The effect of silibinin on protein expression profile in white adipose tissue of obese rats
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive HF-X
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Epididymal White Adipose Tissue
SUBMITTER: 
wang fei
LAB HEAD: Fei Wang
PROVIDER: PXD016635 | Pride | 2020-01-13
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| F8019TQ_1.raw | Raw | |||
| F8019TQ_2.raw | Raw | |||
| F8019TQ_3.raw | Raw | |||
| F8019TQ_4.raw | Raw | |||
| F8019TQ_5.raw | Raw |
Items per page: 5 1 - 5 of 11 |
Similar Datasets
Project description:Explore DNA methylation in chronic epilepsy and its relationship to gene expression. Examination of expression changes in pilocarpine-treated rats compared to controls and pilocarpine-treated rats on a ketogenic diet.
2013-09-09 | E-GEOD-50079 | biostudies-arrayexpress
Project description:Adult male rats of the PD/Cub (PD hereafter) strains were fed a laboratory chow diet (STD, ssniff RZ, ssniff Spezialdiäten GmbH, Soest, Germany). At the age of 12 months, rats within each strain were randomly divided into two groups. The control group was fed a high-sucrose diet (HSD, sucrose 70 cal%) while the experimental group was fed a HSD fortified with quercetin (10 g/kg food, Sigma-Aldrich).
2022-09-15 | E-MTAB-11061 | biostudies-arrayexpress
Project description:Iron is an essential nutritional element; its deficiency in the body causes nutritional problems and a decrease in iron storage that can lead to anemia. The liver not only stores iron but is an important metabolic target as well. Dietary iron deficiency is associated with changes in the metabolism of nutrients such as lipids. However, to the best of our knowledge, a global analysis detailing the consequences of iron deficiency in the body has not yet been reported. We performed a comprehensive transcriptome analysis using DNA microarray technology to reveal the effects of iron deficiency on hepatic gene expression. Four-week-old rats were fed an iron-deficient diet or a control diet for 16 days. On day 17, the rats were sacrificed under anesthesia, and their livers were dissected for DNA microarray analysis. We identified 600 up-regulated and 500 down-regulated probe sets to characterize the iron-deficient diet group. The up-regulated probe sets contained genes for enzymes that are involved in cholesterol, amino acid, and glucose metabolisms, as well as in apoptosis. The down-regulated probe sets included genes for enzymes associated with lipid metabolism. Additionally, the 16-day iron-deficient diet induced anemia. Our gene expression analysis revealed that, as a result, cholesterol biosynthesis, gluconeogenesis, and apoptosis due to endoplasmic reticulum stress were accelerated, while fatty acid biosynthesis was suppressed by dietary iron deficiency. Our analysis also showed that cholesterol metabolism, including bile acid biosynthesis, was accelerated in the initial stages of cholesterol accumulation. Experiment Overall Design: Male 3-week-old Sprague Dawley rats were purchased from Charles River Japan (Kanagawa, Japan) and housed in a room conditioned at 24 ± 1°C and 40 ± 5% humidity with a 12-h light-dark cycle (lights on at 08:00). The rats were given a control diet and water for 24 h ad libitum. Diets for rats were obtained from Research Diets, Inc. (New Brunswick, NJ, USA). The composition of the control diet was based on the AIN93G diet , except that cellulose was replaced by Avicel, since cellulose is an ingredient of variable iron content. The iron-deficient diet was prepared by removal of iron (ferric citrate) from the control diet. At day 8, rats were divided into two groups comprising animals of similar body weights. One group (n = 6) was fed the control diet and the other group (n = 7) was fed the iron-deficient diet (iron-deficient diet group). After iron-deficient diet feeding was started, blood hemoglobin levels were measured every two days. Blood samples for hemoglobin measurements were collected from the tail vein, and hemoglobin levels were measured by using the Wako Hemoglobin B test (Wako Pure Chemical Industries, Osaka, Japan). On day 12 of the iron-deficient diet treatment, diets were removed at 17:00, and feeding was conducted between 09:00 and 17:00 for another 4 days. This protocol was intended to synchronize the ratsâ feeding behavior. On day 17 of the iron-deficient diet treatment, rats were fed for 1.5 h prior to sacrifice under anesthesia. Livers were then excised and subsequently immersed in RNAlater (Applied Biosystems Japan, Tokyo, Japan). Blood hemoglobin level of rats fed an iron-deficient diet decreased significantly over the course of the feeding. On day 17, the hemoglobin level in the iron-deficient diet group was 42% of that of the control diet group (P < 0.01).
