In this study, we investigated effects of inhaled ozone exposure and high-cholesterol diet (HCD) in healthy Wistar and Wistar-derived Goto-Kakizaki (GK) rats, a non-obese model of type 2 diabetes. Male rats (4-week old) were fed normal diet or HCD for 12 weeks and then exposed to filtered air or 1.0 ppm ozone (6hrs/day) for 1 or 2 days. We examined pulmonary, vascular, hematology, and inflammatory responses after each exposure plus an 18-hr recovery period.

This dataset is associated with the following publication: Snow, S., A. Henriquez, L. Thompson, C. Fisher, M.C. Schladweiler, C. Wood, and U. Kodavanti. Pulmonary and Vascular Effects of Acute Ozone Exposure in Diabetic Rats Fed an Atherogenic Diet. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 415(115430): 1, (2021).

Consumption of a shiitake mushroom diet has been reported to have effects on serum phospholipids. However, much less is known about the effect on serum polar lipids including lysophospholipids and free fatty acids. In the present study, the effects of a shiitake diet were evaluated on the basis of identification and quantification of individual polar lipid components in rat serum using liquid chromatography−mass spectrometry/mass spectrometry. By comparison with standards and published data, 50 lysophospholipids and 32 free fatty acids were identified, and the concentrations of 27 polar lipids in rat serum were determined. Shiitake diets decreased the levels of all individual polar lipid components in the serum of male rat. The total level of serum polar lipids in males fed 4% shiitake diets (1365.71 mol/L) was significantly lower than that of the control (2270.26 mol/L). However, shiitake diets did not significantly affect the levels of serum polar lipids in female rats.

Background: Diet deeply affects the food selection and ingestion both in humans and rodents, often resulting in excess energy intake. Methods: We investigated this process comparing two different high-fat dietary approaches to induce obesity, in which all rats received about 40% of their energy intake as lipids. The main nutrient difference between the diets, when compared with controls fed standard lab chow, was the lipid content. Cafeteria diets (K) were devised to be tasty, and thus highly desirable to the rats, mainly for its diverse mix of tastes, particularly salty and sweet. This diet was compared with another high-fat (HF) potentially obesogenic diet, devised not to be as tasty as K, and prepared just supplementing standard chow pellets with fat. We also analysed the influence of sex on the effects of the diets. Results: K rats grew faster, especially the males, although females showed a higher proportion of body lipid, because of a high lipid, sugar and protein intake. HF weight change rates were not different from those of controls. In addition to high sugar, K rats also ingested large amounts of salt. With this study we have shown that the key factor eliciting the excess energy intake in a high-energy diet rat model was not solely or mainly their fat intake. The changes in body fat accrual were more a consequence of their appetence for the food. Conclusions: The results show that the significant presence of sugar and salt is a powerful factor promoting excess food intake, more effective than increasing diet lipid content. These effects were already observed after a relatively short treatment, additionally confirming the differential effects of sex on the hedonic and obesogenic response to diet.

Background- Resistant starch is a prebiotic metabolized by the gut bacteria. It has been shown to attenuate chronic kidney disease (CKD) progression in rats. Previous studies employed taxonomic analysis using 16S rRNA sequencing and untargeted metabolomics profiling. Here we expand these studies by metaproteomics, gaining new insight into the host-microbiome interaction. Methods- Differences between cecum contents in CKD rats fed a diet containing resistant starch with those fed a diet containing digestible starch were examined by comparative metaproteomics analysis. Taxonomic information was obtained using unique protein sequences. Our methodology results in quantitative data covering both host and bacterial proteins. Results - 5,834 proteins were quantified, with 947 proteins originating from the host organism. Taxonomic information derived from metaproteomics data surpassed previous 16S RNA analysis, and reached species resolutions for moderately abundant taxonomic groups. In particular, the Ruminococcaceae family becomes well resolved – with butyrate producers and amylolytic species such as R. bromii clearly visible and significantly higher while fibrolytic species such as R. flavefaciens are significantly lower with resistant starch feeding. The observed changes in protein patterns are consistent with fiber-associated improvement in CKD phenotype. Several known host CKD-associated proteins and biomarkers of impaired kidney function were significantly reduced with resistant starch supplementation. Conclusions- Metaproteomics analysis of cecum contents of CKD rats with and without resistant starch supplementation reveals changes within gut microbiota at unprecedented resolution, providing both functional and taxonomic information. Proteins and organisms differentially abundant with RS supplementation point toward a shift from mucin degraders to butyrate producers.

