Genome-wide analysis of gene expression in adipose tissue of female mice after continuous high fat diet feeding
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE37238 | GEO | 2013/05/10
SECONDARY ACCESSION(S): PRJNA158967
REPOSITORIES: GEO
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Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes. Total RNA was obtained from adipose tissue of the HFD fed mice, including F0, F1 and F2 generations. Normal chow fed mice were used as controls.
2013-05-10 | E-GEOD-37238 | biostudies-arrayexpress
Project description:There is a growing body of evidence that inadequate maternal nutrition during gestation can have immediate and life-long effects on offspring. However, little is known about the reproductive effects of maternal gestational nutrition in offspring males. Here, using a sheep model of poor maternal nutrition (restricted- or over-feeding) during gestation, we found that poor maternal gestational nutrition does not affect semen characteristics (i.e. volume, sperm concentration, pH, sperm motility, sperm morphology) and scrotal circumference in offspring. However, by evaluating associations between poor maternal gestational nutrition and altered small non-cording RNAs (sncRNAs) and DNA methylation in offspring sperm, we demonstrated that poor maternal gestational nutrition alters sperm sncRNA composition and expression. Whole genome bisulfite sequencing further identified genomic regions with increased or decreased DNA methylation in sperm in response to poor maternal gestational nutrition. These findings imply that maternal diet-induced epigenetic errors can accumulate in sperm to worsen developmental outcomes of future generations.
2024-04-04 | GSE225924 | GEO
Project description:There is a growing body of evidence that inadequate maternal nutrition during gestation can have immediate and life-long effects on offspring. However, little is known about the reproductive effects of maternal gestational nutrition in offspring males. Here, using a sheep model of poor maternal nutrition (restricted- or over-feeding) during gestation, we found that poor maternal gestational nutrition does not affect semen characteristics (i.e. volume, sperm concentration, pH, sperm motility, sperm morphology) and scrotal circumference in offspring. However, by evaluating associations between poor maternal gestational nutrition and altered small non-cording RNAs (sncRNAs) and DNA methylation in offspring sperm, we demonstrated that poor maternal gestational nutrition alters sperm sncRNA composition and expression. Whole genome bisulfite sequencing further identified genomic regions with increased or decreased DNA methylation in sperm in response to poor maternal gestational nutrition. These findings imply that maternal diet-induced epigenetic errors can accumulate in sperm to worsen developmental outcomes of future generations.
2024-04-04 | GSE225985 | GEO
Project description:Physical inactivity and over-nutrition are key risk factors for metabolic diseases, with impaired skeletal muscle gene transcription and metabolic function proposed as key etiological factors. Here, we have used RNA-seq to assessed the skeletal muscle transcriptome from mice fed a control or high fat diet (HFD), both pre- and 3h post-exercise. HFD up-regulated genes involved in lipid catabolism in skeletal muscle (quadriceps), while decreasing 241 exercise-responsive genes related to skeletal muscle plasticity. Collectively, this experimental approach provides a suitable resource to study transcriptional and metabolic networks in skeletal muscle in the context of health and disease.
2017-10-31 | GSE97718 | GEO
Project description:Childhood obesity traces its roots to the parental lifestyle and eating habits. Familial clustering of obesity indicates that children’s feeding behavior is a result of a complex interplay between cultural inheritance, genetics, and epigenetics. In the current study, we asked a question if epigenetic factors, such as ancestral diet, could program offspring feeding behavior in a fruit fly model. Here we show that ancestral caloric overload produces a generational shift in the offspring’s feeding behavior, with a concomitant alteration in activity, triglycerides, and brain mitochondrial density. Mechanistically, we find the generational changes to be associated with alterations in brain mitochondrial proteome and miRNAs. The findings identify ancestral nutrition as a critical factor in the generational programming of feeding behavior.
2023-04-22 | PXD033363 | JPOST Repository
Project description:Purpose: To investiagte why maternal obesity induces the susceptibility of offspring to diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) over generations upon over nutrition.The goals of this study are to find over-generationally altered genes and miRNAs which may contribute the accumulative progeny susceptibility to HCC under over nutrition. Methods: C57BL/6 female mice (F0 generation) were fed with either normal chow (NC) or HFD (60% kcal fat) from 1-month to 3-month old, and mated with NC-fed male mice to produce F1 generation. The F2 generation was similarly created. Male offspring of the F0, F1 and F2 generations were intraperitoneally injected with DEN at 2-weeks-old, and kept inmaintained on HFD and named as H1D, H2D and H3D groups, respectively. Male offspring of the F0 generation injected with PBS (Nor group) or DEN (NCD group) at the same age and kept inmaintained on NC. All groups were sacrificed at 40-weeks-old. Liver mRNA profiles and miRNA profiles from the different offspring groups were generated by LncRNA sequencing and small RNA sequencing. Results: We identified many over-generationally changed genes and miRNAs in the offspring by RNA-sequencing. Conclusions: The study revealed an important role of miRNA and targeting genes in regulating the incidence of HCC in the offspring of maternal-lineage under multi-generational HFD exposure, which has a profound effect on exploring the link between maternal obesity and the development of diseases in offspring.