2009-07-11 | E-GEOD-16899 | biostudies-arrayexpress
Project description:Vitamin A (retinol) is an essential precursor for the production of retinoic acid (RA), which in turn is a major regulator of gene expression, affecting cell differentiation throughout the body. Understanding how vitamin A nutritional status, as well as therapeutic retinoid treatment, regulates the expression of retinoid homeostatic genes is important for improving dietary recommendations and therapeutic strategies using retinoids. This study investigated genes central to processes of retinoid uptake and storage, release to plasma, and oxidation in the liver of rats under steady-state conditions after different exposures to dietary vitamin A (deficient, marginal, adequate and supplemented), and acutely after administration of a therapeutic dose of all-trans-RA. Over a very wide range of dietary vitamin A, lecithin:retinol acyltransferase (LRAT) as well as multiple cytochrome P450s (CYP26A1, CYP26B1, and CYP2C22) differed by diet and were highly correlated with one another and with vitamin A status assessed by liver retinol concentration (all correlations, P<0.05). After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding RARß, a classical direct target of RA. CYP26A1 mRNA exhibited the greatest dynamic range (change of log26 in 3 h). Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naïve rats. By in situ hybridization, CYP26A1 mRNA was strongly regulated within hepatocytes, closely resembling RBP4 in location. Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change. All rats were housed in a room maintained at 22°C with a 12-h dark:light cycle, and food and water were freely available. For the Steady-State Vitamin A Study (experiment 1) and the Retinoic Acid 16-hour Kinetic Study (experiment 2), lactating female Sprague-Dawley rats with 12 female pups (purchased from Charles River Laboratories, Willmington, MA) were fed a vitamin A-deficient purified diet [AIN-93G diet, prepared by Research Diets, New Brunswick, NJ] to reduce the transfer of vitamin A in milk from mother to pups prior to the start of the study. For experiment 1, from weaning, the offspring were fed the same diet modified to contain vitamin A at one of four levels: 0 (vitamin A deficient), 0.4 mg retinol/kg diet (vitamin A marginal), 4 mg retinol/kg diet (vitamin A adequate control), or 100 mg retinol/kg diet (vitamin A supplemented). All rats were studied at 8 weeks of age. Rats were euthanized by carbon dioxide asphyxiation and blood and liver were collected rapidly and frozen in liquid nitrogen for storage at -80°C before analysis. In experiment 2, at 8 weeks of age female vitamin A-deficient rats were treated with ~100 ug of All-trans-Retinoic acid (at-RA) for 0 (vehicle only), 3, 6, 10 or 16 h (n=3-4/group). Tissues were collected and RNA was prepared in the same manner as in experiment 1. In the 90-minute "first pass" kinetic study (experiment 3), female rats were purchased at 6 weeks of age and fed a stock rodent diet. When the rats were 8 weeks old they were assigned to a control (naïve) group. Rats in the naive group received an equal amount of vehicle only (vegetable oil/5% ethanol). Food was removed immediately. Sixteen hours after priming, each rat was lightly anesthetized by isoflurane-oxygen inhalation and treated with ~25 ug all-trans-RA bound to albumin [10 ug RA per 100 g bo dy weight], injected into the exposed left common iliac vein. The incision was closed with a surgical staple. The rats were allowed to recover from the anesthesia. Rats were killed at 0 minute (vehicle injection), and 30, 60, and 90 min (n = 3/group) after injection of the RA test dose. Rats were euthanized by carbon dioxide asphyxiation and blood and liver were collected rapidly and frozen in liquid nitrogen for storage at -80°C before analysis. For experiment 1, five biological repeats were Vitamin A deficient, seven biological repeats were Vitamin A marginal, six biological repeats were Vitamin A adequate, and two biological repeats were Vitamin A supplemented. In experiment 2, three biological repeats were performed for each of the following treatments: untreated, at-RA for 3 hours, at-RA for 6 hours and at-RA for 16 hours. Four biological repeats were treated with at-RA for 10 hours. For experiment 3, two biological repeats were untreated and three biological repeats were performed for each of the following at-RA treatment times: 30, 60 and 90 minutes. A total of 47 samples were analyzed.
