Effect of ecdysterone on the hepatic transcriptome and lipid metabolism in lean and obese Zucker rats
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PROVIDER: PRJNA707205 | ENA |
REPOSITORIES: ENA
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Project description:Ecdysteroids are a class of steroid hormones occurring in insects, where they are referred as zooecdysteroids, and in plants, where they are termed phytoecdysteroids. While zooecdysteroids in insects regulate important developmental processes, such as embryogenesis, molting (ecdysis), metamorphosis, reproduction, and diapause, phytoecdysteroids provide protection against invertebrate predators by acting as feeding deterrents and by disrupting critical developmental processes of such invertebrates. The ecdysteroids in insects and plants comprise a great number of different analogues, with 20‐hydroxyecdysone, also called ecdysterone, being the quantitatively dominating biologically active analogue in both, insects and plants. Although phytoecdysteroids are effective toxins or antifeedants towards non-adapted herbivorous invertebrate predators, ecdysteroids are apparently non-toxic to mammals and even have been shown to exert a variety of interesting metabolic actions, such as antiobesity, hypoglycemic and protein-anabolic effects. In the present study aimed to test the hypothesis that ecdysterone causes lipid-lowering effects in obese Zucker rats. To test this hypothesis, two groups of obese Zucker rats were fed a nutrient-adequate diet supplemented without or with 0.05% ecdysterone. This ecdysterone concentration was appropriate to achieve a similar dose of ecdysterone per kg body weight BW as applied in other rodent studies, in which ecdysterone caused either hepatic and plasma lipid-lowering effects or antiobesity effects in different rodent models. In order to decipher the potential lipid-lowering actions of ecdysteroids in Zucker rats, measurements of liver and plasma lipid concentrations and hepatic transcriptome analysis was carried out. To further study if ecdysterone is capable of alleviating the strong lipid-synthetic activity in the liver of obese Zucker rats, the study included also two groups of lean Zucker rats which also received either the ecdysterone-supplemented or the non-supplemented diet.
2021-03-07 | GSE168390 | GEO
Project description:Endurance exercise training has been shown to decrease whole-body and skeletal muscle insulin resistance and increase glucose tolerance in conditions of both pre-diabetes and overt type 2 diabetes. However, the adaptive responses in skeletal muscle at the molecular and genetic level for these beneficial effects of exercise training have not been clearly established in an animal model of pre-diabetes. The present study identifies alterations in skeletal muscle gene expression that occur with exercise training in pre-diabetic, insulin-resistant obese Zucker (fa/fa) rats and insulin-sensitive lean Zucker (Fa/-) rats. Treadmill running for up to 4 weeks caused significant enhancements of glucose tolerance as assessed by the integrated area under the curve for glucose (AUCg) during an oral glucose tolerance test in both lean and obese animals. Using microarray analysis, a set of only 12 genes was identified as both significantly altered (>1.5-fold change relative to sedentary controls; p<0.05) and significantly correlated (p<0.05) with the AUCg. Two of these genes, peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a) and the z-isoform of protein kinase C (PKC-z), have known involvement in the regulation of skeletal muscle glucose transport. We confirmed that protein expression levels of PGC-1a and PKC-z were positively correlated with the mRNA expression levels for these two genes. Overall, this study has identified a limited number of genes in soleus muscle of lean and obese Zucker rats that are associated with decreased insulin resistance and increase glucose tolerance following endurance exercise training. These findings could guide the development of pharmaceutical M-^Sexercise mimeticsM-^T in the treatment of insulin-resistant, pre-diabetic or overtly type 2 diabetic individuals.
2009-11-16 | E-TABM-213 | biostudies-arrayexpress
Project description:Thiazolidinediones increase tissue insulin sensitivity and are protective against worsening of nephropathy and hypertension in diabetes. Mechanisms underlying protection at the renal level likely involve a variety of unknown changes in gene expression. We examined kidney gene expression in obese and lean Zucker rats in response to rosiglitazone (Avandia®), a peroxisome proliferator activated receptor (gamma-subtype) agonist. Lean and obese Zucker rats were treated with either control chow or chow with added rosiglitazone (3 mg/kg�bw) for 12 weeks (n = 3/group). Total kidney mRNA expression was evaluated using the Affymetrix Rat Genome 230 2.0 GeneChip. 903 probe sets were significantly (P < 0.05) altered with at least 1.5-fold changes between groups. In untreated obese rats, 300 probe sets were increased and 244 decreased, relative to lean. Increased genes included the β-subunit of the epithelial sodium channel (ENaC), the thiazide-sensitive Na-Cl cotransporter, and aquaporin 3. Decreased genes included angiotensin converting enzyme, type 1 (ACE1). FatiGO analysis showed that the highest number of altered genes between lean and obese belonged to the categories: ion binding, hydrolase activity, and protein binding. RGZ increased expression of uncoupling protein 1 (UCP1), CD36, and fatty acid binding protein 4 (FAbp4) in both lean and obese rats. In obese rats, 33 genes were normalized by RGZ (no longer different from lean) including ACE1, fatty acid synthase (Fasn), and stearoyl-coenzyme A desaturase 2 (Scd2). Ingenuity Pathways System analysis of genes upregulated by RGZ in obese rats revealed two major nodes affected: PPAR-gamma and tumor necrosis factor alpha (TNF-alpha). Experiment Overall Design: Twelve male Zucker rats (6 Lean and 6 Obese) were used in the study. Three rats from each body type were fed either with control diet (ground chow diet) or control diet with rosiglitazone (3 mg/kg body weight). The rats were weighed weekly and fed diets and recieved water ad libitum for 12 weeks.
