in this rat prostate carcinogenesis model. The contrast with the inhibitory effects of MSeA in the TRAMP and pten-deficient mouse models may be due to differences in administered dose or fundamental rat-mouse differences in Se metabolism that impact chemoprevention by Se compounds. Supported by NIH grant CA172169. Citation Format: Maarten C. Bosland, Michael J. Schlicht, Yibin Deng, Junxuan Lu. Effect of dietary methylseleninic acid and Se-methylselenocysteine on carcinogen-induced, androgen-promoted prostate carcinogenesis in rats [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 270.

Abstract 2237: Diclofenac as a dual inhibitor of cyclooxygenase and aldo-keto-reductase 1B10 inhibits pancreatitis-enhanced carcinogenesis in LSL-Kras G12D -Pdx-1-Cremice

Abstract Diclofenac is one of non-steroid anti-inflammatory drugs and is recently identified as a competitive inhibitor of aldo-keto reductase family 1B10 (AKR1B10). AKR1B10 is an NADPH-dependent enzyme that exhibits lipid substrate specificity, especially for farnesyl and geranylgeranyl involved in protein prenylation (such as for Kras) and plays an oncogenic role in pancreatic carcinogenesis. In the present study, we determined the chemopreventive effects and mechanism of diclofenac on inhibiting pancreatitis-carcinogenesis in LSL-KrasG12D/Pdx1-Cre mice (called Pankras mice), particularly on Kras prenylation. Pancreatitis was induced by single i.p. injection of Cearulein (250ug/Kg body weight) for 5-week old mice, and one week after caerulein treatment, Pankras mice were fed an AIN-93M diet or a diet with 5 or 20ppm diclofenac (n=12 mice/group) for 7 months. The results showed that Diclofenac significantly reduced the severity of chronic pancreatitis, as measured by the extent of acini loss, inflammatory cell infiltration and stromal fibrosis. The progression of low-grade mPanIN I to high-grade mPanIN II/III and to invasive carcinoma was significantly suppressed and the tumor incidence significantly reduced to 50% and 17% in the mice treated with either 5ppm or 20 diclofenac compared to 86% in Pankras mice. Inhibition of membrane-bound mutant Kras (prenylated) and its transmitted phosphorylation of mitogen-activated protein kinase's kinase/extracellular signal-regulated kinases were demonstrated in pancreatic tissues by western blot assay. Analysis of the eicosanoid profile revealed a significant reduction of prostaglandin E2. These results indicate that diclofenac is a highly potential agent for preventing chronic pancreatitis and carcinogenesis, mainly via targeting mutant Kras and inflammation (Supported by NIH R01 CA164041). Citation Format: Jie Liao, Leyu Sun, Haonan Li, Rong Xia, Xiaoming You, Dandan Xu, Guang-Yu Yang. Diclofenac as a dual inhibitor of cyclooxygenase and aldo-keto-reductase 1B10 inhibits pancreatitis-enhanced carcinogenesis in LSL-KrasG12D-Pdx-1-Cremice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2237.

Resistance training alone or combined with leucine supplementation improves the serum lipid profile of diabetic rats, whereas leucine alone does not.

Diabetes mellitus is associated with dyslipidemia, which contributes to a higher risk of thrombosis, atherosclerosis and cardiovascular disease. This study evaluated the effects of leucine and resistance training on the serum lipid profile in rats with streptozotocin-induced diabetes for 8 weeks. Wistar rats with neonatal streptozotocin-induced diabetes were treated with leucine supplementation (5%) and/or resistance training (3 days per week) for 8 weeks, and divided in DL (diabetic and leucine), DT (diabetic and resistance training group) and DLT (diabetic, leucine and resistance training) groups. Others 2 groups of animals received isonitrogen AIN-93M diet that was defined as a control diet: group D (diabetic untreated) and group C (non-diabetic). The decrease in serum total cholesterol and increase in high-density lipoprotein cholesterol (HDL-C) was observed in the resistance training-induced diabetic rats when compared with diabetic rats. There was no change in serum lipid profile in leucine-supplemented diabetic rats and no synergistic effect of leucine and resistance training. The fasting glucose levels were reduced in all animals treated compared to D group. The diabetic trained rats demonstrate a protective effect of resistance training on the serum lipid profile.

