Increased adipose tissue fibrogenesis, not impaired expandability, is associated with nonalcoholic fatty liver disease
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ABSTRACT:
PROVIDER: PRJNA670900 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12883700.fastq.gz | Fastqsanger.gz | |||
| SRR12883701.fastq.gz | Fastqsanger.gz | |||
| SRR12883702.fastq.gz | Fastqsanger.gz | |||
| SRR12883703.fastq.gz | Fastqsanger.gz | |||
| SRR12883704.fastq.gz | Fastqsanger.gz |
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Project description:BACKGROUND AND AIMS: It is proposed that impaired expansion of subcutaneous adipose tissue (SAT), caused in part by an increase in adipose tissue fibrosis, redirects fatty acids to the liver and other organs, leading to ectopic lipid accumulation and insulin resistance. We therefore evaluated whether a decrease in SAT expandability, assessed by measuring SAT lipogenesis (triglyceride production), and an increase in SAT fibrogenesis (collagen production) are associated with nonalcoholic fatty liver disease (NAFLD) and insulin resistance in people with obesity. APPROACH AND RESULTS: In vivo SAT lipogenesis and fibrogenesis, the expression of SAT genes involved in extracellular matrix (ECM) formation, and insulin sensitivity were assessed in three groups stratified by adiposity, insulin sensitivity and intrahepatic triglyceride (IHTG) content: 1) healthy lean (Lean-NL; n=12); 2) obese with normal IHTG content and normal glucose tolerance (Ob-NL; n=25); and 3) obese with NAFLD and abnormal glucose metabolism (Ob-NAFLD; n=25). Abdominal SAT total triglyceride synthesis rates were greater in the Ob-NL (65.9±4.6 g/wk) and Ob-NAFLD (71.1±6.7 g/wk) than the Lean-NL group (16.2±2.8 g/wk), without a difference between the obese groups. Abdominal SAT collagen synthesis rate and the composite expression of collagen genes progressively increased from Lean-NL to Ob-NL to Ob-NAFLD and were greater in the Ob-NAFLD than the Ob-NL group (P<0.05). Collagen synthesis rate and the composite expression of collagen genes correlated with factors that regulate collagen production, including circulating insulin and fibrogenic factors in SAT (all P<0.001). CONCLUSIONS: Adipose tissue lipogenesis and expandability are not impaired in people with obesity and NAFLD. However, SAT fibrogenesis and extracellular matrix remodeling are greater in people with obesity and NAFLD than in those with obesity and normal IHTG content. ClinicalTrials.gov number: NCT02706262.
2021-10-01 | GSE159924 | GEO
Project description:The current study was designed to determine if dietary fatty acid concentration and composition affects the development and progression of nonalcoholic fatty liver disease. Male SD rats were overfed diets low (5%) or high (70%) fat diets via total enteral nutrition where the fat source was olive oil (monounsaturated), or corn oil (polyunsaturated). Overfeeding 5% corn oil produced little steatosis relative to feeding 5% olive oil. This was associated with lower fatty acid synthesis and reduced SREBP-c signaling in the 5% corn oil group. Overfeeding 70% fat diets increased steatosis and lead to increased liver necrosis in the 70% corn oil but not olive oil group. Increased injury after feeding polyunsaturated fat diets was linked to peroxidizability of hepatic free fatty acids and triglycerides and appearance of peroxidaized lipid products HETES and HODES previously linked to clinical nonalcoholic steatohepatitis. Male SD rats were overfed diets low (5%) or high (70%) fat diets via total enteral nutrition where the fat source was olive oil (monounsaturated) or corn oil (polyunsaturated).
2011-10-23 | E-GEOD-33166 | biostudies-arrayexpress
Project description:The aim of this sudy is to investigate the prevalence of colorectal cancer (CRC) in patients with nonalcoholic fatty liver disease (NAFLD) and evaluate whether NAFLD is a risk factor for CRC.
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Project description:This SuperSeries is composed of the following subset Series: GSE30447: Foxa1 Reduces Lipid Accumulation in Human Hepatocytes and Is Down-regulated in Nonalcoholic Fatty Liver (HepG2 data) GSE30450: Foxa1 Reduces Lipid Accumulation in Human Hepatocytes and Is Down-regulated in Nonalcoholic Fatty Liver (hepatocytes data) Refer to individual Series
2011-07-07 | E-GEOD-30451 | biostudies-arrayexpress
Project description:The current study was designed to determine if dietary fatty acid concentration and composition affects the development and progression of nonalcoholic fatty liver disease. Male SD rats were overfed diets low (5%) or high (70%) fat diets via total enteral nutrition where the fat source was olive oil (monounsaturated), or corn oil (polyunsaturated). Overfeeding 5% corn oil produced little steatosis relative to feeding 5% olive oil. This was associated with lower fatty acid synthesis and reduced SREBP-c signaling in the 5% corn oil group. Overfeeding 70% fat diets increased steatosis and lead to increased liver necrosis in the 70% corn oil but not olive oil group. Increased injury after feeding polyunsaturated fat diets was linked to peroxidizability of hepatic free fatty acids and triglycerides and appearance of peroxidaized lipid products HETES and HODES previously linked to clinical nonalcoholic steatohepatitis.
