Mus musculus
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PROVIDER: PRJNA391497 | ENA |
REPOSITORIES: ENA
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Project description:To elucidate the bioactive property of the dietary antioxidant curcumin, we examined tissue distribution and the gene expression- and lipidomic-profiles in epididymal white adipose tissue (eWAT) of the diet-induced obese mice. Dietary intake of curcumin (0.1% W/W) didn’t affect the eWAT weight and the plasma lipid levels but reduced the levels of lipid peroxidation marker in eWAT. Curcumin was a slightly accumulated in eWAT and altered the gene expression associated with eukaryotic translation initiation factor 2 (EIF2) signaling. Curcumin suppressed the endoplasmic reticulum (ER) stress-related eIF2 phospholyration, the accumulation of macrophages and the expression of oxidative stress-sensitive transcription factor NF-κB p65 and leptin, whereas anti-inflammatory effect wasn’t enough to reduce the TNF-α and IFN-γ levels. Lipidomic- and gene expression analysis suggests that curcumin reduced the contents of some diacylglyverols (DAGs) and DAG derived glycerophospholipids by suppressing the expressions of lipogenesis-related glycerol-3-phosphate acyltransferase 1 and lipolysis-related adipose triglyceride lipase.
2018-07-02 | GSE100388 | GEO
Project description:Although aging is a physiological process to which all organisms are subject, the presence of obesity and type 2 diabetes accelerates biological aging. Recent studies have demonstrated the causal relationships between dietary interventions suppressing obesity and type 2 diabetes and delaying the onset of age-related endocrine changes. Curcumin, a natural antioxidant, has putative therapeutic properties such as reinstating insulin sensitivity in obese mice. However, how curcumin contributes to maintaining insulin homeostasis in aged organisms largely remains unclear. Thus, the objective of this study is to examine the pleiotropic effect of dietary curcumin on insulin homeostasis in a diet-induced obese (DIO) aged mouse model. Aged (18-20 months old) male mice given a high-fat high-sugar diet supplemented with curcumin displayed a different metabolic phenotype compared to mice given a high-fat high-sugar diet alone. Furthermore, curcumin supplementation altered hepatic gene expression profiling, especially insulin signaling and senescence pathways. We then mechanistically investigated how curcumin functions to fine-tune insulin sensitivity. We found that curcumin supplementation increased hepatic insulin degrading enzyme (IDE) expression levels and preserved islet integrity, both of which are beneficial during aging. Our findings suggest that the multifaceted therapeutic potential of curcumin can be used as a protective agent for age-induced metabolic diseases.
2021-11-04 | GSE186971 | GEO
Project description:Melanoma is the most aggressive form of skin cancer with estimated 48,000 deaths worldwide. The polyphenol curcumin derived from the plant Curcuma longa is well known for its anti-inflammatory and anti-cancerogenic properties. Accordingly, dietary intake of this compound may be suitable for melanoma prevention. However, how this compound affects basic cellular mechanisms in developing melanoma still remains elusive. Therefore, the aim of this study was to investigate for the first time the impact of oral curcumin administration on the miRNA signature of engrafting melanoma. For this purpose, the effects of a 4% curcumin diet on murine B78H1 melanoma were tested in a flank model. Curcumin diet or standard chow (control) was administered two weeks prior to tumor initiation until termination of the experiment. Highly significant chip-based miRNA array analysis was deployed to detect alterations in the miRNA signature of the tumors. Curcumin treatment significantly reduced the growth of the flank tumors. Furthermore the miRNA expression signature in tumors was substantially altered by curcumin intake with mmu-miR-205-5p over 100 times higher expressed when compared to controls. Putative targets of curcumin-induced up-regulated miRNAs were enriched in o-glycan biosynthesis, endoplasmatic reticulum protein processing and different cancer-related pathways. These findings demonstrate a profound alteration of the miRNA expression signature in engrafting curcumin-treated melanoma with mmu-miR-205-5p being up-regulated most significantly. Treatment of male C57BL/6 mice with induced flank tumors (injection of B78H1 cells) either with standard mouse chow (control n=6) or chow enriched with 4% of curcumin (treatment group n=7 )
2013-12-31 | E-GEOD-47211 | biostudies-arrayexpress
Project description:Melanoma is the most aggressive form of skin cancer with estimated 48,000 deaths worldwide. The polyphenol curcumin derived from the plant Curcuma longa is well known for its anti-inflammatory and anti-cancerogenic properties. Accordingly, dietary intake of this compound may be suitable for melanoma prevention. However, how this compound affects basic cellular mechanisms in developing melanoma still remains elusive. Therefore, the aim of this study was to investigate for the first time the impact of oral curcumin administration on the miRNA signature of engrafting melanoma. For this purpose, the effects of a 4% curcumin diet on murine B78H1 melanoma were tested in a flank model. Curcumin diet or standard chow (control) was administered two weeks prior to tumor initiation until termination of the experiment. Highly significant chip-based miRNA array analysis was deployed to detect alterations in the miRNA signature of the tumors. Curcumin treatment significantly reduced the growth of the flank tumors. Furthermore the miRNA expression signature in tumors was substantially altered by curcumin intake with mmu-miR-205-5p over 100 times higher expressed when compared to controls. Putative targets of curcumin-induced up-regulated miRNAs were enriched in o-glycan biosynthesis, endoplasmatic reticulum protein processing and different cancer-related pathways. These findings demonstrate a profound alteration of the miRNA expression signature in engrafting curcumin-treated melanoma with mmu-miR-205-5p being up-regulated most significantly.