Wistar Kyoto, inbred male rats (M & B, Ry, Denmark) were randomized and fed a semisynthetic pellet diet deficient in folate (TD350, Harland, Madison, Wisconsin, USA) or an identical diet with a normal amount of folate (TD351, Harland). Special analyses were performed to establish the content of Methionine, Vitamin B12, Folate and Vitamin B6 in the two diets. The folate content was <0.06 mg/kg and 1.63 mg/Kg, respectively. Detailed specification of the diets has been published previously. Animals were housed in stainless steel cages with a bed of sawdust, two to a cage, and were allowed free access to food and drinking water. The room temperature was 23„a C and the humidity was 45-55 %. Light cycles consisted of 12 h light/12 h darkness. The animals were weighed at randomization and subsequently every seven days. The animal experiments were carried out in accordance with the guidelines of the International Scientific Committee for Thrombosis and Hemostasis, and the Danish Ethical Committee for Animal Experimentation had approved the study protocol. This study consisted of twelve rats fed the folate deficient diet and twelve rats fed the normal diet for 28 days.

A high phosphorus (HP) diet causes disorders of renal function, bone metabolism, and vascular function. We previously demonstrated that DNA microarray analysis is an appropriate method to comprehensively evaluate the effects of a HP diet on kidney dysfunction such as calcification, fibrillization, and inflammation. We reported that type IIb sodium-dependent phosphate transporter is significantly up-regulated in this context. In the present study, we performed DNA microarray analysis to investigate the effects of a HP diet on the liver, which plays a pivotal role in energy metabolism. DNA microarray analysis was performed with total RNA isolated from the livers of rats fed a control diet (containing 0.3% phosphorus) or a HP diet (containing 1.2% phosphorus). Gene Ontology analysis of differentially expressed genes (DEGs) revealed that the HP diet induced down-regulation of genes involved in hepatic amino acid catabolism and lipogenesis, while genes related to fatty acid β-oxidation process were up-regulated. Although genes related to fatty acid biosynthesis were down-regulated in HP diet-fed rats, genes important for the elongation and desaturation reactions of omega-3 and -6 fatty acids were up-regulated. Concentrations of hepatic arachidonic acid and eicosapentaenoic acid were increased in HP diet-fed rats. These essential fatty acids activate peroxisome proliferator-activated receptor alpha (PPARα), a transcription factor for fatty acid β-oxidation. Evaluation of the upstream regulators of DEGs using Ingenuity Pathway Analysis indicated that PPARα was activated in the livers of HP diet-fed rats. Furthermore, the serum concentration of fibroblast growth factor 21, a hormone secreted from the liver that promotes fatty acid utilization in adipose tissue as a PPARα target gene, was higher (p = 0.054) in HP diet-fed rats than in control diet-fed rats. These data suggest that a HP diet enhances energy expenditure through the utilization of free fatty acids released via lipolysis of white adipose tissue. Male Wistar rats (4 weeks old) were purchased from Japan SLC Co. (Hamamatsu, Japan) and individually housed in metabolic cages under controlled conditions of 22±1°C and a 12-hour light/dark cycle (lights on from 08:00 to 20:00 daily). Two different diets containing 0.3% phosphorous (control diet) and 1.2% phosphorous (HP diet) were prepared based on the AIN-93G diet (Table 1).9) All rats were fed the control diet for a 7-day acclimatization period. After acclimatization, rats were divided into two groups of similar mean body weight (n = 5 each) and then fed either the control or the HP diet for 24 days. The animals were allowed to eat ad libitum and had free access to water (MilliQ water).The protocol for the animal experiments was approved by the Animal Use Committee of the Faculty of Agriculture at The University of Tokyo. Please note that the animals used in this study are identical to those used in GSE31973.