2021-07-01 | GSE117539 | GEO
Project description:To understand how gonadal adpose tissue is altered via maternal HFD feeding, we fed dams a 60% HFD only during weaning. These data are from the offspring, both control and HFD fed male mice
2023-12-08 | GSE227337 | GEO
Project description:Maternal nutrition during embryonic development and lactation influences multiple aspects of offspring health. Using mice, this study investigates the effects of maternal caloric restriction (CR) during mid-gestation and lactation on offspring neonatal development and on adult metabolic function when challenged by a high fat diet (HFD). The CR maternal model produced male and female offspring that were significantly smaller, in terms of weight and length, and females had delayed puberty. Adult offspring born to CR dams had a sexually dimorphic response to the high fat diet. Compared to offspring of maternal control dams, adult female, but not male, CR offspring gained more weight in response to high fat diet at 10 weeks. In adipose tissue of male HFD offspring, maternal undernutrition resulted in blunted expression of genes associated with weight gain and increased expression of genes that protect against weight gain. Regardless of maternal nutrition status, HFD male offspring showed increased expression of genes associated with nonalcoholic liver disease (NAFLD). Furthermore, we observed significant, sexually dimorphic differences in serum TSH. These data reveal tissue- and sex-specific changes in gene and hormone regulation following mild maternal undernutrition, which may offer protection against diet induced weight gain in adult male offspring.
2024-01-04 | GSE247985 | GEO
Project description:To identify novel neurocircuits activated upon short-term HFD feeding, we employed phosphoribotrap-profiling, which allows for the unbiased identification of alterations in neuronal activation via immunoprecipitation of phosphorylated S6 ribosomal protein-tagged ribosomes from hypothalamic extracts of mice exposed to either 3 days of normal chow diet or HFD-feeding. We have analyzed mRNA selectively expressed in hypothalamic cells activated by a either normal chow diet (NCD)-feeding for 3 days or high fat diet (HFD)-feeding for 3 days. 10-week-old male C57/BL6N mice were put either on a normal chow diet or a high fat diet for 3 days. Afterwards, mice were sacrificed by cervical dislocation. The hypothalamus was rapidly dissected using a stainless steel brain matrix and immediately frozen in liquid nitrogen. Hypothalamic tissues were pooled (8 per IP).
2020-04-16 | GSE137737 | GEO
Project description:Using standardized, semipurified diets is a crucial factor for reproducibility of experimental nutritional studies. For the purpose of comparability and integration of research, two European consortia, Mitofood and BIOCLAIMS, proposed an AIN-93-based standard reference diet, the standardized BIOCLAIMS low-fat diet (LFD) as well as a high-fat diet (HFD). In order to evaluate the BIOCLAIMS LFD and HFD, we performed short-term (5 days) and long-term (12 weeks) feeding experiments using male C57BL/6 mice. The HFD has the same composition as the LFD except the fat content is increased to 40% energy in exchange for carbohydrates. Both diets were accepted by the animals and proof of principle was given that the BIOCLAIMS HFD increases body weight and body fat and affects glucose homeostasis. Short-term feeding trials (5 days) were performed in order to identify metabolic and molecular parameters which can serve as acute predictors for metabolic disorders due to high-fat diet-induced obesity. We analyzed gene expression in gonadal white adipose tissue of short- and long-term fed animals with whole genome microarrays. The BIOCLAIMS HFD strongly influenced gene expression in white adipose tissue after short- and long-term intervention. A total number of 973 and 4678 transcripts were significantly different between both diets after 5 days feeding and 12 weeks feeding, respectively. A total number of 764 transcripts encoding 549 genes were significantly differentially regulated between LF and HF animals after 12 weeks feeding as well as after 5 days feeding. Of these 549 overlapping genes, a substantial number (434 genes) were expressed at a lower level and 115 genes were expressed at a higher level in the HF mice compared to the LF mice. Without exception, all genes were regulated equally. Pathway analysis revealed a prominent role for genes involved in lipid metabolism, carbohydrate metabolism and oxidative phosphorylation. This was confirmed by quantitative real-time reverse transcription PCR. The high predictive value of gene expression changes in our short-term study compared to long-term high fat feeding is a promising step to get well-defined, early biomarkers that could shorten animal trials considerably and allow a more rapid and efficient screening of different compounds. C57BL/6J wildtype male mice, aged 12 weeks, received a low-fat diet or a high-fat diet for 5 days or 12 weeks. After sacrification, white adipose tissue depots were dissected, and immediately snap frozen in liquid nitrogen. Total RNA was isolated, quantified and qualified, and subsequently used for global gene expression profiling using Agilent 4x44K microarrays.
2013-08-27 | E-GEOD-38337 | biostudies-arrayexpress