Ontology highlight
ABSTRACT:
PROVIDER: PRJNA889082 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21855500_1.fastq.gz | Fastqsanger.gz | |||
| SRR21855500_2.fastq.gz | Fastqsanger.gz | |||
| SRR21855600_1.fastq.gz | Fastqsanger.gz | |||
| SRR21855600_2.fastq.gz | Fastqsanger.gz | |||
| SRR21855700_1.fastq.gz | Fastqsanger.gz |
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Project description:The aim of this study was to investigate transcriptome signatures in human subcutaneous white adipose tissue (sWAT) before and after long-term weight changes and assess their predictive value for body weight change. Long-term body weight change in adult women associates with altered sWAT transcriptome. Expression of genes associated with inflammation, insulin response, adipogenesis and lipogenesis are linked to weight loss. However, other pathways such as protein homeostasis not only associate with but also predict future weight gain suggesting that intrinsic factors in sWAT impact tissue expansion.
2019-05-01 | GSE126963 | GEO
Project description:Background: Diet induced weight reduction promotes a decrease in resting energy expenditure that could partly explain the difficulty to maintain reduced body mass. Whether this reduction remains after stabilized weight loss is still controversial. The molecular mechanisms are unknown. Objective: To investigate the effect of a stabilized 10%-weight loss on resting metabolic rate, body composition and skeletal muscle gene expression profile in obese women. Design: Obese women were successively submitted to a 4-w very low-calorie diet, a 3-6-wk low-calorie diet, and a 4-wk weight maintenance program to achieve a 10% weight loss. Resting energy expenditure, body composition, plasma parameters and skeletal muscle transcriptome were compared before weight loss and during stabilized weight reduction. Results: Energy restriction caused an 11% weight loss. Stabilization to the new weight was accompanied by an 11% decrease of the resting metabolic rate normalized to the body cellular mass which was below that of lean subjects. The range of the changes in the skeletal muscle transcriptome was modest. The main regulated genes were that of slow/oxidative fiber markers which were overexpressed and the gene encoding the glucose metabolism inhibitor PDK4 which was down-regulated. The knowledge based approach, gene set enrichment analysis, identified pathways related to insulin and interleukin 6 and long term calorie restriction adaptations during weight loss. Set of arrays that are part of repeated experiments Keywords: Biological Replicate
2008-03-26 | GSE9917 | GEO
Project description:Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity. However, maintaining weight loss is a considerable challenge, especially as the body appears to retain an obesogenic memory that defends against body weight changes. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nuclei RNA-sequencing, we show that both human and mouse adipose tissue retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the mouse adipocyte epigenome, negatively affecting their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely based on stable epigenetic changes, in mouse adipocytes, and likely other cell types. These changes appear to prime cells for pathological responses in an obesogenic environment, contributing to the problematic "yo-yo" effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.
2024-11-14 | GSE236579 | GEO
Project description:Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity. However, maintaining weight loss is a considerable challenge, especially as the body appears to retain an obesogenic memory that defends against body weight changes. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nuclei RNA-sequencing, we show that both human and mouse adipose tissue retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the mouse adipocyte epigenome, negatively affecting their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely based on stable epigenetic changes, in mouse adipocytes, and likely other cell types. These changes appear to prime cells for pathological responses in an obesogenic environment, contributing to the problematic "yo-yo" effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.
2024-11-14 | GSE236575 | GEO
Project description:Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity. However, maintaining weight loss is a considerable challenge, especially as the body appears to retain an obesogenic memory that defends against body weight changes. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nuclei RNA-sequencing, we show that both human and mouse adipose tissue retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the mouse adipocyte epigenome, negatively affecting their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely based on stable epigenetic changes, in mouse adipocytes, and likely other cell types. These changes appear to prime cells for pathological responses in an obesogenic environment, contributing to the problematic "yo-yo" effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.
2024-11-14 | GSE236578 | GEO
Project description:Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity. However, maintaining weight loss is a considerable challenge, especially as the body appears to retain an obesogenic memory that defends against body weight changes. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nuclei RNA-sequencing, we show that both human and mouse adipose tissue retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the mouse adipocyte epigenome, negatively affecting their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely based on stable epigenetic changes, in mouse adipocytes, and likely other cell types. These changes appear to prime cells for pathological responses in an obesogenic environment, contributing to the problematic "yo-yo" effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.
2024-11-14 | GSE236577 | GEO
Project description:We explored the effect of long-term high-concentrate diet feeding on ruminal pH and fermentation, and its effect on the rumen epithelial transcriptomes in Japanese Black beef cattle during a 20-month fattening period.