Effects of gut microbiota and time of treatment on tissue levels of green tea polyphenols in mice.

The previous studies have shown that tea polyphenols are metabolized by gut microbiota. This study investigated the effect of gut microbiota on the bioavailability, tissue levels, and degradation of tea polyphenols. Mice were treated with antibiotics (ampicillin/sulfamethoxazole/trimethoprim) in drinking water and the control mice received water for 11 days, and they were given an AIN93M diet enriched with 0.32% of Polyphenon E. The levels of catechins and their metabolites (if present) in the serum, liver, urine, and fecal samples were determined by high-performance liquid chromatography. The results showed that treatment with antibiotics significantly increased the levels of the major polyphenol, (-)-epigallocatechin-3-gallate (EGCG), in serum and liver samples. Antibiotics also raised the levels of some catechins in urine and fecal samples but decreased the levels of their metabolites. These results suggest that antibiotics eliminated gut microbes and increased the bioavailabilities of these tea catechins. In a second study, mice were given different concentrations of green tea infusions as the drinking fluid. The plasma levels of EGCG and (-)-epicatechin-3-gallate (ECG) at day 112 were significantly lower than those at day 5. The urine levels of EGCG and ECG increased in the first 4 or 5 days, and then decreased to much lower levels at day 23 and beyond. In contrast, the levels of (-)-epigallocatechin and (-)-epicatechin showed a trend of increase during the 112-day experiment, likely owing to microbial hydrolysis of EGCG and ECG. Both sets of experiments support the idea that the degradation of EGCG and ECG by gut microbiota decreases their bioavailabilities. © 2018 BioFactors, 2018.

The effect of micronized corn fiber on body weight, glycemia, and lipid metabolism in rats fed cafeteria diet

Abstract During corn industrial dry milling, a residue rich in dietary fibers is generated. This study aimed to evaluate the effects of micronized corn fiber (MCF) as part of a cafeteria diet in the macronutrient metabolism and body weight. Wistar male rats, with initial body weight of 249 ± 14 g (n = 13), received AIN-93M diet (Group 1) or cafeteria diet (Groups 2, 3 and 4), composed of commercial ration, cookies, fried potato sticks, milk chocolate, bacon and chicken liver pâte. Groups 3 and 4 received MCF to replace 100 and 50% of the cellulose from the AIN-93M diet, respectively. After 35 days, blood, tissues and feces were collected. Data were analyzed by ANOVA followed by Tukey test (p < 0.10). The weight gain of the animals increased by 25.9%, 20.8% and 22.0%, when fed cafeteria diet or 100 and 50% of MCF respectively, compared to the control group, although food consumption did not differ between them. Body weight and food efficiency ratio did not differ between the groups fed cafeteria diet with or without MCF. The addition of MCF to the cafeteria diet did not alter the animal lipid profile and glycemia, however, the accumulation of lipids in their livers was similar to the control group. The intake of 100% MCF resulted in higher fecal weight and fecal excretion of lipids, and lower fecal nitrogen, lipid absorption and lipid deposition in the liver than the cafeteria diet. In conclusion, MCF has a potential to improve intestinal transit and lipid excretion, but showed no benefit on blood lipid and glucose levels.

Effects of bound phenolic from defatted Moringa oleifera seed flour on diet-induced hypercholesterolemic mice