2013-12-31 | GSE47211 | GEO
Project description:OBJECTIVE Diet intervention in obese adults is the first strategy to induce weight loss and to improve insulin sensitivity. We hypothesized that improvements in insulin sensitivity after weight loss from a short-term dietary intervention tracks with alterations in expression of metabolic genes and abundance of specific lipid species. RESEARCH DESIGN AND METHODS Eight obese, insulin resistant, non-diabetic adults were recruited to participate in a three-week low calorie diet intervention study (1000 kcal/day). Fasting blood samples and vastus lateralis skeletal muscle biopsies were obtained before and after the dietary intervention. Clinical chemistry and measures of insulin sensitivity were determined. Unbiased microarray gene expression and targeted lipidomic analysis of skeletal muscle was performed. RESULTS Body weight was reduced, insulin sensitivity (HOMA-IR) was enhanced, and serum insulin concentration and blood lipid (triglyceride, cholesterol, LDL and HDL) levels were improved after dietary intervention. Gene set enrichment analysis of skeletal muscle revealed that oxidative phosphorylation and inflammatory processes were among the most enriched KEGG-pathways identified after dietary intervention. mRNA expression of PDK4 and MLYCD increased, while SCD decreased in skeletal muscle after dietary intervention. Dietary intervention altered the intramuscular lipid profile of skeletal muscle, with changes in content of phosphatidylcholine and triglyceride species among the pronounced. CONCLUSIONS Short-term diet intervention and weight loss in obese adults alters metabolic gene expression and reduces specific phosphatidylcholine and triglyceride species in skeletal muscle, concomitant with improvements in clinical outcomes and enhanced insulin sensitivity.
2019-02-05 | GSE103682 | GEO
Project description:The type and the amount of dietary fat have a significant influence on the metabolic pathways involved in the development of obesity, metabolic syndrome, diabetes type 2 and cardiovascular diseases. However, it is unknown to what extent this modulation is achieved through DNA methylation. We assessed the effects of cholesterol intake, the proportion of energy intake derived from fat, the ratio of polyunsaturated fatty acids (PUFA) to saturated fatty acids (SFA), the ratio of monounsaturated fatty acids (MUFA) to SFA, and the ratio of (MUFA+PUFA) to SFA on genome-wide DNA methylation patterns in normal-weight and obese children. We determined the genome-wide methylation profile in blood of 69 Greek preadolescents (~10 y old), as well as their dietary intake for two consecutive weekdays and one weekend day. The methylation levels of four sites and a CpG island were significantly correlated with total fat intake. The methylation levels of 13 islands and 16 sites were significantly correlated with PUFA/SFA; of 35 islands and 158 sites with MUFA/SFA; and of 50 islands and 130 sites with (MUFA+PUFA)/SFA. We found significant gene enrichment in 26 pathways for PUFA/SFA, including the leptin pathway, and a significant enrichment in three pathways for (MUFA+PUFA)/SFA. Our results suggest that the quality, and to a lesser extent the quantity of fat intake, influences DNA methylation, including genes involved in metabolism. Thus, specific changes in DNA methylation may play an important role in the mechanisms involved in the physiological responses to different types of dietary fat. Bisulphite converted DNA from 22 boys were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2.Both obese and normal-weight indiviudals were included.