Body weight, feed intake, NMR body composition and internal organs weight in rats fed experimental diets; intestinal parameters in rats fed experimental diets; blood plasma parameters in rats fed experimental diets; small intestinal biochemical parameters in rats fed experimental diets; level of gene expression in the small intestine of rats fed experimental diets; morphological effects of different Cu sources or type of fibre in the diet on the small intestine of rats. Rats were randomly divided into 10 groups. The first two groups were fed a control diet that contained cellulose, and a mineral mixture with standard or enhanced content of CuCO3. Experimental groups were fed a diet supplemented with CuNPs (6.5 or 13 mg/kg) and combined with different types of fibre (cellulose, pectin, inulin or psyllium).

We performed carefully designed and controlled animal feeding studies. We devided 9 adult rats in three group and each group fed with one type of diets in 28 days: rice, potatoes and chow. We fed piglets in triplicate either with cow milk or let them feed from sows milk for 4 weeks followed by 7 weeks of maize diet. Based on the small RNA sequencing data from 9 rat and 6 pig serum samples, we detected no transfer of plant miRNAs into rat blood, or bovine milk sequences into piglet blood. The miRNA profiles in serum of chow-fed, potato-fed and rice-fed rats in 28 days and the miRNA profiles in serum of cow milk and sows milk fed pigs were generated by sequencing, in triplicate, Illumina TruSeq small RNA.

The number of animals was 10 rats/sex/group; data is presented as group mean values±SD.

Global Journal of Pure and Applied Sciences.

This study considers the physiological modulation of liver proteins due to the supplementation with fish oils under two different dietary backgrounds: low- or high- fat and sucrose diets, and the effect of their combination with an antioxidant agent (grape polyphenols) which provides reducing power. For this scope, a quantitative proteomics approach based on the Isobaric Tag for relative and Absolute Quantitation methodology (iTRAQ)-coupled to nano-LC-MS/MS and complemented with 2D-DIGE analysis were used for determining the regulation of liver proteins exerted by the supplementation with fish oils, polyphenols or their combination of Wistar Kyoto rats in the two chosen dietary backgrounds. This experimental design was useful to investigate if the behavior of fish oils changes when the dietary background is modified and the possible synergy between fish oils and polyphenols. Results show that the capacity of fish oils, polyphenols or their combination for down or up-regulating liver proteins depends on the dietary context. In the background of low-fat low-sucrose healthy diets, 10 different proteins were altered by the sum of three supplements, in opposite to the 45 altered proteins found in the high-fat high-sucrose unhealthy diets. In both situations, fish oils seemed to be the main force for regulating liver proteins, although the addition of polyphenols was able to modulate some fish oils effects. Moreover, we provide evidence of the effect of fish oils and their combination with grape polyphenols for improving biochemical parameters and for reducing enzymes of hepatic lipogenesis and glycolysis, for enhancing fatty acid beta oxidation and insulin signaling and for the amelioration of endoplasmic reticule stress and protein oxidation when are included in an unhealthy diet.

Diet-induced obesity in rat pregnancy has been shown previously to be associated with consistently raised blood pressure in the offspring, attributed to sympathetic over-activation, but the relative contributions to this phenotype of maternal obesity versus raised dietary fat is unknown. Sprague-Dawley female rats were fed either a control (4.3% fat, n = 11) or lard-enriched (23.6% fat, n = 16) chow 10 days prior to mating, throughout pregnancy and lactation. In conscious adult (9-month-old) offspring cardiovascular parameters were measured (radiotelemetry). The short period of fat-feeding did not increase maternal weight versus controls and the baseline blood pressure was similar in offspring of fat fed dams (OF) and controls (OC). However, adult male OF showed heightened cardiovascular reactivity to acute restraint stress (p

Transmission electron micrograph of the junctional complexes at the intersection of three hepatocytes. This image was taken from liver tissues from an ethanol fed rat and also shows the bile canaliculus. Smooth endoplasmic reticulum and ...

