Similar Datasets
Project description:Transcriptome of GCKR-P446L-EMI-B6N on a high-fat high-sugar diet
| PRJNA951224 | ENA
Project description:Liver transcriptome of GCKR-P446L-EMI-B6N male and female mice
2023-04-19 | GSE228697 | GEO
Project description:Liver transcriptome of GCKR-P446L-EMI-B6N male and female mice
| PRJNA951222 | ENA
Project description:Rats were fed either a control diet or high fat and refined sugar (HFS) diet and hippocampus was resected for proteomic analysis
2012-09-14 | PXD000028 | Pride
Project description:Purpose: NGS was used to determine if a distinct transcriptomic profile is observed among the experimental mice fed four different dietary components. Methods: We carried out RNA-Seq analysis of ileum tissue from 6 weeks male mice ad libitum fed for 10 weeks a high liquid sugar (23% (w/v)) or/and high fat (60% Kcal from fat) diet. The combined effect of sugar drink and high fat diet (HF-Sugar) was compared with sugar drink only (NF-Sugar), or high fat diet only (HF), or control diet that was plain water and normal fat diet (NF). Results: RNA-Seq revealed sample-specific clusters that included genes responding to each experimental diet. We found only addition of sugar drink to high fat group (HF-Sugar) not NF-Sugar and HF, there was a significant enrichment in biological functions relating to Inflammatory/Immune Responses, especially including dendritic cell (DC) and T cell related signaling pathway. Conclusions: Taken together, our data demonstrate that sugar drink synergistically promotes and exacerbates inflammatory responses driven by the high fat diet.
2021-11-25 | GSE140972 | GEO
Project description:High sugar consumption, as well as high-fat diet, is a known cause of obesity and metabolic syndrome. However, the synergistic effect of high-sugar and high-fat consumption rarely has been evaluated, especially in terms of transcriptional regulation. Therefore, we focused on the effect of high sugar consumption on hepatic transcriptional networks in normal and high fat-fed mice. C57BL/6J mice were divided into four groups and were provided either 23%(w/v) sugar solution or plain water with either high-fat or normal-fat diet for 10 weeks. As a result, high sugar consumption significantly altered lipid metabolism-related genes in normal fat-fed mice; however, in high fat-fed mice, high sugar consumption altered inflammation-responsive genes rather than lipid metabolism. After all, these modulations eventually increased lipid accumulation in the liver and caused systemic metabolic disturbances. These observations for the first time suggested that high sugar consumption along with high-fat diet could lead to the development of severe metabolic syndrome via altering hepatic transcriptional networks.
2017-01-01 | GSE70477 | GEO
Project description:X-box binding protein 1 (XBP1) is a key component of the unfolded protein response (UPR) and plays important roles in the pathogenesis of nonalcoholic fatty liver diseases (NAFLD). Mice with liver-specific XBP1 deletion developed great liver injury and fibrosis in a dietary model of NAFLD. This project is to investigate hepatocyte-specific transcriptome profiling in XBP1-deficient mice fed a high fat sugar diet.
2022-01-03 | GSE190947 | GEO
Project description:Obesity has been linked with a host of metabolic and reproductive disorders including polycystic ovary syndrome (PCOS). While a distinct link exists between obesity and PCOS, the exact pathogenesis of the disease remains less understood and limited research has explored the impact of diet on the development of PCOS. With the primary symptoms of PCOS including hyperandrogenism, anovulation, and polycystic ovaries, most animal models utilize androgen treatment to effectively induce PCOS. However, these models fail to address the underlying causes of disease symptoms and do not effectively demonstrate the metabolic features of the disease such as hyperinsulinemia. Here, we present a novel rodent model of diet-induced obesity that recapitulates both the metabolic and reproductive phenotypes of human PCOS. In utilizing a high-fat high-sugar (HFHS) diet, we have created a model of PCOS that allows for the study of metabolic parameters and their impact on ovarian follicle development and reproductive health. Animals on the HFHS diet not only demonstrated signs of metabolic impairment, but they also developed polycystic ovaries and experienced irregular estrous cycling marked by an extended period spent in estrus. Though hyperandrogenism was not characteristic of HFHS diet animals as a group, testosterone levels were predictive of a polycystic ovarian morphology. Importantly, PCOS was induced similarly to the disease etiology in humans, allowing this model to offer the unique opportunity to study PCOS at its genesis rather than following the development of disease symptoms.
2017-06-01 | GSE83220 | GEO
Project description:Conditionally pathogenic gut microbes promote larval growth by increasing redox-dependent fat storage in high sugar diet-fed Drosophila melanogaster
| PRJEB10235 | ENA
Project description:Non-alcoholic fatty liver disease (NAFLD) is a major public health burden and it covers a spectrum of diseases. NAFLD starts with the accumulation of lipid droplets (LDs) within hepatocytes (steatosis). Part of the challenge of studying the mechanistic processes involved in LD accumulation and their implications on the pathogenesis of human NAFLD is due to the available models. Investigating hepatic LDs in humans is challenging and relies on liver biopsies, meaning only cross-sectional data be obtained. On the other hand, LD patterns in in vitro models are poorly defined and rarely reported. Diacylgylcerol acyltransferase (DGAT)2 is one of two enzymes that carry out the final committed step in triacylglycerol (TAG) synthesis. It is unclear whether the enzymes are able to compensate for each other or whether they have distinct roles. It has been hypothesised that DGAT1 primarily utilises exogenous fatty acids and DGAT2 uses de novo-derived fatty acids. Given the important role of this enzyme in TAG synthesis and accumulation, the aims of this study are first to create a cellular model of intrahepatocellular TAG accumulation by manipulating nutritional substrates and to investigate intracellular metabolism in wildtype and DGAT2 knockout cells under these conditions. The experimental workflow for this study is as follows: Huh7 cells (either wild type or knockout) were grown in media containing 11 mM glucose and 2% human serum (HS) for seven days before additional sugars and fatty acids (FAs) were added for a further seven days. All treatments contained 11 mM glucose and 2% HS, either with 200 µM FAs (low fat low sugar; LFLS), 5.5 mM fructose + 200 µM FAs (low fat high sugar; LFHS) or 5.5 mM fructose + 800 µM FAs (high fat high sugar; HFHS). FA metabolism, lipid droplet characteristics and transcriptomic signatures were investigated.
2020-08-21 | E-MTAB-7884 | biostudies-arrayexpress