Gene expression of p53 deficient, mutant p53R245W, and wildtype murine livers from animals fed a high fat, choline defficient diet
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE230057 | GEO | 2024/01/10
REPOSITORIES: GEO
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Project description:Gene expression of p53 deficient, mutant p53R245W, and wildtype murine livers from animals fed a high fat, choline defficient diet
| PRJNA957292 | ENA
Project description:BACKGROUND:Arjunarishta (AA), a formulation used as cardiotonic is a hydroalcoholic formulation of Terminalia arjuna (Roxb.) Wight and Arn. (TA) belonging to family Combretaceae. OBJECTIVE:To evaluate the anti-hyperglycemic and anti-hyperlipidemic effect of Arjunarishta on high-fat diet fed animals. MATERIALS AND METHODS:High-fat diet fed (HFD) Wistar rats were randomly divided into three groups and treated with phytochemically standardized Arjunarishta (1.8 ml/kg), and hydroalcoholic extract of T. arjuna (TAHA) (250 mg/kg) and rosuvastatin (10 mg/kg), for 3 months. Intraperitoneal glucose tolerance test, blood biochemistry, liver triglyceride and systolic blood pressure were performed in all the groups. Effect of these drugs on the expression of tumor necrosis factor-α (TNF-α) and insulin receptor substrate-1 (IRS-1) and peroxisome proliferators activated receptor γ coactivator 1-α (PGC-1α) were studied in liver tissue using Quantitative Real-time PCR. RESULTS:HFD increased fasting blood glucose, liver triglyceride, systolic blood pressure and gene expression of TNF-α, IRS-1 and PGC-1α. Treatment of AA and TAHA significantly reduced fasting blood glucose, systolic blood pressure, total cholesterol and triglyceride levels. These treatments significantly decreased gene expression of TNF-α (2.4, 2.2 and 2.6 fold change); increased IRS-1 (2.8, 2.9 and 2.8 fold change) and PGC-1α (2.9, 3.7 and 3.3 fold change) as compared to untreated HFD. CONCLUSION:Anti-hyperglycemic, anti-hyperlipidemic effect of Arjunarishta may be mediated by decreased TNF-α and increased PGC-1α and IRS-1.
| S-EPMC5884182 | biostudies-literature
Project description:Obesity has been correlating with low levels of glutathione (GSH) and 25-hydroxyvitamin D3 (25(OH)VD3). The liver is the principal site for the 25(OH)VD3 biosynthesis. This study investigated whether GSH deficiency induces epigenetic alterations that impair Vitamin D (VD) metabolism genes in the livers of HFD-fed mice. The expression of the VD metabolism genes CYP2R1 and CYP27A1 (25-hydroxylase), CYP27B1 (1-α-hydroxylase), and vitamin D receptor (VDR) were downregulated in the livers of mice fed an HFD (GSH- deficient) compared with control diet-fed group. The expression of CYP24A1 (24-hydroxylase) was significantly increased, which catabolizes both 25(OH)VD3 and 1α,25-hydroxyvitaminD3. Gene-specific hypermethylation of 25-hydroxylase, 1-α-hydroxylase, and VDR, and hypomethylation of CYP24A1 was observed in HFD-fed mice. GSH deficiency induced in cultured hepatocytes caused an increase in oxidative stress and alterations in VD regulatory genes. Similarly, elevated global DNA methylation, Dnmt activity, and 5-methylcytosine but decreased Tet activity and 5-hydroxymethylcytosine were observed in the GSH-deficient hepatocytes and the liver of HFD-fed mice. Replenishment of GSH by its prodrugs treatment beneficially altered epigenetic enzymes, and VD-metabolism genes in hepatocytes. HFD-induces GSH deficiency and epigenetically alters VD-biosynthesis pathway genes. This provides a biochemical mechanism for the VD-deficiency and potential benefits of GSH treatment in reducing 25(OH)VD3-deficiency.