2011-08-31 | E-GEOD-24104 | biostudies-arrayexpress
Project description:Rats fed a 20%-maple syrup diet (maple syrup group) for 11 days showed significantly lower values of the hepatic function markers than those fed a 20%-sugar mix syrup diet (control) likewise. One reasons was suggested by DNA microarray analysis which revealed that the expression of genes for enzymes of ammonia production were down-regulated in the liver of maple syrup group. Rats were quarantined and conditioned by administration of the authentic AIN93G diet for 4 days. Rats had free access to the diet and drinking water during this preliminary feeding. For feeding tests, they were dichotomized (n = 7 and 8) for maple syrup and sugar mix syrup group, respectively, and then fed for 11 days on either the AIN93G diet containing 20% maple syrup or on the 20% sugar mix syrup with a similar sugar composition; the amount of maple syrup or the sugar mix syrup was arranged. Rats in both diet groups were fasted for 16 hours, prior to being anesthetically sacrificed for dissection.
2011-08-31 | E-GEOD-30532 | biostudies-arrayexpress
Project description:Iron deficiency-induced anemia is generally a representative nutritional problem in most populations. We reported that the anemia due to dietary iron deficiency causes a variety of changes in nutrient metabolism, even leading to apoptosis as a result of associated endoplasmic reticulum (ER) stress in the rat liver. On the other hand, it appears that non-anemic iron-deficiency causes no serious problem because no appreciable down-regulation of hemoglobin synthesis occurs. Biochemically, iron is essential for activation of cytochrome-related enzymes and its deficiency should yield some physiological problems. We performed a comprehensive transcriptome analysis to define the effects of non-anemic iron deficiency on hepatic gene expression. Four-week-old rats were fed a low-iron diet (ca. 3 ppm iron) for 2 days. These rats were compared with those fed a control diet (48 ppm iron) by pair feeding. On day 3, the rats were sacrificed under anesthesia, and their livers were dissected for DNA microarray analysis. Rats in the iron-deficient diet group, showed that their serum ferritin and iron levels decreased with an increase in the serum total iron binding capacity (TIBC) level, while the hemoglobin level was not changed. In the DNA microarray study, we identified 91 up-regulated and 186 down-regulated probe sets that characterized the iron-deficient diet group. In the up-regulated probe sets, genes involved in glucose and lipid metabolic processes were significantly enriched, whereas genes related to organic acid metabolic process, cellular ketone metabolic process, lipid metabolic process, oxidation reduction, response to drug, response to extracellular stimulus and gas transport were significantly enriched in the down-regulated probe sets. These results suggest that even the non-anemic iron-deficiency exerts various influences on nutrient metabolisms in the liver. Three-week-old male rats (Sprague Dawley) were purchased from Charles River Japan (Kanagawa, Japan) and housed in a room maintained at 24 M-BM-1 1M-BM-0C and 40 M-BM-1 5% humidity with a 12-h light/dark cycle (light 08:00M-bM-^@M-^S20:00; dark 20:00M-bM-^@M-^S08:00). Rats were given a normal diet (Research Diets, Inc., New Brunswick, NJ, USA) as control and water for 24 h ad libitum. The composition of the control diet, 48 ppm iron, was based on the AIN-93G diet; Avicel was used in place of cellulose which may contain a trace amount of iron. On day 3, diet was removed at 18:00 and the feeding was conducted between 09:00 and 17:00 for another 4 days to synchronize the feeding behaviors. On day 8, rats were divided into two groups with similar average body weights. Rats in the one group (n = 5) were given ad libitum an iron-deficient diet, ca. 3 ppm iron, that was prepared by removal of iron (ferric citrate) from the control diet, and those in the other group (n = 5) were fed the control diet by pair feeding. On day 1 and day 3 of feeding with the experiment diet, the hemoglobin level of each rat was measured for the blood samples collected from the tail vein. On day 3, each rat was sacrificed under anesthesia after 1.5 h feeding, prior to excising the liver which was soon immersed in RNAlater.
2013-03-21 | E-GEOD-30533 | biostudies-arrayexpress
Project description:In the experiment two groups of rats were compared. The control group consisted of 10 male, 5- to 6-weeks old, Fischer 344 (F344) rats (Nossan, Correzzana, Milan, Italy) fed a high fat, high sucrose, low fibre diet (control diet) for two weeks. This diet was based on the AIN76 diet [19], and was modified to contain 23% (w/w) fat (from corn oil) and a low level of cellulose (2% w/w), to mimic the high risk of colon cancer in human populations consuming high fat diets. The experimental group consisted of 10 male, 4- to 5-weeks old, F344 rats fed the same high fat diet as the control group in combination with 50 mg/kg red wine polyphenols for two weeks. The red wine polyphenol extract was prepared as described by Femia et al.<br> Total RNA was extracted using the RNeasy Midi kit (Qiagen, Milan, Italy). Equally amounts of RNA extracted from the colon mucosa of control diet-fed rats (n=10) were pooled and used as common reference for all hybridizations.