2011-10-24 | GSE33166 | GEO
Project description:Background and aimsIt is proposed that impaired expansion of subcutaneous adipose tissue (SAT) and an increase in adipose tissue (AT) fibrosis causes ectopic lipid accumulation, insulin resistance (IR), and metabolically unhealthy obesity. We therefore evaluated whether a decrease in SAT expandability, assessed by measuring SAT lipogenesis (triglyceride [TG] production), and an increase in SAT fibrogenesis (collagen production) are associated with NAFLD and IR in persons with obesity.Approach and resultsIn vivo abdominal SAT lipogenesis and fibrogenesis, expression of SAT genes involved in extracellular matrix (ECM) formation, and insulin sensitivity were assessed in three groups of participants stratified by adiposity and intrahepatic TG (IHTG) content: (1) healthy lean with normal IHTG content (Lean-NL; n = 12); (2) obese with normal IHTG content and normal glucose tolerance (Ob-NL; n = 25); and (3) obese with NAFLD and abnormal glucose metabolism (Ob-NAFLD; n = 25). Abdominal SAT TG synthesis rates were greater (P < 0.05) in both the Ob-NL (65.9 ± 4.6 g/wk) and Ob-NAFLD groups (71.1 ± 6.7 g/wk) than the Lean-NL group (16.2 ± 2.8 g/wk) without a difference between the Ob-NL and Ob-NAFLD groups. Abdominal SAT collagen synthesis rate and the composite expression of genes encoding collagens progressively increased from the Lean-NL to the Ob-NL to the Ob-NAFLD groups and were greater in the Ob-NAFLD than the Ob-NL group (P < 0.05). Composite expression of collagen genes was inversely correlated with both hepatic and whole-body insulin sensitivity (P < 0.001).ConclusionsAT expandability is not impaired in persons with obesity and NAFLD. However, SAT fibrogenesis is greater in persons with obesity and NAFLD than in those with obesity and normal IHTG content, and is inversely correlated with both hepatic and whole-body insulin sensitivity.
| S-EPMC8559258 | biostudies-literature
Project description:Nonalcoholic fatty liver disease represents a spectrum of pathology that ranges from benign steatosis to potentially-progressive steatohepatitis and affects more than 30% of US adults. Advanced NAFLD is associated with increased morbidity and mortality from cirrhosis, primary liver cancer, cardiovascular disease and extrahepatic cancers. Accurate identification of patients at risk for advanced NAFLD is challenging. The aims of this study were to define the liver gene expression patterns that distinguish mild from advanced NAFLD and to develop a gene expression profile associated with advanced NAFLD. We analyzed total RNA from 72 patients with NAFLD (40 with mild NAFLD, fibrosis stage 0-1 and 32 with advanced NAFLD, fibrosis stage 3-4) and developed a gene profile associated with advanced NAFLD. This dataset is part of the TransQST collection.
2013-08-30 | E-GEOD-49541 | biostudies-arrayexpress
Project description:Purpose: We investigated the tetrachloroethylene associated changes in kidney transcriptomes among healthy mice, nonalcoholic fatty liver disease mice, and nonalcoholic steatohepatitis mice.
2019-02-13 | GSE115641 | GEO
Project description:We analyzed the transcriptome for drug metabolism genes of 35 human (17 healthy control (HC), and 18 nonalcoholic fatty liver disease (NAFLD)) liver tissues, obtained during laparoscopic cholecystectomy. The aim of our study is to identify the drug metabolism genes significantly regulated by NAFLD at the transcriptome level.
2022-12-19 | E-MTAB-12445 | biostudies-arrayexpress
Project description:Background & Aims: Overnutrition is one of the major causes of non-alcoholic fatty liver disease (NAFLD) and its advanced form non-alcoholic steatohepatitis (NASH). Besides the quantity of consumed calories, distinct dietary components are increasingly recognized as important contributor to the pathogenesis of NASH. We aimed to develop and characterize a hitherto missing murine model which resembles both the pathology and nutritional situation of NASH-patients in Western societies. Methods: We developed a NASH-inducing diet (ND) enriched with sucrose, cholesterol and a high concentration of fats rich in saturated fatty acids in a composition which mimics Western food. C57Bl6/N mice were fed with the ND or control chow for 12 weeks. Biochemical, real-time polymerase chain reaction, Western Blot and immunohistochemical analyses were performed to characterize systemic and hepatic changes induced by ND-feeding. Immunohistochemistry was used to assess c-Jun levels and activation in 110 human NAFLD and control liver specimens applying tissue micro array technology. Results: ND-fed mice showed significant body weight gain, impaired glucose tolerance, elevated fasting blood glucose levels as well as decreased adiponectin and increased leptin serum levels compared to control mice. In the liver, ND-feeding led to marked steatosis, enhanced cholesterol levels, distinct signs of oxidative stress, hepatocellular damage, inflammation, activation of hepatic stellate cells, and beginning fibrosis. Transcriptome-wide hepatic gene expression analysis comparing ND-fed mice and control mice indicated main alterations in lipid metabolism and inflammatory processes. Search for over-represented transcription factor target sites among the differentially expressed genes identified AP-1 as the most likely factor to cause the transcriptional changes in ND-livers. Combining differentially expressed gene and protein-protein interaction network analysis identified c-Jun (a component of the AP-1 complex) as hub in the largest connected deregulated sub-network in ND-livers. In accordance, ND-livers revealed c-Jun-phosphorylation and nuclear translocation. Moreover, hepatic c-Jun RNA and protein expression was enhanced in ND-fed compared to control mice. Also NAFLD-patients showed enhanced hepatic c-Jun levels, which correlated with inflammation, and notably, with the degree of hepatic steatosis. Conclusions: The new dietary mouse-model shows important pathological changes also found in human NASH and indicates c-jun/AP-1 activation as critical regulator of hepatic alterations. Abundance of c-jun in NAFLD likely facilitates development and progression of NASH, and thus, c-jun appears as attractive prognostic and therapeutic target of NAFLD progression. 14-weeks old male C57BL/6N mice were fed with either regular diet or a newly designed NASH-inducing diet for 12 weeks. Hepatic gene expression levels were measured thereafter.
2014-02-01 | E-GEOD-52748 | biostudies-arrayexpress