In this study, we analyzed the effects of chronic alcohol consumption on liver repair and regeneration after partial hepatectomy (PHx). Rats were fed a liquid diet containing 36% of total calories derived from ethanol for 5 weeks; corresponding pair-fed calorie-matched controls were fed diets in which ethanol calories were replaced either by carbohydrate or by fat. After 5 weeks, rats were subjected to 70% PHx and liver samples were collected at 1, 6 and 24h after the surgery. The excised liver samples at t=0 served as within-animal controls. We used Affymetrix Rat Gene 1.0 ST arrays to obtain global gene expression data from each liver sample (n=4 replicate rats, 72 arrays total). Gene expression was profiled in the chronic ethanol-fed (EtOH) and carbohydrate control pair-fed (CHO) liver prior to (control) and 1 h, 6 h, 12 h, and 24 h after partial hepatectomy (PHx).

The Dahl salt-sensitive (S) rat model develops chronic hypertensive disease when fed a high salt diet that ultimately results in renal and heart failure, as well as prevalent cerebrovascular pathologies. Phenotypic changes in the cerebral vasculature are preceded by changes in gene expression, and evidence supports a role for extracellular signal-regulated kinase 1/2 (ERK1/2) in vascular cell proliferation, yet little is known regarding ERK1/2 –regulated gene transcription in cerebrovascular smooth muscle during hypertension. Findings presented here support the hypothesis that salt-induced hypertensive disease results in upregulation of ERK1/2 activity and ERK1/2-regulated genes that promote remodeling in cerebral resistance arteries. Dahl S rats were fed either a 0.4% NaCl (low salt, LS) or 8% NaCl (high salt, HS) diet until evidence of left ventricular dysfunction. Gene expression profiling using oligonucleotide array analysis detected a significant fold-change of 1.5 or greater in 133 out of 15,923 genes examined. Mitogen-activated protein kinase (MAPK)-regulated genes were overrepresented and provided a link to genes involved in proliferation and extracellular matrix signaling including plasminogen activator inhibitor I (PAI-1), osteopontin (OPN) and junB. These data suggests that salt induced hypertensive disease promotes hyperplasia and changes in matricellular genes that are likely important in vascular remodeling. Experiment Overall Design: Analysis was based on a comparison between the Low Salt and High Salt groups. Arteries from 3 animals were pooled for each sample, thus there were 9 animals/group. Analysis of significance amongst all genes as well as prospective hypotheses correlating to disease were performed.

Insulin resistance drives the development of type 2 diabetes (T2D). In liver, diacylglycerol (DAG) is a key mediator of lipid-induced insulin resistance. DAG activates protein kinase C epsilon (PKCε), which phosphorylates and inhibits the insulin receptor. In rats, a 3-day high fat diet produces hepatic insulin resistance through this mechanism, and knockdown of hepatic PKCε protects against high fat diet-induced hepatic insulin resistance. Here we employ a systems level approach to uncover additional signaling pathways involved in high fat diet-induced hepatic insulin resistance. We used quantitative phosphoproteomics to map global in vivo changes in hepatic protein phosphorylation in chow-fed, high fat-fed, and high fat-fed with PKCε knockdown rats to distinguish the impact of lipid- and PKCε-induced protein phosphorylation.

