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Expression profiling of aging liver in low-fat diet mice

ABSTRACT: Dietary interventions are effective ways to extend or shorten lifespan. By examining midlife hepatic gene expressions in mice under different dietary conditions, which resulted in different lifespans and aging-related phenotypes, we were able to identify genes and pathways that modulate the aging process. To determine how our dietary intervention-based transcriptomic approach for predicting aging-regulatory genes compares to more traditional approach of using age-dependent transcriptional changes, we examined the hepatic gene expression changes in LF-fed mice during aging at 4, 8, 13 and 21 months. Male C57BL/6J mice at 4 weeks of age were purchased from Shanghai Animal Co, Ltd. Mice were maintained under a 12-hour dark/light cycle (lights on at 6:30 am) at a temperature of 22 ± 3 °C in accredited animal facilities. Prior to the start of experiment, mice were maintained on a low-fat diet (Research Diets Inc., New Brunswick, NJ) for one week. Liver RNAs extracted from six male C57BL/6J mice of the same age were pooled at each age point to obtain an average microarray profile at 4, 8, 13 and 21 months.

ORGANISM(S): Mus musculus

SUBMITTER: Bing Zhou

PROVIDER: E-GEOD-36836 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression profiling of aging liver in low-fat diet mice

2012-03-28 | GSE36836 | GEO

Expression profiling of the effect of high-fat diet, low-fat diet, CR and exercise on mice liver

Project description:Dietary interventions are effective ways to extend or shorten lifespan. By examining midlife hepatic gene expressions in mice under different dietary conditions, which resulted in different lifespans and aging-related phenotypes, we were able to identify genes and pathways that modulate the aging process. We found that pathways transcriptionally correlated with diet-modulated lifespan and physiological changes were enriched for lifespan-modifying genes. Male C57BL/6J mice at 4 weeks of age were purchased from Shanghai Animal Co, Ltd. Mice were maintained under a 12-hour dark/light cycle (lights on at 6:30 am) at a temperature of 22 ± 3 °C in accredited animal facilities. Prior to the start of experiment, mice were maintained on a low-fat diet (Research Diets Inc., New Brunswick, NJ) for one week. At the age of 5 weeks, animals were randomly assigned to one of the 6 intervention groups (n = 30 for each group): feeding of a low-fat diet (10% fat, D12450B, Research Diets) ad libitum (LF) or with 30% calorie restriction (LF+CR) or with voluntary running exercise (LF+Ex), feeding of a high-fat diet (60% fat, D12492, Research Diets) ad libitum (HF) or with 30% calorie restriction (HF+CR) or with voluntary running exercise (HF+Ex). All mice were housed individually during the study. The daily consumption of food in LF and HF groups was recorded over a week and averaged to determine the amount of food for the following week for the LF+CR and HF+CR groups, respectively. After 1 week acclimation in cage with the locked running wheels, mice in the LF+Ex and HF+Ex groups were allowed free access to a running wheel, and the running distance and time were recorded automatically by the equipment. The hepatic transcriptional level for 3 mice from each intervention group at 62 weeks of age was analyzed using Affymetrix Mouse Genome 430 2.0 Arrays.

2012-03-27 | E-GEOD-36838 | biostudies-arrayexpress

Plasticity of life-long calorie restricted C57BL/6J mice in adapting to a medium-fat diet intervention at old age

Project description:Calorie restriction (CR) is a dietary regimen that supports healthy aging. In this study we investigated the systemic and liver-specific responses caused by a diet switch to a medium-fat (MF) diet in 24-month-old life-long, CR-exposed mice. This study aimed to increase the knowledge base on dietary alterations of gerontological relevance. Nine-week-old C57BL/6J mice were exposed either to a control, CR or MF diet. At the age of 24 months, a subset of mice of the CR group was transferred to ad libitum MF feeding (CR-MF).The mice were sacrificed at the age of 28 months, then biochemical and molecular analyses were performed. Our results showed that, despite the long-term exposure to the CR regimen, mice in the CR-MF group displayed hyperphagia, rapid weight gain, and hepatic steatosis. However, no hepatic fibrosis/injury or alteration in CR-improved survival was observed in the diet switch group. The liver transcriptomic profile of CR-MF mice largely shifted to a profile similar to the MF-fed animals but leaving ~22% of the 1578 differentially regulated genes between the CR and MF diet groups comparable with the expression of the life-long CR group. Therefore, although the diet switch was performed at an old age, the CR-MF-exposed mice showed plasticity in coping with the challenge of a MF diet without developing severe liver pathologies.