2019-06-22 | GSE133152 | GEO
Project description:The experiment was conducted at the Kołuda Wielka Experimental Station of the National Research Institute of Animal Production (Kołuda Wielka, Poland). All birds were kept in semi-intensive rearing system according to the oat-fattening technology. At 15.5 weeks of age, 8 geese were selected and divided into two groups (n=4) depending on final body weight. Group I (light) were geese with the flock average weight of 7,10 kg, group II (heavy) consisted of geese with above-average growth potential, which achieved a body weight of 7,95 kg during the same time. Up to 20 min after slaughter, the whole pituitary and hypothalamus were collected and stabilized in RNAlater solution to RNA isolation purpose.
2021-03-02 | GSE167941 | GEO
Project description:Background. Differential gene expression in adipose tissue during diet-induced weight loss followed by a weight stability period is not well characterized. Markers of these processes may provide a deeper understanding of the underlying mechanisms. Objective. To identify differentially expressed genes in human adipose tissue during weight loss and weight maintenance after weight loss. Design. RNA from subcutaneous abdominal adipose tissue from nine obese subjects was obtained and analyzed at baseline, after weight reduction on a low calorie diet (LCD), and after a period of group therapy in order to maintain weight stability. Results. Subjects lost 18.8 + 5.4% of their body weight during the LCD and maintained this weight during group therapy. Insulin sensitivity (HOMA) improved after weight loss with no further improvement during weight maintenance. Cyclin-dependent kinase inhibitor 2B (CDKN2B) and JAZF zinc finger 1 (JAZF1), associated with type 2 diabetes, were downregulated. We could also confirm the downregulation of candidates for obesity and related traits, such as tenomodulin (TNMD) and matrix metallopeptidase 9 (MMP9), with weight loss. The expression of other candidates, such as cell death-inducing DFFA-like effector A (CIDEA) and stearoyl-CoA desaturase (SCD) were upregulated during weight loss but returned to baseline levels during weight maintenance. Conclusion. Genes in the adipose tissue are differentially expressed during weight loss and weight maintenance after weight loss. Genes that show sustained regulation may be of potential interest as markers of the beneficial effects of weight loss whereas others seem to be primarily involved in the process of weight loss itself. Nine participants were prescribed a low calorie diet (LCD) containing 1200 kcal/day for approximately three months (101 ± 26 days). Following the weight reduction phase the participants attended a six month follow-up period (167 ± 37 days). By protocol design, subjects were eligible to enter the study if they had lost at least 10% of their initial body weight during the LCD-period and maintained this weight (+5%) after group therapy. Subcutaneous adipose tissue samples were obtained at three time-points: (i) at baseline, (ii) after weight reduction when subjects were no longer losing weight, and (iii) after the group therapy weight maintenance phase.
2012-01-31 | E-GEOD-35411 | biostudies-arrayexpress
Project description:Purpose: The present study was designed to identify both differentially expressed (DE) genes in the liver tissues of fattening Merino lambs and differences in metabolites accumulated in plasma, thus trying to identify modified metabolic pathways as a consequence of milk restriction during the suckling period. Methods: Twenty-four male Merino lambs were assigned to 2 different groups (n=12 per dietary treatment). The first group (ad libitum, ADL) was kept permanently with the dams whereas the other group (restricted, RES) was milk restricted. When they reached 15 kg of live body weight, all the lambs were offered the same complete pelleted diet at the same level to ensure no differences in dry matter intake. All the lambs were slaughtered with 27 kg. For transcriptomic analysis, 4 liver samples representative from each group (8 samples in total) were selected for RNA sequencing methodology (RNA-seq). Results: 38 DE annotated genes were identified by RNA-seq, with 23 DE genes being down-regulated and 15 up-regulated in the liver of RES relative to the ADL group (P < 0.10). In general, those genes and pathways involved in protein synthesis or protease inhibitors were down-regulated in the RES group, whereas those related to proteolytic degradation were up-regultated, thus suggesting a higher catabolism of proteins in these lambs. Contrarily, RES lambs showed over-expression of xenobiotic metabolism pathways, whereas those genes related to β-oxidation of fatty acids were down expressed. Conclusions: According to the data obtained, early feed restriction during the suckling period of Merino lambs promoted long-term effects on hepatic transcriptomic profile and plasma metabolic profile wich might have modified fatty acids metabolism, catabolism of proteins and detoxification of xenobiotics, thus reducing feed efficiency of fattening period.
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