Identification of factors associated with high fat diet induced insulin resistance
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE48794 | GEO | 2016/07/01
SECONDARY ACCESSION(S): PRJNA211838
REPOSITORIES: GEO
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Project description:Whole genome expression profilling were undertaken in high fat diet (HFD)-fed obese rats to identify the genetic factors associated with metabolic dysfunction, insulin resistance and obesity. Sprague dawley male rats were maintained on HFD for 12 weeks ad libitum regimen. Liver being the principal organ for glucose homeostasis is targeted for microarray profilling. We could identify genes/factors associated with obesity induced metabolic dysfunction. Custom Rat Whole Genome 8x60k Gene Expression Microarray (AMADID:030192 ) designed by Genotypic Technology Private Limited.
2016-07-01 | E-GEOD-48794 | biostudies-arrayexpress
Project description:In order to establish an obese mouse model, female mice were continuously fed with a high-fat diet (HFD) or a normal diet (control) for 16 weeks beginning at three weeks of age. In this paper, these mice are termed ‘HFD mice’ and ‘control mice’, respectively. Accordingly, we call their oocytes ‘HFD oocytes’ and ‘control oocytes’. Substantial evidence indicates that the effects of maternal obesity on embryo/offspring development can be attributed to factors within the oocyte (9). To identify such potential effectors, we performed a comparative proteomic analysis of ovulated MII oocytes from control and HFD mice.
2018-05-24 | PXD006641 | Pride
Project description:Folic acid (FA) supplementation may protect from obesity and insulin resistance, the effects and mechanism of FA on chronic high-fat-diet-induced obesity-related metabolic disorders are not well elucidated. We adopted a genome-wide approach to directly examine whether FA supplementation affects the DNA methylation profile of mouse adipose tissue and identify the functional consequences of these changes. Mice were fed a high-fat diet (HFD), normal diet (ND) or an HFD supplemented with folic acid (20 μg/ml in drinking water) for 10 weeks, epididymal fat was harvested, and genome-wide DNA methylation analyses were performed using methylated DNA immunoprecipitation sequencing (MeDIP-seq). Mice exposed to the HFD expanded their adipose mass, which was accompanied by a significant increase in circulating glucose and insulin levels. FA supplementation reduced the fat mass and serum glucose levels and improved insulin resistance in HFD-fed mice. MeDIP-seq revealed distribution of differentially methylated regions (DMRs) throughout the adipocyte genome, with more hypermethylated regions in HFD mice. Methylome profiling identified DMRs associated with 3787 annotated genes from HFD mice in response to FA supplementation. Pathway analyses showed novel DNA methylation changes in adipose genes associated with insulin secretion, pancreatic secretion and type 2 diabetes. The differential DNA methylation corresponded to changes in the adipose tissue gene expression of Adcy3 and Rapgef4 in mice exposed to a diet containing FA. FA supplementation improved insulin resistance, decreased the fat mass, and induced DNA methylation and gene expression changes in genes associated with obesity and insulin secretion in obese mice fed a HFD.
2018-06-30 | GSE97576 | GEO
Project description:High fat diet (HFD), if prolonged, leads to obesity thereby accelerating the development of many ageing-related pathologies including chronic inflammation, cardiovascular disease, diabetes, and a higher predisposition to develop cancer. We asked whether HFD could reprogram the circadian output of young stem cells in a manner similar to what we observed during physiological ageing. HFD has been recently shown to induce a rewiring of the liver circadian transcriptome and metabolome, although in an obesity-independent manner. We therefore fed young (8 week old) C57Bl6 mice with HFD or its control diet for 7-weeks, a time when mice had not yet become obese, and performed circadian transcriptome analysis.
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Project description:High-fat diet (HFD) induces diminished ovarian reserve and subfertility in female mice, irrespective of obesity. To further assess the impact of HFD on ovarian function, female mice were fed a 60% HFD or standard chow for 10 weeks and then HFD fed mice were separated into obese (HFOB) and lean (HFLN) groups. RNA-sequencing of whole ovaries identified multiple differentially expressed genes involved in normal ovarian function (ovulation, luteinization, luteolysis) in both the HFLN and HFOB mice compared to the chow fed mice (q<0.05). Taken together, elevated dietary fat intake, regardless of obesity, is associated with impaired estrous cycles and altered expression of genes critical to normal ovulatory function.
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Project description:High fat diet (HFD), if prolonged, leads to obesity thereby accelerating the development of many ageing-related pathologies including chronic inflammation, cardiovascular disease, diabetes, and a higher predisposition to develop cancer. We asked whether HFD could reprogram the circadian output of young stem cells in a manner similar to what we observed during physiological ageing. HFD has been recently shown to induce a rewiring of the liver circadian transcriptome and metabolome, although in an obesity-independent manner. We therefore fed young (8 week old) C57Bl6 mice with HFD or its control diet for 7-weeks, a time when mice had not yet become obese, and performed circadian transcriptome analysis.