In previous in vitro study, we reported potential mechanism of cholesterol-lowering effect of Lactobacillus brevis119-2 (119-2) isolated from turnip “Tsuda kabu” is due to incorporation of cholesterol into 119-2 cell. In this study, we analyzed serum cholesterol and hepatic gene expression of Sprague-Dawley (SD) rat fed diet containing cholesterol with or without 119-2 for 2 weeks, to evaluate the cholesterol-lowering effect of 119-2 in vivo. Serum cholesterol of SD rat fed diet with 119-2 significantly decreased compared to SD rat fed diet without 119-2, and both viable and dead 119-2 indicated the effect. The result of hepatic gene analysis using DNA microarray suggested that potential mechanism of the cholesterol-lowering effect of 119-2 in vivo is inhibiting the activity of 3-hydroxy-3-methylglutaryl-CoA reductase by Insig (insulin induced gene) that is endoplasmic reticulum membrane protein, and catabolizing cholesterol to bile acid by Cyp7a1 (cytochrome P450 a1) that is the rate-limiting enzyme in the synthesis of bile acid from cholesterol. In addition, we concluded feeding 119-2 decreased serum low density lipoprotein (LDL) cholesterol by overexpression of Ldlr (LDL receptor gene). On the other hand, feeding Lactobacillus acidophilus ATCC43121 (ATCC) increased high density lipoprotein (HDL) cholesterol by over expression of Abca1 (ATP binding cassette sub-family A member 1 gene) and Angplt3 (Angiopoietin-like 3). These results suggested that 119-2 decrease the risk of atherosclerosis by serum cholesterol-lowering effect and improving effect of fatty liver and the LH (LDL cholesterol / HDL cholesterol) ratio. Lactobacillus brevis119-2 (119-2) was isolated from turnip “Tsuda kabu” harvested in Matsue city, Shimane Prefecture, Japan, and was stored at Shimane Institute for industrial Technology. Male Jcl: SD rat (4 weeks of age) were obtained from CLEA Japan, Inc. (Tokyo, Japan). Rats were maintained under controlled environmental conditions (temperature 23 ± 3 ˚C, relative humidity 55% ± 25%, 12/12hr light - dark cycle) and given food and water ad libitum. All rats were acclimated 1 week prior to the experiment. Two groups of 11 rats each were treated respective group diets for 2weeks. Control group was fed high-cholesterol diet containing 10 g cholesterol/kg, 5 g cholic acid/kg, 985 g mouse & rat & rabbit diet (CRF-1) /kg obtained from Oriental yeast Co., Ltd (Tokyo, Japan). The other group was fed same highcholesterol diet with 10 g freeze-dried viable 119-2 /kg. This study and all procedures were approved by regulations and code of ethics in experimental animals Chitose Japan Food Research Laboratories.

Rationale: We investigated isotopic diet-excreta offset (Ddiet-excreta) for predatory birds, and the isotopic influence of bird digestion on consumed prey tissues. The foraging ecology of predatory birds can be non-invasively monitored using excreta or regurgitated prey. However, one must account for Ddiet-excreta and any influence of digestion on prey tissues. Neither of these has been previously evaluated for predatory birds. Methods: We worked with a captive Eurasian eagle owl (Bubo bubo) and red-tailed hawk (Buteo jamaicensis) fed frozen rats. We collected rat feet, as well as regurgitated pellets and excreta from each bird’s enclosure. We analyzed carbon (d13C) and nitrogen (d15N) isotopes in undigested rat muscle, undigested and digested fur and bone collagen (extracted from pellets); d13C, oxygen (d18O), and strontium (87Sr/86Sr) isotopes in rat bone bioapatite; and d13C, d15N and 87Sr/86Sr in bird excreta. Results: Diet-excreta offset differed slightly between individuals, ..., This dataset summarizes raw isotope data for rat tissues before and after digestion by Rhett, the red-tailed hawk, or Caspian, the eagle owl, who were individually housed at the Cincinnati zoo. We have also included isotope data for excreta produced by the birds. The study was conducted for a total of 11 days. A foot from each consumed rat was collected before feeding the birds, and then a regurgitated casting and excreta sample were collected from each bird's enclosure the following day. Rat collagen was isolated by soaking samples in 0.5 N HCl at 4°C ultil they were demineralized, rinsing in ultrapure water five times. Lipids were removed from rat muscle, hair and bone by sonicating samples in trace metal grade petroleum ether 2 to 5 times, then sonicating in ultra pure water 2 to 5 times, and drying. Rat bioapatite was processed by soaking powdered sample in 30% H2O2 for 72 hours, rinsing with ultrapure water five times, soaking in 1 M Acetic Acid buffered with calcium acetate,..., , # Details and raw isotope data for samples related to a semi-controlled feeding study involving rats fed to a red-tailed hawk (Buteo jamaicensis) and Eurasian eagle owl (Bubo bubo).

