Comparative study of sesame lignans affecting gene expression profile and fatty acid oxidation in rat liver
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Takashi Ide
PROVIDER: E-GEOD-42693 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The impact of sesamin, episesamin and sesamolin (sesame lignans) on hepatic gene expression profiles was compared with a DNA microarray. Male Sprague-Dawley rats were fed experimental diets containing 0.2% sesamin, episesamin or sesamolin, and a control diet free of lignans for 15 d. Compared to a lignan-free diet, a diet containing sesamin, episesamin and sesamolin caused 1.5- and 2-fold changes in the expression of 128 and 40, 526 and 152, and 516 and 140 genes, respectively. The lignans modified not only the mRNA levels of many enzymes involved in hepatic fatty acid oxidation, but also those of proteins involved in the transportation of fatty acids into hepatocytes and their organelles, and regulate hepatic concentrations of carnitine, CoA and malonyl-CoA. It is apparent that sesame lignans stimulate hepatic fatty acid oxidation by affecting the gene expression of various proteins regulating hepatic fatty acid metabolism. We also observed that lignans modified the gene expression of various proteins involved in hepatic lipogenesis, cholesterogenesis and glucose metabolism. The changes were generally greater with episesamin and sesamolin than with sesamin. In terms of the amounts accumulated in serum and the liver, the lignans ranked in the order sesamolin, episesamin and sesamin. The differences in bio-availability among these lignans appear to be important to their divergent physiological activities.
2012-12-04 | GSE42693 | GEO
Project description:Soybean and fish contains various active components that were reported to prevent cardiovasucular diseases. Epidemiological studies indicated that Asian eating patterns, consisting of daily seafood and/or soy consumption, confer protection against cardiovascular diseases. In this context, we expected that simultaneous intake of soybean and fish may be greatly beneficial in a manner different from the ingestion of the individual food. To understand the detailed mechanism for modulating the lipid metabolism by co-ingestion of a soy food (tofu) and fish oil, we investigated the global changes in hepatic mRNA expression in rats by using a microarray analysis. Generally, ingestion of tofu contributed to prevent the mRNA expressions involved in hepatic lipogenesis, whereas fish oil facilitated the mRNA expressions related to the degradation of hepatic fatty acids. In terms of mRNA expression, the interaction of two dietary factors was limited. The expression data was normalized and summarized by using SuperNORM data service (Skylight Biotech Inc.). Significance of expressional change among groups was tested by 2-way ANOVA on the normalized CEL data, which was deposited in a tab-separated ASCII text format. Principal components were identified on the summarized gene data. Rats were divided into four groups each with similar average body weights and assigned experimental diets for 21 days as follows: casein and soybean oil diet (CS); casein and fish oil diet (CF); tofu and soybean oil diet (TS); tofu and fish oil diet (TF). Total protein and fat content of each diet was 200 and 150 g/kg, respectively. Soybean oil diets (CS and TS) contain 150 g/kg diet of soybean-derived fat (i.e. soybean oil and freeze-dried tofu), and 50 g/kg of fish oil was replaced with the same amount of soybean-derived fat for fish oil diets (CF and TF). Animals were allowed free access to food and water.
2015-09-01 | E-GEOD-66371 | 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:The effects of the administration of molecular hydrogen-saturated drinking water (hydrogen water) on hepatic gene expression were investigated in rats. Using DNA microarrays, 548 upregulated and 695 downregulated genes were detected in the liver after a 4-week administration of hydrogen water. Gene Ontology analysis revealed that genes for oxidoreduction-related proteins, including hydroxymethylglutaryl CoA reductase, were significantly enriched in the upregulated genes. 4-week-old male Sprague-Dawley rats were acclimatized for 4 days in a room maintained at 24 ± 3°C with a relative humidity of 55 ± 15% with a 12-h light-dark cycle (lights on at 7:00, off at 19:00) and were fed ad libitum on a commercial diet (MF, Oriental Yeast Co., Yokohama, Japan). After acclimatization, the rats were divided into two groups (n = 8 per group) with similar mean body weights. During a period of 4 weeks, one group (control group) was supplied with sterilized distilled water and the other (HW group) with hydrogen water produced by MiZ Co. Ltd. (Fujisawa, Japan), which contains 0.7 mM dissolved hydrogen (pH 7.4). All the animals drank water ad libitum. After 4 weeks, each rat was anesthetized with diethyl ether and blood samples were collected from the abdominal aorta. The liver was then excised and analyzed the effect of hydrogen water extract administration on hepatic gene expression.