2007-11-13 | E-MEXP-934 | biostudies-arrayexpress
Project description:Gene expression along the crypt-villus (C-V) axis was analyzed using cryostat sectioning to isolate fractions representing the crypts (bottom) and villus tops (top). These fractions were used for analyzing gene expression in iron replete Wistar rats (++), iron deficient Wistar rats (low iron), and in iron deficient Wistar rats fed iron for 3 and 6 days (iron-fed). Differences were observed between the crypts and villus tops in the expression of genes associated with Wnt and BNP signaling, cell proliferation and apoptosis, lipid and iron transport and metabolism. Gene expression in villus crypts and tops was also compared between Wistar and Belgrade rats (bb) and Belgrade rats fed iron (iron-fed) particularly as related to iron absorption and metabolism to define the affects of the mutation in DMT1 in the Belgrade rat on the expression of genes related to iron absorption and metabolism and the response to iron feeding. Keywords: iron stress response A colony of Wistar strain rats (++) and Belgrade (bb) rats on a Wistar background maintained in our animal quarters was used for this study. Twelve one-month old ++ rats were separated into 3 groups of four rats each. Group 1 rats (samples 1-8) were fed a normal diet and served as control animals. Group 2 (samples 9-16) and Group 3 rats (samples 17-22) were fed a low iron diet and bled 2-3 ml every three days for 4 weeks and served as iron deficient rats (low-iron). Group 3 rats, of which one rat died during anesthesia while undergoing phlebotomy, were fed iron supplementation in drinking water (50 µM Ferric ammonium citrate) for the three days before sacrifice (iron-fed). Rats were fasted overnight, killed by injection of pentobarbital sodium and a 1-cm duodenal segment 1 cm distal from the pylorus was cryostat sectioned at the right angle to the crypt-villus axis and the sections representing the top one-third of villus (top) and the bottom one-third of the villus were pooled for RNA isolation. For the study of Belgrade rats, eleven bb rats were divided into 3 groups with the 4 rats in Group 1 (samples 23-30) maintained on a normal diet, the 4 rats in Group 2 (samples 31-38) fed iron for 3 days prior to sacrifice, and the 3 rats in Group 3 (samples 39-44) fed iron for 6 days prior to sacrifice. All procedures for the bb rats were the same as described above for the ++ rats. An additional ++ rat (samples 45-46) was similarly analyzed in a separate experiment.
2010-05-27 | E-GEOD-7970 | biostudies-arrayexpress
Project description:We used Affymetrix microarrays to investigate gene expression changes in the liver of lean female Zucker rats exposed to a normal diet supplemented with a rosemary extract rich in the diterpenic compound, carnosic acid (CA). The aim of this work was to determine whether the daily intake (with the standard diet) of the rosemary extract (RE) enriched in CA (40%) for 64 days exerted any modulatory effects, at the level of gene expression, in the liver of lean Zucker female rats. Female lean Zucker rats were randomly assigned to two experimental groups (n= 7 animals per group) as follows: (1) control group, fed a standard diet (CT); (2) treated group, fed a standard diet supplemented (0.05% w/w) with the RE rich in CA (RE). At the end of the experimental procedure (64 days), total RNA was extracted from the liver to compare differential gene expression between the two groups. Liver differential gene expression after 64 days of supplementation between the CT group and the RE group (effects of the extract supplementation).
2013-09-15 | E-GEOD-48373 | biostudies-arrayexpress
Project description:Gene expression of rat peripheral blood mononuclear cells was analyzed by microarray analysis in normoweight and in diet-induced obese rats (cafeteria rats). The aim of this study was to identify genes involved in energy homeostasis that are altered in the obese state. Keywords: Dietary treatment, obese-state analysis This study analyzed the gene expression of PBMC in normoweight and in diet-induced obese (cafeteria-fed) Wistar rats submitted to ad libitum feed conditions. Two-month-old male Wistar rats (n=10) were assigned into two dietary groups for 4 months: the control group (n=5) was fed with a standard chow diet, whereas the second group (cafeteria group, n=5) was fed with a fat-rich hypercaloric cafeteria diet in addition to the standard chow. At 6 months of age, blood samples were collected in feeding conditions from the safena vein. Peripheral blood mononuclear cells were isolated by Ficoll gradient separation, and RNA was extracted. One sample in the control group was excluded because of a low amount of RNA. Gene expression changes were assessed using an Agilent rat whole genome microarray (G4131F Agilent Technologies).
2009-12-01 | E-GEOD-14094 | biostudies-arrayexpress