2017-08-10 | GSE84508 | GEO
Project description:Male C57BL/6J mice were fed a high-fat diet (HFD, 60 kcal% fat, D12492, Research Diets, Inc) or normal standard chow diet with 10 kal% fat (ND, D09100304, Research Diets, Inc). Specifically, 6-week-old mice were fed a HFD for 12 weeks to induce insulin resistance (HFD-12w group); 14-week-old mice were fed a HFD for 4 weeks to induce obesity (HFD-4w group). Control mice were fed a ND continuously for 12 weeks starting at 6 weeks of age (ND group). All mice reached the experimental endpoint at 18 weeks of age. Insulin sensitivity was measured by glucose tolerance test and insulin tolerance test. Mice that developed insulin resistance in HFD-12w group and obese mice with normal insulin sensitivity in HFD-4w group were used for further experiments. Mice in ND group were used as controls. Upon reaching the experimental endpoint, livers from three insulin-resistant mice, three insulin-sensitive obese mice, and three control mice were removed for RNA sequencing.
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Project description:To investigate whether lncRNAs are involved in intergenerational inheritance of obesity and obesity-induced decline in fertility, we divided mice into obesity (F0 mice fed a high-fat diet, F0-HFD) and non-obese (F0 mice fed normal chow, F0-NC) model groups and their male offspring (F1-HFD and F1-NC, respectively). We examined the differences in the expression levels of lncRNAs and mRNAs in the F0-HFD/F0-normal and F1-HFD/F1-normal groups. The results revealed similar expression patterns in the F1-HFD/F0-HFD groups at both the lncRNA and mRNA levels. The maximum difference in the lncRNA expression was observed between the F0-HFD and F0-NC groups. The differentially expressed lncRNA targets and mRNAs identified in our study are mainly involved in GnRH signalling pathway, metabolic process, and Hippo signalling pathway; similarly expressed lncRNAs and mRNAs in F1-HFD/F0-HFD are closely linked with G-protein coupled receptor signalling pathway, pancreatic polypeptide receptor activity, and lysine biosynthesis, which may play an important role in the molecular mechanism of intergenerational inheritance of obesity. Furthermore, potential genes that might play important roles in the pathogenesis of obesity-related low fertility were revealed by lncRNA-and mRNA-interaction studies based on the microarray expression profiles. In conclusion, we found that lncRNA could be involved in obesity-induced infertility by expressing abnormalities, which could act as genetic vectors of paternal inheritance of obesity.
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Project description:Younger age and obesity increase the incidence and rates of metastasis of triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer. The tissue microenvironment, specifically the extracellular matrix (ECM), is known to promote tumor invasion and metastasis. We sought to characterize the effect of both age and obesity on the ECM of mammary fat pads. We used a diet-induced obesity (DIO) model where 10-week-old female mice were fed a high-fat diet (HFD) for 16 weeks or a control chow diet (CD) where time points were every 4 weeks to monitor age and obesity HFD progression. We isolated the mammary fat pads to characterize the ECM at each time point. Utilizing proteomics, we found that the early stages of obesity were sufficient to induce distinct differences in the ECM composition of mammary fat pads that promote TNBC cell invasion. ECM proteins previously implicated in driving TNBC invasion Collagen IV and Collagen VI, were enriched with weight gain. Together these data implicate ECM changes in the primary tumor microenvironment as mechanisms by which age and obesity contribute to breast cancer progression.
2024-06-06 | PXD050250 | Pride
Project description:Although there are studies on obesity and sarcopenia, our understanding of obesity-mediated sarcopenia is insufficient. Additionally, no studies have investigated the application of luteolin in sarcopenia. We attempted to determine the effect of luteolin on obese sarcopenia in mice with high-fat diet (HFD)-induced obesity. Luteolin exerted suppressive effects on obesity, inflammation, and protein degradation in HFD-fed obese mice. Luteolin inhibited lipid infiltration into the muscle and decreased p38 and JNK activity and mRNA expression of inflammatory factors, such as TNFα, Tlr2, Tlr4, MCP1, and MMP2, in the muscle. Suppression of muscle inflammation by luteolin led to the inhibition of myostatin, FoxO, atrogin, and MuRF expression, which reduced protein degradation and improved muscle function. This is the first study to demonstrate that luteolin exerts a protective effect against obese sarcopenia, as its anti-obesity and anti-inflammatory activities inhibited protein degradation. Therefore, luteolin may be a useful supplement for prevention of obese sarcopenia.
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