2018-01-24 | GSE102593 | GEO

Fibroblast growth factor 21 reflects liver fat accumulation and dysregulation of signalling pathways in the liver of C57BL/6J mice

Project description:Fibroblast growth factor 21 (Fgf21) has emerged as a potential plasma marker to diagnose non-alcoholic fatty liver disease (NAFLD). To study the molecular processes underlying the association of plasma Fgf21 with NAFLD, we explored the liver transcriptome data of a mild NAFLD model of aging C57BL/6J mice at 12, 24, and 28 months of age. The plasma Fgf21 level significantly correlated with intrahepatic triglyceride content. At the molecular level, elevated plasma Fgf21 levels were associated with dysregulated metabolic and cancer-related pathways. The up-regulated Fgf21 levels in NAFLD were implied to be a protective response against the NAFLD-induced adverse effects, e.g. lipotoxicity, oxidative stress and endoplasmic reticulum stress. An in vivo PPARalpha challenge demonstrated the dysregulation of PPARalpha signalling in the presence of NAFLD, which resulted in a stochastically increasing hepatic expression of Fgf21. Notably, elevated plasma Fgf21 was associated with declining expression of Klb, Fgf21â??s crucial co-receptor, which suggests a resistance to Fgf21. Therefore, although liver fat accumulation is a benign stage of NAFLD, the elevated plasma Fgf21 likely indicated vulnerability to metabolic stressors that may contribute towards progression to end-stage NAFLD. In conclusion, plasma levels of Fgf21 reflect liver fat accumulation and dysregulation of metabolic pathways in the liver. Male C57Bl/6J mice were divided to 3 dietary intervention groups: Control (AIN-93W), 30% calorie restriction (CR; AIN-93W-CR) and medium fat (MF; AIN-93W-MF; 25% energy from fat). Dietary interventions started at the age of 9 weeks and sacrifice was performed at the age of 6, 12, 24 and 28 months. We performed various measurements on metabolic parameters and gene expression analysis. This entry represents the microarray data.

2016-08-09 | E-GEOD-84495 | biostudies-arrayexpress

Expression data from mouse bone marrow adipocytes with age

Project description:The aim of this study was to characterize the age-related gene expression profiles between bone marrow adipocytes and peripheral white adipocytes. Alterations of gene expression with aging were analyzed in bone marrow and peripheral white adipocytes isolated from C57BL/6J male mice using Affymetrix Mouse Gene 1.0 ST arrays. Bone marrow adipocytes and peripheral white adipocytes (n=6-10 animals per group) were isolated from male C57BL/6J mice (6-months, 14-months and 18-months of age). Samples were grouped into cell type (bone marrow adipocytes vs. peripheral adipocytes) and age (6-month (6M), 14-month (14M) and 18-month (18M)).

