Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA149237 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 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:A time course of orotic acid induced fatty liver disease. Kyoto and Wistar strain rats were exposed to orotic acid for days 1, 3 and 14. Controls are also included.
2007-10-11 | E-GEOD-665 | biostudies-arrayexpress
Project description:Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic diseases globally and nonalcoholic steatohepatitis is its progressive stage with limited therapeutic options. Here a role for intestinal peroxisome proliferator-activated receptor α (PPARα)-fatty acid binding protein 1 (FABP1) in obesity-associated metabolic syndrome, fatty liver and nonalcoholic steatohepatitis via modulating dietary fat absorption was uncovered. Intestinal PPARα is highly activated accompanied by marked upregulation of FABP1 by high-fat diet (HFD) in mice and obese humans. Intestine-specific PPARα or FABP1 disruption in mice decreases HFD-induced obesity, fatty liver and nonalcoholic steatohepatitis and intestinal PPARα disruption fails to further decrease obesity and NASH. Chemical PPARα antagonism improves metabolic disorders depending on the presence of intestinal PPARα or FABP1. Translationally, GW6471 decreases human PPARα-driven intestinal fatty acid uptake and therapeutically improves obesity in PPARA-humanized, but not Ppara-null, mice. These results suggest that intestinal PPARα-FABP1 axis could be a therapeutic target for NASH.
2022-09-01 | GSE190140 | GEO
Project description:Luciferase activity screen identifies Oxymatrine regulating obesity-related gene enhancer activity in nonalcoholic fatty liver disease
| PRJNA693665 | ENA
Project description:Influence of dietary sucrose and copper content in a rat model of non-alcoholic fatty-liver disease
| PRJNA253783 | ENA
Project description:Nonalcoholic fatty liver disease (NAFLD), a progressive hepatic disease with ectopic fat accumulation, can evolve toward nonalcoholic steatohepatitis (NASH). To date, there is still no approved drug therapy, which remains a major unmet need. Previous study has indicated that tranilast ameliorates hepatic fibrosis and stellate cells activation in dietary rat model of NASH. However, the precise mechanism of tranilast in anti-NASH remains unclear.
2025-02-19 | GSE249350 | GEO
Project description:Nonalcoholic fatty liver disease (NAFLD) is a hepatic condition characterized by excessive fat accumulation, leading to liver fibrosis, cirrhosis, and cancer. Currently, invasive liver biopsy is the only method for identifying and classifying NASH. Mass spectrometry-based proteomics can detect crucial proteins and pathways involved in NASH development. A study using liver and serum samples from mice and humans found altered proteins involved in detoxification, fibrosis, inflammation, and fatty acid metabolism. These findings provide insights into NASH molecular mechanisms and potential diagnostic biomarkers for early diagnosis.
2025-05-07 | PXD053187 | Pride