2010-12-31 | E-GEOD-26363 | biostudies-arrayexpress
Project description:Persimmon (Diospyros kaki L. f.) is a most popular fruit in Asian countries but its peels are totally wasted despite of containing a plenty of antioxidants such as carotenoids and polyphenols. We prepared a fat-soluble extract from a persimmon peel (PP) fraction and fed type 2 diabetic Goto-Kakizaki (GK) rats with a PP extract-containing AIN-93G diet (PP diet) for 12 weeks. Compared with the control AIN-93G diet, the feeding of the PP diet reduced the plasma glutamic-pyruvate transaminase activity significantly, with accumulation of M-NM-2-cryptoxanthin in the liver. A DNA microarray analysis revealed that the PP diet altered the hepatic gene expression profiles. In particular, insulin signaling pathway-related genes were significantly enriched in differentially expressed gene sets. Moreover, Western blotting analysis actually showed the promotion of IRM-NM-2 tyrosine phosphorylation. All these data suggest that the PP extract administration to the GK rats improves their insulin resistance. Male GK rats (90M-bM-^@M-^S107 g), aged 5 weeks, were purchased from Japan SLC Co. (Hamamatsu, Japan). The rats were maintained in a room at 22 M-BM-1 1M-BM-0C under a 12-h light-dark cycle (lights on at 0800) and administered a commercial diet (AIN-93G, Research Diets, Inc., New Brunswick, NJ, USA) for a week. The rats were allowed free access to diet and water. After one week, they were divided into two groups with similar average body weights. The control group rats (n = 4) were fed on the commercial diet, and the PP group rats (n = 4) on the same diet containing the PP extract. After the 12-week-feeding the liver was excised and analyzed the effect of PP extract administration on hepatic gene expression.
2011-03-17 | E-GEOD-21417 | biostudies-arrayexpress
Project description: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.
2016-05-18 | E-GEOD-71201 | 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:Protein malnutrition promotes hepatic steatosis, decreases insulin-like growth factor (IGF)-I production, and retards growth. In order to identify new molecules involved in such changes, we conducted DNA microarray analysis for liver samples of rats fed isoenergetic low protein diet for 8 hours, and identified fibroblast growth factor 21 (Fgf21) as one of the most strongly up-regulated genes under conditions of acute protein malnutrition (P<0.05, FDR<0.001). In addition, amino acid deprivation from the culture media increased Fgf21 mRNA levels in rat liver-derived RL-34 cells (P<0.01). Thus, it was suggested that amino acid limitation directly increases Fgf21 expression. FGF21 is a polypeptide hormone that regulates glucose and lipid metabolism. Using transgenic mice, FGF21 has also been shown to promote a growth hormone-resistant state and suppress IGF-I. Therefore, to further determine whether the up-regulation of Fgf21 under protein malnutrition causes hepatic steatosis and growth retardation following decrease in IGF-I, we fed isoenergetic low protein diet to Fgf21-knockout (KO) mice. Fgf21-KO did not rescue growth retardation and reduced plasma IGF-I concentration of mice fed the low-protein diet. Meanwhile, Fgf21-KO mice showed greater epididymal white adipose tissue weight as well as hepatic triglyceride and cholesterol levels under protein malnutrition (P<0.05). Taken together, we showed that protein deprivation directly increases Fgf21 expression. However, growth retardation and decreased IGF-I were not mediated by increased FGF21 expression under protein malnutrition. Furthermore, up-regulated FGF21 rather appears to have a protective effect against obesity and hepatic steatosis in protein malnourished animals. Livers of rats from 2 groups (control (15P) or low-protain (5P) diet fed groups), total of 6 samples (3 replicates for each group) were analyzed.
2015-01-15 | E-GEOD-64970 | 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:The aim of this study was to compare the effects of cocoa butter and safflower oil on hepatic transcript profiles, lipid metabolism and insulin sensitivity in healthy rats. Cocoa butter-based high-fat feeding for three days did not affect plasma total triglyceride (TG) levels or TG-rich VLDL particles or hepatic insulin sensitivity, but changes in hepatic gene expression were induced that might lead to increased lipid synthesis, lipotoxicity, inflammation and insulin resistance if maintained. Safflower oil increased hepatic β-oxidation, was beneficial in terms of circulating TG-rich VLDL particles, but led to reduced hepatic insulin sensitivity. The effects of safflower oil on hepatic gene expression were partly overlapping with those exerted by cocoa butter, but fewer transcripts from anabolic pathways were altered. Increased hepatic cholesterol levels and increased expression of hepatic CYP7A1 and ABCG5 mRNA, important gene products in bile acid production and cholesterol excretion, were specific effects elicited by safflower oil only. Common effects on gene expression included increased levels of p8, DIG-1 IGFBP-1 and FGF21, and reduced levels of SCD-1 and SCD-2. This indicates that a lipid-induced program for hepatic lipid disposal and cell survival was induced by three days of high-fat feeding, independent on the lipid source. Based on the results, we speculate that hepatic TG infiltration leads to reduced expression of SCD-1, which might mediate either neutral, beneficial or unfavourable effects on hepatic metabolism upon high-fat feeding, depending on which fatty acids were provided by the diet. Keywords: Hepatic gene expression Two-condition experiment. Biological replicates: 4 male rat livers from rats on a standard diet, 4 male rat livers from rats on a cocoa butter diet, 4 male rat livers from rats on a high-fat (safflower oil) diet. One replicate per array.
2010-05-18 | E-GEOD-13936 | biostudies-arrayexpress