2011-11-29 | E-GEOD-25905 | biostudies-arrayexpress

Negative reciprocal regulation between Sirt1 and Per2 modulates the circadian clock and aging (microarray expression)

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2016-08-08 | E-GEOD-54436 | biostudies-arrayexpress

Transcription profiling of mouse heart, brain, and skeletal muscle to determine the rffect of age, calorie restriction and resveratrol on gene expression

Project description:Resveratrol in high doses has been shown to extend lifespan in some studies in invertebrates and to prevent early mortality in mice fed a high-fat diet. We fed mice from middle age (14-months) to old age (30-months) either a control diet, a low dose of resveratrol (4.9 mg kg-1 day-1), or a calorie restricted (CR) diet and examined genome-wide transcriptional profiles. We report a striking transcriptional overlap of CR and resveratrol in heart, skeletal muscle and brain. Both dietary interventions inhibit gene expression profiles associated with cardiac and skeletal muscle aging. Gene expression profiling suggests that both CR and resveratrol may retard some aspects of aging through alterations in chromatin structure and transcription. Resveratrol, at doses that can be readily achieved in humans, fulfills the definition of a dietary compound that mimics some aspects of CR. Experiment Overall Design: Heart, neocortex tissue, and gastrocnemius muscle was collected from young and old mice at 5 and 30 months of age, respectively; mice were subjected to either a calorie restricted diet or a control diet supplemented with resveratrol

2008-06-18 | E-GEOD-11291 | biostudies-arrayexpress

Dietary curcumin ameliorates perturbed insulin homeostasis in the diet-induced obese aged mice

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.

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Expression data from liver of young and old rats fed on different dietary fat sources, namely virgin olive, sunflower or fish oils

Project description:Since the liver is the central organ of metabolism, changes in diet have a great impact on this organ and overall on health with aging. It is well known that dietary fat source strongly influences many parameters of the hepatic mitochondria. These changes includes modification of lipid composition of mitochondrial membrane, affecting the mtETC functions, oxidative stress and mtDNA alterations. We used microarrays to detail the changes in gene expression provides by feeding lifelong on different dietary fat sources, and identified distinct classes of up and down-regulated genes during aging under different dietary conditions. Rats were fed lifelong on a normolipidic diet (4% w/w) with virgin olive, sunflower or fish oil as dietary fat source. At 6 and 24 months, animals were killed and liver were removed for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain changes in gene expression due to both aging and dietary conditions. There were 6 experimental groups (virgin olive oil at 6 months, sunflower oil at 6 months, fish oil at 6 months, virgin olive oil at 24 months, sunflower oil at 24 months and fish oil at 24 months. 3 animals were studied of each experimental group, so a total of 18 samples were analyzed.

2014-03-26 | E-GEOD-56166 | biostudies-arrayexpress

Olive oil phenols and GE in the aging mouse brain

Project description:The aim of this study was to evaluate whether the dietary treatment with olive oil phenols modifies the profile of microRNA and gene expression in different areas of the aging mouse brain and to correlate these changes with the cognitive and motor changes observed in the same aging animals. C57Bl/6J mice were fed from middle age to senescence with extra-virgin olive oil (10% wt/wt dry diet) rich in polyphenols (H-EVOO group, total polyphenol dose/day, 6mg/kg) or with the same extra-virgin olive oil deprived of phenolic compounds (L-EVOO group). By whole gene expression analysis we identified 53 genes differentially expressed in the cortex of H-EVOO mice compared to L-EVOO mice and no genes differentially expressed in the cerebellum. Gene Set Expression analysis (GSEA) found 6 gene sets significantly modulated by the dietary treatments in cortex, like the agrin-related postsynaptic differentiation gene set, involved in cholinergic synaptic differentiation and maintenance, exerting effects on axonal and dendritic growth. miRNA profiling found only 6 miRNA differentially modulated after 12 months of feeding and 63 after six months. Among them we noted miRNAs previously associated to neurodegenerative disorders such as mir101, 8.5 time more expressed in the cortex of L-EVOO fed mice compared to the H-EVOO group and no expressed in young mice. We extended our analysis on cortex harvested from transgenic TgCRND8 mice, a model of Alzheimer's disease, observing an overall down-regulation of miRNAs compared to mice of the same age. On the contrary, the H-EVOO fed mice cortex showed expression profiles similar to those of young mice, results supporting our previous data demonstrating that extra virgin olive oil rich in polyphenols may improve some age-related dysfunctions.

2013-09-10 | E-MTAB-1530 | biostudies-arrayexpress

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