Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA325290 | ENA |
REPOSITORIES: ENA
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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: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:Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovaries. In this study, we induced a PCOS rat model by oral administration of letrozole combined with a high-fat diet and then treated with mogroside V (MV) to evaluate the protective roles on endocrine and follicle development in PCOS rats and the underlying mechanisms. Purpose: To detect the difference of ovary transcriptome profiling between PCOS model and Control rat and to evaluate the effect of mogroside V on the transcriptome profiling of ovaries of PCOS model rats. Methods: Ovarian mRNA profiles of 15-week-old Control, PCOS and PCOS-MV group rats (4 rats per group) were generated by deep sequencing,using Illumina PE150.
2022-04-20 | GSE194398 | GEO
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 fat diet (HF) rodent models have contributed significantly to the dissection of the pathophysiology of the insulin resistance syndrome, but their phenotype varies distinctly between different studies. Here, we have analyzed gene expression patterns in livers of animals fed with different HF with varying fatty acid compositions. Experiment Overall Design: Male Wistar rats were fed with high fat diets (42 energy%, fat sources: lard, olive oil; coconut fat; cod liver oil). Weight, food intake, whole body insulin tolerance and plasma parameters of glucose and lipid metabolism were measured during a 12 week diet course. Liver histologies and hepatic gene expression profiles using AffymetrixR gene chips were obtained.
2007-10-10 | E-GEOD-3512 | biostudies-arrayexpress
Project description:rattus Transcriptome of polycystic ovary syndrome and Premature Ovarian Failure
| PRJNA703763 | ENA
Project description:High fat diet (HF) rodent models have contributed significantly to the dissection of the pathophysiology of the insulin resistance syndrome, but their phenotype varies distinctly between different studies. Here, we have analyzed gene expression patterns in livers of animals fed with different HF with varying fatty acid compositions. Keywords: diet-gene interaction
2005-10-28 | GSE3512 | GEO
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. These phenotypes are controlled by the fat body, a liver- and adipose- like tissue in Drosophila flies. To gain insight into the mechanisms underlying the connection between diet and insulin sensitivity, we used Illumina RNA-seq to profile gene expression in fat bodies isolated from chronically high sugar fed, wandering (post-prandial) third instar wild type larvae w(L3). These data were compared to control-fed wild-type wL3 fat bodies as well as those expressing transgenic interfering RNA (i) targeting CG18362 (Mio/dChREBP) in the fat body on both diets. Female VDRC w1118, cgGAL4, UAS-Dcr2 or UAS-ChREBPi(52606), cgGAL4, UAS-Dcr2 wandering third instar larvae were fed control (0.15M) or high (0.7M) sucrose and fat bodies isolated for RNA extraction.
2013-01-25 | E-GEOD-43734 | biostudies-arrayexpress
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. These phenotypes are controlled by the fat body, a liver- and adipose- like tissue in Drosophila flies. To gain insight into the mechanisms underlying the connection between diet and insulin sensitivity, we used Illumina RNA-seq to profile gene expression in fat bodies isolated from chronically high sugar fed, wandering (post-prandial) third instar wild type larvae w(L3). These data were compared to control-fed wild-type wL3 fat bodies as well as those expressing transgenic interfering RNA (i) targeting CG18362 (Mio/dChREBP) in the fat body on both diets.
2013-01-25 | GSE43734 | GEO