| S-EPMC6794254 | biostudies-literature
Project description:Background & aimsActivation of the renin-angiotensin-system is known to play a role in nonalcoholic steatohepatitis. Renin knockout mice manifest decreased hepatic steatosis. Aliskiren is the first direct renin inhibitor to be approved for clinical use. Our study aims to evaluate the possible therapeutic effects and mechanism of the chronic administration of aliskiren in a dietary steatohepatitis murine model.MethodsMale C57BL/6 mice were fed with a methionine and choline-deficient (MCD) diet to induce steatohepatitis. After 8 weeks of feeding, the injured mice were randomly assigned to receive aliskiren (50 mg·kg(-1) per day) or vehicle administration for 4 weeks. Normal controls were also administered aliskiren (50 mg·kg(-1) per day) or a vehicle for 4 weeks.ResultsIn the MCD mice, aliskiren attenuated hepatic steatosis, inflammation and fibrosis. Aliskiren did not change expression of lipogenic genes but increase turnover of hepatic fat by up-regulating peroxisome proliferator-activated receptor ?, carnitine palmitoyltransferase 1a, cytochrome P450-4A14 and phosphorylated AMP-activated protein kinase. Furthermore, aliskiren decreased the hepatic expression of angiotensin II and nuclear factor ?B. The levels of oxidative stress, hepatocyte apoptosis, activation of Kupffer cells and hepatic stellate cells, and pro-fibrotic markers were also reduced in the livers of the MCD mice receiving aliskiren.ConclusionsAliskiren attenuates steatohepatitis and fibrosis in mice fed with a MCD diet. Thus, the noted therapeutic effects might come from not only the reduction of angiotensin II but also the up-regulation of fatty acid oxidation-related genes.
| S-EPMC3804600 | biostudies-literature
Project description:To investigate the mechanisms of lipid-activated protein kinase C (PKC) family, PKCδ or PKCɛ, involved in insulin resistance and fatty acid metabolism, we employed an in vivo adaptation of SILAC to examine the effects of a fat diet together with deletion of PKCδ or PKCɛ on the expression of liver proteins.
2014-11-04 | PXD000971 | Pride
Project description:Beyond the DNA sequence difference between humans and closely related apes, there are large differences in the environments that these species experience. One prominent example for this is diet. The human diet diverges from those of other primates in various aspects, such as having a high calorie and protein content, as well as being cooked. Here, we used a laboratory mouse model to identify gene expression differences related to dietary differences. Experiment Overall Design: We fed four groups of six genetically identical 8-week-old female NMR1 mice one of four diets ad libidum: (1) a diet consisting of vegetables, fruit and yogurt identical to the diet fed to chimpanzees in our ape facility ('Chimpanzee'); (2) a diet consisting exclusively of McDonalds. fast food ('FastFood'); (3) a diet consisting of cooked food eaten by our staff in the Institute cafeteria ('HumanCafe'); (4) the mouse pellet diet on which they were raised ('Pellet'). At the end of a 2-week period, mice were euthanized by cervical dislocation and both liver and brain (right cerebral hemisphere) tissue were dissected. RNA was extracted from the 24 liver and brain samples as per established lab protocols and processed in two batches (containing equal numbers of individuals from all groups).
2009-04-08 | E-GEOD-6297 | biostudies-arrayexpress
Project description:Analysis of liver gene transcription during feeding of a ketogenic diet. Ketogenic diets may alter physiologic and metabolic profiles in a direction that favors weight loss. C57BL/6J mice were maintained for six weeks on either chow or ketogenic diet. Mice eating KD had lower weights, 90% reduction in insulin levels and increased energy expenditure compared to animals fed chow. Despite consumption of a very high fat diet serum lipids remained normal. Here we show that consumption of KD shifted liver metabolism to drastically increased fatty acid oxidation. Concurrently, expression of genes involved in fatty acid synthesis were markedly suppressed. Reference: A high fat, ketogenic diet induces a unique metabolic state in mice. Kennedy AR, Pissios P, Out H, Xue B, Asakura K, Furukawa N, Marino FE, Liu FF, Kahn BB, Liberman TA, Maratos-Flier E. in press, 2007, Am J Physiol Metab 292. Experiment Overall Design: Eight week old C57BL/6 mice were fed either chow (Labdiet 5008, Pharmserv) or KD (F3666, Bio-Serv) for six weeks. Livers were harvested in the morning in ad lib fed animals. Total RNA from 2-3 animals in each group was used for Affymetrix analysis.