2008-04-06 | E-GEOD-7193 | biostudies-arrayexpress
Project description:Hepatic steatosis is a very common response to liver injury and often attributed to metabolic disorders. Prior studies have demonstrated the efficacy of a biotechnologically produced oyster mushroom (Pleurotus sajor-caju, PSC) in alleviating hepatic steatosis in obese Zucker rats. This study aims to elucidate molecular events underlying the anti-steatotic effects of PSC.
2021-07-27 | PXD022905 | Pride
Project description:Gene expression profiles in tissues of Zucker diabetic fatty (ZDF) rats compared with age matched Zucker lean control (ZLC) rats. Keywords: other
2004-03-01 | GSE1080 | GEO
Project description:Analysis of the gene signature of steatosis associated to obesity in hepatocytes of Zucker fa/fa obese rats and their controls; identifying target genes linked to steatosis progression. or Obesity and insulin resistance-associated steatosis can be a non-inflammatory condition affecting hepatocytes or progress to steatohepatitis: a condition that can result in end-stage liver disease. Although molecular events leading to accumulation of lipid droplets in the liver have been identified individually, the complexity of the condition suggested that emergent target would be uncovered by a more comprehensive examination. Then, this study was aimed at establishing a gene signature of steatosis in hepatocytes and at identifying target genes linked to steatosis progression. Using Affymetrix oligonucleotide arrays, we compared transcriptomes of hepatocytes isolated from Zucker "fa/fa" obese rats with three different age-related grades of steatosis with those of their counterpart non-steatotic cells.
2008-07-31 | E-MEXP-1414 | biostudies-arrayexpress
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days. Adipose tissue (epididymal), skeletal muscle (gastrocnemius), and liver were harvested from lean (LC) and insulin resistant, obese Zucker rats untreated (FC) or treated with one of four PPARγ ligands (pioglitazone [Pio], rosiglitazone [Rosi], troglitazone [Tro], and AG035029 [AG]).
2011-02-11 | E-GEOD-21329 | biostudies-arrayexpress
Project description:Conflicting reports exist with regard to the effect of ecdysterone, the predominating representative of steroid hormones in insects and plants, on hepatic and plasma lipid concentrations in different rodent models of obesity, fatty liver, and diabetes, indicating that the effect is dependent on the rodent model used. Here, the hypothesis was tested for the first time that ecdysterone causes lipid-lowering effects in genetically obese Zucker rats. To test this hypothesis, two groups of male obese Zucker rats (n = 8) were fed a nutrient-adequate diet supplemented without or with 0.5 g ecdysterone per kg diet. To study further if ecdysterone is capable of alleviating the strong lipid-synthetic activity in the liver of obese Zucker rats, the study included also two groups of male lean Zucker rats (n = 8) which also received either the ecdysterone-supplemented or the non-supplemented diet. While hepatic and plasma concentrations of triglycerides and cholesterol were markedly higher in the obese compared to the lean rats (p < 0.05), hepatic and plasma triglyceride and cholesterol concentrations did not differ between rats of the same genotype fed the diets without or with ecdysterone. In conclusion, the present study clearly shows that ecdysterone supplementation does not exhibit lipid-lowering actions in the liver and plasma of lean and obese Zucker rats.
| S-EPMC8156757 | biostudies-literature
Project description:The hypothesis was tested that biotechnologically produced Pleurotus sajor-caju (PSC) influences metabolic health of obese Zucker rats. To test this, obese Zucker rats were randomly assigned to 2 groups of 12 rats each with similar body weights (BW) and fed diets either without (OC) or with 5 % PSC (OPSC) for 4 weeks and hepatic transcript profiling was performed. Transcriptomics of the liver revealed a total of 580 transcripts differentially expressed between OPSC and OC.
2020-06-06 | GSE151882 | GEO
Project description:Background In the past, numerous studies revealed that supplementation with carnitine has multiple effects on performance characteristics and gene expression in livestock and model animals. The molecular mechanisms underlying these observations are still largely unknown. Increasing evidence suggests that microRNAs (miRNAs), a class of small non-coding RNA molecules, play an important role in post-transcriptional regulation of gene expression and thereby influencing several physiological and pathological processes. Based on these findings, the aim of the present study was to investigate the influence of carnitine supplementation on the miRNA expression profile in skeletal muscle of obese Zucker rats using miRNA microarray analysis. Results miRNA expression profiling in skeletal muscle revealed a subset of 152 miRNAs out of the total number of miRNAs analysed (259) were identified to be differentially regulated (adjusted P-value ˂ 0.05) by carnitine supplementation. Compared to the obese control group, 111 miRNAs were up-regulated and 41 down-regulated by carnitine supplementation (adjusted P-value ˂ 0.05). 14 of these miRNAs showed a log2 ratio ≥ 0.5 and 7 miRNAs showed a log2 ratio ≤ -0.5 (adjusted P-value ˂ 0.05). Conclusion The present study shows for the first time that supplementation of carnitine affects a large set of miRNAs in skeletal muscle of obese Zucker rats suggesting a novel mechanism through which carnitine exerts its multiple effects on gene expression, which were observed during the past. For microarray analyses, six RNA samples each, for the obese control group (n = 6) and the obese carnitine group (n = 6), were prepared from skeletal muscle tissue.
2014-06-17 | E-GEOD-58537 | biostudies-arrayexpress