The effect of bound phenolic and catechins extracted from defatted Moringa oleifera seed (DMSF) flour on diet-induced hypercholesterolemia was evaluated in this study. The animals (C57BL6 mice) were divided into four groups: group one received AIN 93M diet (control) group two received high-fat cholesterol diet (HFCD), three and four received HFCD along with bound phenolic and catechins, respectively, through oral administration at the dose of 25 mg/kg body weight daily for 8 weeks. Blood and tissue analysis showed that bound phenolic and catechins were able to reduce plasma and liver cholesterol significantly (p < .05). And these extracts were also able to reduce stress enzymes and molecules level in liver. The bound phenolic and catechins extracts from DMSF were able to increase plasma HDL level and lower atherogenic index in the treated groups. The data suggests that the combination of HFCD and bound phenolic or catechins extracted from DMSF as a source of antioxidants was beneficial. Practical applications In the present study the bound phenolic and catechins extracted from DMSF was studied for its effect on reducing cholesterol. DMSF is a processing waste left over after extraction of oil, hence prove to be cost-effective. In this study catechins (catechin and epicatechin) as well as combination of catechin-rich bound phenolic containing gallic acid, protocatechuic acid, ferulic acid, and catechin gallate were studied for its hypocholesterolemic effect. The results revealed that the combination of bound phenolic or catechins were comparably beneficial in reducing cholesterol and atherogenic index in diet induced mice model, which is the critical risk factor for atherosclerosis.

Prolonged Dietary Curcumin Supplementation Augments Nrf2 Nuclear Translocation and Attenuates Oxidative Stress in Skeletal Muscle of Aging Rats

The development of sarcopenia, which is the aging‐related loss of muscle mass, function and quality, can be attributed to a myriad of factors. Oxidative stress has received particular attention as a key factor in the development of sarcopenia and can collectively be a result of a decreased antioxidant reserve and increased production of reactive oxygen species (ROS). Interestingly, nuclear factor erythroid‐2‐related factor 2 (Nrf2), a transcription factor responsible for activating the antioxidant response element (ARE), has shown decreased nuclear activation with age. Curcumin, the active ingredient in the spice turmeric, has properties that can both increase antioxidant capacity through the activation of Nrf2 and directly quench ROS. These beneficial traits of curcumin were documented in numerous studies that implemented an oral administration method of supplementation. Hence, it is possible that curcumin supplementation through the diet can favorably alter the redox status of muscle and attenuate sarcopenia. This study examined the effects of 4‐months of dietary curcumin exposure on oxidative stress, Nrf2 activation, and the antioxidant response in a rodent model of aging skeletal muscle. Thirty‐two‐month‐old male F344xBN rats (n=54) were provided a purified AIN‐93M diet with or without 0.2% curcumin per food weight for a period of 4 months. One group received the control diet ad libitum (CON, n=18) and another received the same diet containing 0.2% curcumin (CUR, n=18). A third group received the control purified diet, but in equal amounts to those consumed by the CUR animals (PAIR, n=18) to account for any changes in food consumption due to curcumin palatability. After the 4‐month supplementation period, plantaris muscle was tested in vivo for force measures and hindlimb muscle tissue was harvested for biochemical and functional analyses. Body mass, muscle mass, contractile force, measures of oxidative damage, antioxidant expression/activity, and Nrf2 nuclear activation were analyzed using 1‐way ANOVA. All values are reported as mean ± SEM. CUR animals consumed less food than CON rats, and thus a difference between the CON and PAIR groups was also observed (p &lt; 0.05). The CUR rats displayed a significantly larger plantaris mass compared to the PAIR animals (0.198 ± 0.013g vs. 0.326 ± 0.018g; p &lt; 0.05). Plantaris twitch and tetanic force largely mirrored muscle mass changes, where the CUR rats produced larger force than the PAIR rats (p &lt; 0.05). No significant difference in measures of antioxidant expression were observed between the groups (p &gt; 0.05). However, Nrf2 nuclear levels (p &lt; 0.01), and measures of oxidative damage including 3‐nitrotyrosine (3NT; 1.16 ± 0.226 vs. 0.337 ± 0.108 O.D.; p &lt; 0.05), and protein carbonyls (2.29 ± 0.195 vs. 1.43 ± 0.328 O.D.; p &lt; 0.05) were significantly different between the PAIR and CUR groups, respectively. Thus, this study suggests that curcumin supplementation exerts favorable effects on aging muscle that include changes in oxidative stress and muscle mass and function when animals are subjected to food restriction.Support or Funding InformationSupported by the NIH, National Institute on Aging, Grant #1R36AG050734 ‐ 01 (CNR).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of Black Raspberry on Dibenzo[a,l]Pyrene Diol Epoxide Induced DNA Adducts, Mutagenesis, and Tumorigenesis in the Mouse Oral Cavity.