https://doi.org/10.5061/dryad.ksn02v7ft

Description of the data and file structure

Files and variables

File: Dryad_dataset.xlsx

Description:Â

This dataset summarizes raw isotope data for rat tissues before and after digestion by Rhett, the red-tailed hawk, or Caspian, the eagle owl, who were individually housed at the Cincinnati zoo. We have also included isotope data for excreta produced by the birds. The study was conducted for a total of 11 days. A foot from each consumed rat was collected before feeding the birds, and then a regurgitated casting and excreta sample were collected from each bird's enclosure the following day.Â

Within the dataset, blank cells indicate analyses that were not performed for specific samples. No data were exclud...,

Protein-Protein, Genetic, and Chemical Interactions for Fukaya N (2009):The alpha-glucosidase inhibitor miglitol delays the development of diabetes and dysfunctional insulin secretion in pancreatic beta-cells in OLETF rats. curated by BioGRID (https://thebiogrid.org); ABSTRACT: The Otsuka Long-Evans Tokushima Fatty (OLETF) rat, an animal model of type 2 diabetes, exhibits obesity, hyperglycemia and hyperlipidemia, with late onset of chronic and slowly progressive hyperinsulinemia. In this study, we examined effects of long-term dietary supplementation with the alpha-glucosidase inhibitor miglitol on the development of diabetes and the reduction of beta-cells in the pancreas of OLETF rats. The OLETF rats were fed a control diet or a diet containing 800 ppm miglitol (miglitol diet) for 65 weeks from pre-onset stage (5 weeks old). The non-fasting blood glucose concentrations gradually increased in OLETF rats fed the control diet and, at week 64, were significantly higher than those in OLETF rats fed the miglitol diet and age-matched Long-Evans Tokushima Otsuka (LETO) rats, which are control, non-diabetic, non-obese rats of the same strain. Oral glucose tolerance tests revealed that OLETF rats fed the control diet showed pronounced impaired glucose tolerance, but those fed the miglitol diet did not. Furthermore, insulin concentrations after glucose-loading were significantly lower in OLETF rats fed the control diet than in those fed the miglitol diet. The islets of 65-week-old OLETF rats fed the control diet showed significant fibrosis and loss of beta-cells, while those of age-matched control LETO rats had a normal appearance. Feeding OLETF rats a miglitol diet reduced fibrosis and the loss of beta-cells. Our results suggest that dietary supplementation with miglitol from pre-onset stage in OLETF rats delays the onset and development of diabetes and preserves the insulin secretory function of pancreatic islets.

Fructus Xanthii (FX) has been widely used as a traditional herbal medicine for rhinitis, headache, cold, etc. Modern pharmacological studies revealed that FX possesses anti-inflammatory, anti-oxidative, and anti-hyperglycemic properties. The present study was designed to investigate the effects of FX on glucose and insulin tolerance, and hepatic lipid metabolism in rats fed on high-fat diet (HFD). Hepatic steatosis was induced by HFD feeding. Aqueous extraction fractions of FX or vehicle were orally administered by gavage for 6 weeks. Body weight and blood glucose were monitored. Glucose and insulin tolerance test were performed. Liver morphology was visualized by hematoxylin and eosin, and oil red O staining. Expression of liver lipogenic and lipolytic genes was measured by real-time PCR. We showed here that FX improved glucose tolerance and insulin sensitivity in HFD rats. FX significantly decreased the expression of lipogenic genes and increased the expression of lipolytic genes, ameliorated lipid accumulation and decreased the total liver triglyceride (TG) content, and thus attenuated HFD-induced hepatic steatosis. In conclusion, FX improves glucose tolerance and insulin sensitivity, decreases lipogenesis and increases lipid oxidation in the liver of HFD rats, implying a potential application in the treatment of non-alcoholic fatty liver disease.