2014-05-09 | E-GEOD-57484 | biostudies-arrayexpress
Project description:Excessive intake of dietary fat is known to be a contributing factor in the development of obesity. In this study, we determined the dose-dependent effects of dietary fat on the development of this metabolic condition with a focus on changes in gene expression in the small intestine. C57BL/6J mice were fed diets with either 10, 20, 30 or 45 energy% (E%) derived from fat for four weeks (n=10 mice/diet). We found a significant higher weight gain in mice fed the 30E% and 45E% fat diet compared to mice on the control diet. These data indicate that the main shift towards an obese phenotype lies between a 20E% and 30E% dietary fat intake. Analysis of differential gene expression in the small intestine showed a fat-dose dependent gradient in differentially expressed genes, with the highest numbers in mice fed the 45E% fat diet. The main shift in fat-induced differential gene expression was found between the 30E% and 45E% fat diet. Furthermore, approximately 70% of the differentially expressed genes were regulated in a fat-dose dependent manner. Many of these genes were involved in lipid metabolism-related processes and were already differentially expressed on a 30E% fat diet. Taken together, we conclude that up to 20E% of dietary fat, the small intestine has an effective ‘buffer capacity’ for fat handling. From 30E% of dietary fat, a switch towards an obese phenotype is triggered. We further speculate that especially fat-dose dependently regulated lipid metabolism-related genes are involved in development of obesity. The proximal, middle, and distal parts of the intestine of mice fed 10, 20, 30, or 45E% dietary fat were analyzed. 10 replicates each.
2011-04-26 | E-GEOD-26300 | biostudies-arrayexpress
Project description:The molecular mechanisms linking the stress of unfolded proteins in the endoplasmic reticulum (ER stress) to glucose intolerance in obese animals are poorly understood. In this study enforced expression of a translation initiation 2α (eIF2α)-specific phosphatase, GADD34, was used to selectively compromise signaling in the eIF2(αP)-dependent arm of the ER unfolded protein response in liver of transgenic mice. The transgene resulted in lower liver glycogen levels and susceptibility to fasting hypoglycemia in lean mice and glucose tolerance and diminished hepato-steatosis in animals fed a high fat diet. Attenuated eIF2(αP) correlated with lower expression of the adipogenic nuclear receptor PPARγ and its upstream regulators, the transcription factors C/EBPα and C/EBPβ, in transgenic mouse liver, whereas eIF2α phosphorylation promoted C/EBP translation in cultured cells and primary hepatocytes. These observations suggest that eIF2(αP)-mediated translation of key hepatic transcriptional regulators of intermediary metabolism contributes to the detrimental consequences of nutrient excess. Keywords: genotype comparison The low expressing Ttr::Fv2E-Perk transgene (#58) was bred into the Atf4 knockout strain and the derivative compound heterozygous mice (in the mixed FvB/n; Swiss Webster background) were backcrossed to the Atf4+/- parental stock and Ttr::Fv2E-PERK positive siblings with Atf4+/+ and Atf4-/- genetypes were analyzed.
2011-12-23 | E-GEOD-11116 | biostudies-arrayexpress
Project description:Methionine, a sulfur-containing essential amino acid, is a key component of dietary proteins important for protein synthesis, sulfur metabolism, antioxidant defense, and signaling. However, the role of methionine in cancer progression remains inconclusive. On one hand, dietary methionine restriction is known to repress cancer growth and improve cancer therapy in xenografted tumors. On the other hand, methionine is also critical for T cell activation and differentiation, making it a potential tumor suppression nutrient by enhancing T cell-mediated anti-tumor immunity. Here we investigated the interaction between dietary methionine, immune cells, and cancer cells by allografting CT26.WT mouse colon carcinoma cells into immunocompetent Balb/c mice or immunodeficient NSG mice, then analyzed how dietary methionine contents affect their growth. Our results show that dietary methionine restriction suppresses tumor growth in immunodeficient NSG mice but promotes tumor progression in immunocompetentt Balb/c mice.
2023-06-14 | GSE165993 | GEO