We previously showed that metabolic activation of the environmental and tobacco smoke constituent dibenzo[a,l]pyrene (DB[a,l]P) to its active fjord region diol epoxide (DB[a,l]PDE) is required to induce DNA damage, mutagenesis, and squamous cell carcinoma (SCC) in the mouse oral cavity. In contrast to procarcinogens, which were employed previously to induce SCC, DB[a,l]PDE does not require metabolic activation to exert its biological effects, and thus, this study was initiated to examine, for the first time, whether black raspberry powder (BRB) inhibits postmetabolic processes, such as DNA damage, mutagenesis, and tumorigenesis. Prior to long-term chemoprevention studies, we initially examined the effect of BRB (5% added to AIN-93M diet) on DNA damage in B6C3F1 mice using LC/MS-MS and on mutagenesis in the lacI gene in the mouse oral cavity. We showed that BRB inhibited DB[a,l]PDE-induced DNA damage (P < 0.05) and mutagenesis (P = 0.053) in the oral cavity. Tumor incidence in the oral cavity (oral mucosa and tongue) of mice fed diet containing 5% BRB was significantly (P < 0.05) reduced from 93% to 66%. Specifically, the incidence of benign tumor was significantly (P < 0.001) reduced from 90% to 31% (62% to 28% in the oral cavity and 28% to 2% in the tongue), a nonsignificant reduction of malignant tumors from 52% to 45%. Our preclinical findings demonstrate for the first time that the chemopreventive efficacy of BRB can be extended to direct-acting carcinogens that do not require phase I enzymes and is not just limited to procarcinogens. Cancer Prev Res; 11(3); 157-64. ©2017 AACR.

Extensive Degradation and Low Bioavailability of Orally Consumed Corn miRNAs in Mice

The current study seeks to resolve the discrepancy in the literature regarding the cross-kingdom transfer of plant microRNAs (miRNAs) into mammals using an improved miRNA processing and detection method. Two studies utilizing C57BL/6 mice were performed. In the first study, mice were fed an AIN-93M diet and gavaged with water, random deoxynucleotide triphosphates (dNTP) or isolated corn miRNAs for two weeks (n = 10 per group). In the second study, mice were fed an AIN-93M diet, or the diet supplemented with 3% fresh or autoclaved corn powder for two weeks (n = 10 per group). Corn miRNA levels were analyzed in blood and tissue samples by real-time PCR (RT-PCR) following periodate oxidation and β elimination treatments to eliminate artifacts. After removing false positive detections, there were no differences in corn miRNA levels between control and treated groups in cecal, fecal, liver and blood samples. Using an in vitro digestion system, corn miRNAs in AIN-93M diet or in the extracts were found to be extensively degraded. Less than 1% was recovered in the gastrointestinal tract after oral and gastric phases. In conclusion, no evidence of increased levels of corn miRNAs in whole blood or tissues after supplementation of corn miRNAs in the diet was observed in a mouse model.

Effects of soybean isoflavones on the energy metabolism of swimming mice

To establish an animal model for loaded swimming, so as to investigate the energy metabolism effects of soybean isoflavones (SI) on swimming mice. Thirty male Kunming mice were randomly divided into three groups:normal control, swimming group, and swimming+SI group. The normal control group mice were fed a basic AIN-93M diet, the SI groups were supplied with soybean isoflavones(4 g/kg).Two weeks later, the mice were forced to swim for an hour,and then all the mice were killed, the samples of blood, liver and muscles of hind were collected.The serum contents of lactic acid(Lac), the activities of lactic dehydrogenase (LDH), succinate dehydrogenase (SDH), creatine kinase (CK) and ATPase were measured. Compared with normal control,the serum content of Lac was significantly improved in the group of the swimming control and SI(P<0.05),the activity of LDH in the serum was obviously improved in the group of the swimming control and SI, and the activity of CK and SDH were both significantly improved in the group of the swimming control and SI except the activity of SDH in the liver of the group SI; compared with the swimming control,the serum contents of Lac,the activities of LDH, ATPase, SDH, CK were obviously improved(P<0.05). Soybean isoflavones can improve the energy metabolism,antioxidant capacity of the swimming mice.