Weight loss resulted in increased expression of the anti-inflammatory protein, CRISPLD2, in mouse adipose tissue
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ABSTRACT:
PROVIDER: PRJNA558135 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9881220_1.fastq.gz | Fastqsanger.gz | |||
| SRR9881220_2.fastq.gz | Fastqsanger.gz | |||
| SRR9881221_1.fastq.gz | Fastqsanger.gz | |||
| SRR9881221_2.fastq.gz | Fastqsanger.gz | |||
| SRR9881222_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: NGS was used to determine if a distinct transcriptomic profile is observed between lean, obese and weight loss fat Methods: We carried out RNA-Seq analysis of epididymal adipose mice ad libitum fed for 10 weeks either a high fat diet (HFD) or a regular chow diet (RD), versus a cohort of mice fed HFD for the first 5 weeks before swapping to RD for the remainder (SWAP). Results: SWAP feeding resulted in weight loss with a parallel improvement in insulin sensitivity. RNA-Seq revealed several transcriptomic signatures distinct to SWAP adipose, distinguished from both RD and HFD adipose. We found a unique up-regulated mRNA encoding a secreted, LPS-binding glycoprotein, CRISPLD2, in SWAP adipose tissue. While cellular CRISPLD2 protein levels were unchanged, plasma CRIPSLD2 levels increased in SWAP mice following weight loss, and can correlate with insulin sensitivity. Conclusions: Taken together, our data demonstrate that CRISPLD2 is a circulating adipokine that may regulate adipocyte remodeling during weight loss.
2019-08-02 | GSE135239 | GEO
Project description:Most individuals do not maintain weight loss, and weight regain increases cardio-metabolic risk beyond that of obesity. Adipose inflammation directly contributes to insulin resistance; however, immune-related changes that occur with weight loss and weight regain are not well understood. Single cell RNA-sequencing was completed with CITE-sequencing and biological replicates to profile changes in murine immune subpopulations following obesity, weight loss, and weight cycling. Weight loss normalized glucose tolerance, however, type 2 immune cells did not repopulate adipose following weight loss. Many inflammatory populations persisted with weight loss and increased further following weight regain. Obesity drove T cell exhaustion and broad increases in antigen presentation, lipid handing, and inflammation that persisted with weight loss and weight cycling. This work provides critical groundwork for understanding the immunological causes of weight cycling-accelerated metabolic disease.
2022-03-04 | GSE182233 | 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.
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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.
2012-01-31 | GSE35411 | GEO
Project description:The main aim of this experiment was to investigate gene expression on human subcutaneous adipose tissue following bariatric surgery. Our questions consisted in understanding how gene expression was linked to clinical parameters of obese patients and whether this drastic weight loss was discriminated this data.
2015-08-19 | GSE72158 | GEO
Project description:We investigated the regulation of adipose tissue (AT) gene expression during different phases of a dietary weight loss program and its relationship with insulin sensitivity. Obese women followed a weight reduction program composed of an energy restriction phase (ER) with a 4-week very-low-calorie diet and a weight stabilization period (WS) composed of a 2-month low-calorie diet followed by 3 to 4 months of a weight maintenance diet. At each time point, body composition, plasma parameters and glucose disposal rate were assessed and subcutaneous AT biopsies were performed. Variations in mRNA levels were determined using DNA microarrays and reverse transcription-quantitative PCR. Distinct sets of AT genes are regulated during calorie restriction and weight stabilization revealing an unexpected temporal pattern in the link between AT and insulin sensitivity during weight loss.
2009-05-12 | GSE11975 | GEO
Project description:Lipedema is a lipodystrophic disease characterized by marked increases in lower-body subcutaneous adipose tissue, anecdotally reported to: i) increase inflammation and fibrosis and impair microvascular and lymphatic circulation in the affected adipose tissue, ii) reduce risk of developing obesity-related cardiometabolic abnormalities; and iii) be resistant to diet-induced weight loss. To further our understanding of lipedema, we examined body composition, metabolic health and adipose tissue bology in women with obesity and lipedema (Obese-LIP) at baseline and following ~9% diet-induced weight loss. At baseline, people with Obese-LIP had ~23% greater leg fat mass, ~11% lower android-to-gynoid ratio and ~54% greater insulin sensitivity compared to women matched on age, body mass index and whole-body fat mass. In the Obese-LIP group, total and proinflammatory macrophage content and expression of inflammation and fibrosis-related genes were greater while lymph/angiogenesis-related genes were lower in subcutaneous femoral compared to abdominal adipose tissue. Diet-induced weight loss improved insulin sensitivity and decreased total fat mass due to similar reductions in abdominal and leg fat masses, with minimal effect on markers of adipose tissue inflammation/fibrosis and lymph/angiogenesis. Our study provides important insights into the pathophysiology of lipedema and suggests diet-induced weight loss should be the cornerstone therapy in people with Obese-LIP.