2007-12-13 | E-GEOD-7699 | biostudies-arrayexpress
Project description:Maternal choline intakes are below recommendations, potentially impairing the child's later-life metabolic health. This study aims to elucidate the interaction between the choline content of the gestational diet (GD) and fat content of the post-weaning diet (PWD) on metabolic phenotype of male Wistar rats. Pregnant Wistar rats were fed a standard rodent diet (AIN-93G) with either recommended choline (RC, 1 g/kg diet choline bitartrate) or high choline (HC, 2.5-fold). Male pups were weaned to either a normal (16%) fat (NF) or a high (45%) fat (HF) diet for 17 weeks. Body weight, visceral adiposity, food intake, energy expenditure, plasma hormones, triglycerides, and hepatic fatty acids were measured. HC-HF offspring had 7% lower body weight but not food intake, and lower adiposity, plasma triglycerides, and insulin resistance compared to RC-HF. They also had increased hepatic n-3 fatty acids and a reduced n-6/n-3 and C 18:1 n-9/C18:0 ratios. In contrast, HC-NF offspring had 6-8% higher cumulative food intake and body weight, as well as increased leptin and elevated hepatic C16:1 n-7/C16:0 ratio compared to RC-NF. Therefore, gestational choline supplementation associated with improved long-term regulation of several biomarkers of the metabolic syndrome in male Wistar rat offspring fed a HF, but not a NF, PWD.
| S-EPMC8145686 | biostudies-literature
Project description:Nonalcoholic steatohepatitis (NASH) is often associated with obesity, but some patients develop NASH without obesity. The physiological processes by which nonobese patients develop NASH and cirrhosis have not yet been determined. Here, we analyzed the effects of dietary methionine content on NASH induced in mice fed on a choline-deficient, methionine-lowered, l-amino acid-defined high-fat diet (CDAHFD). CDAHFD with insufficient methionine induced insulin sensitivity and enhanced NASH pathology, but without obesity. In contrast, CDAHFD with sufficient methionine induced steatosis, and unlike CDAHFD with insufficient methionine, also induced obesity and insulin resistance. Gene profile analysis revealed that the disease severity in CDAHFD may partially be due to upregulation of the Rho family GTPases pathway and mitochondrial and nuclear receptor signal dysfunction. The signaling factors/pathways detected in this study may assist in future study of NASH regulation, especially its 'nonobese' subtype.
| S-EPMC8564345 | biostudies-literature
Project description:We used fish from two divergent lines of rainbow trout, selected for low or high muscle fat content (respectively L and F lines) and fed two different diets, containing either 10% (LE diet) or 23% (HE diet) lipids. For more details about experimental fish and diets, see Kolditz et al.,Am J Physiol Regul Integr Comp Physiol 294: R1154–R1164, 2008. There are 4 experimental conditions: L-LE, L-HE, F-LE and F-HE. This experiment contain the data derived from the hybridization of the RNA extracted from individual liver of these fish. for each membrane, spots with an oligonucleotide signal lower than three times the background level were excluded from the analysis. After this filtering step, signal processing was performed using the vector oligonucleotide data to correct each spot signal according to the actual amount of DNA present in each spot. After correction, the signal was normalized by dividing each gene expression value by the median value of the array. Keywords: Nutritional genomics, response to divergent selection for muscle fattening, liver metabolism, rainbow trout
2008-09-01 | GSE12031 | GEO