2024-10-15 | GSE274137 | GEO
Project description:ObjectiveObesity is a major risk factor for cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus, whereas weight loss is associated with improved health outcomes. It is therefore important to learn how adipose contraction during weight loss contributes to improved health. It was hypothesized that adipose tissue undergoing weight loss would have a unique transcriptomic profile, expressing specific genes that might improve health.MethodsThis study conducted an RNA-sequencing analysis of the epididymal adipose tissue of mice fed either a high-fat diet (HFD) or a regular rodent chow diet (RD) ad libitum for 10 weeks versus a cohort of mice fed HFD for the first 5 weeks before being swapped to an RD for the remainder of the study (swapped diet [SWAP]).ResultsThe swapped diet resulted in weight loss, with a parallel improvement in insulin sensitivity. RNA sequencing revealed several transcriptomic signatures distinct to adipose tissue in SWAP mice, distinguished from both RD and HFD adipose tissue. The analysis found a unique upregulated mRNA that encodes a secreted lipopolysaccharide-binding glycoprotein (CRISPLD2) in adipose tissue. Whereas cellular CRISPLD2 protein levels were unchanged, plasma CRIPSLD2 levels increased in SWAP mice following weight loss and could correlate with insulin sensitivity.ConclusionsTaken together, these data demonstrate that CRISPLD2 is a circulating adipokine that may regulate adipocyte remodeling during weight loss.
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Project description:RNA Sequencing of human adipose tissue before and after diet-induced weight loss
2017-10-28 | GSE106289 | GEO
Project description:We investigated the regulation of adipose tissue (AT) gene expression during different phases of a dietary weight loss program and its relationship with insulin sensitivity. Obese women followed a weight reduction program composed of an energy restriction phase (ER) with a 4-week very-low-calorie diet and a weight stabilization period (WS) composed of a 2-month low-calorie diet followed by 3 to 4 months of a weight maintenance diet. At each time point, body composition, plasma parameters and glucose disposal rate were assessed and subcutaneous AT biopsies were performed. Variations in mRNA levels were determined using DNA microarrays and reverse transcription-quantitative PCR. Distinct sets of AT genes are regulated during calorie restriction and weight stabilization revealing an unexpected temporal pattern in the link between AT and insulin sensitivity during weight loss. Experiment Overall Design: Fifteen obese premenopausal women were recruited at the Third Faculty of Medicine of Charles University and at the Institute for Mother and Child Care in Prague, Czech Republic. During the first four weeks of the dietary intervention program, the subjects received an energy restricted diet of 800 kcal/day (liquid formula diet, Redita, Promil). During the next two months, a low-calorie diet was designed to provide 600 kcal/day less than the individually estimated energy requirement based on an initial resting metabolic rate multiplied by 1.3. Following this, subjects entered a weight maintenance phase for a period of 3 to 4 months, during which the patients were instructed to keep their weight stable. A complete clinical investigation in the fasting state was realized before and at the end of each phase. Needle microbiopsy of subcutaneous AT was performed under local anesthesia (1% Xylocaine) from the abdominal region (14â20 cm lateral to the umbilicus). Total RNA were isolated from AT samples with Qiagen RNeasy kit. RNA quantity and quality were checked with the Experion automated electrophoresis system (BioRad laboratories). We performed a whole transcriptome analysis comparing 1) before vs. after the initial 4 weeks severe energy restriction (ER), 2) after energy restriction vs. after weight stabilization (WS) and 3) before dietary intervention vs. after weight stabilization (DI). Eight subjects representative of the cohort were selected, matched for high quality of total RNA samples, insulin sensitivity and weight changes during the study. Targets for microarray experiments were generated from 500 ng of total RNA with Agilent low RNA input amplification kit (Agilent Technologies) and hybridized to whole genome 44k oligonucleotide arrays (Agilent Technologies). Each combination of samples was analyzed twice using a dye swap design (i.e., a total of 48 hybridizations). Data acquisition from microarrays was obtained with a GenePix 4000B scanner (Axon instruments) and image processing was performed with Feature Extraction 8.5 (Agilent Technologies). Raw data were normalized with a global Lowess procedure and filtered with R package LIMMA (Bioconductor). Outlier replicates and spots with a signal to noise ratio lesser than 2 on both red and green channel were eliminated from our analyses. Mean log ratios were calculated from paired duplicates before normalization. Differentially expressed genes were identified with Significance Analysis of Microarray (SAM) procedure.
2009-05-16 | E-GEOD-11975 | biostudies-arrayexpress