Effects of Allulose and Erythritol Consumption on a High-Fat Diet
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1176696 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31095800_1.fastq.gz | Fastqsanger.gz | |||
| SRR31095800_2.fastq.gz | Fastqsanger.gz | |||
| SRR31095801_1.fastq.gz | Fastqsanger.gz | |||
| SRR31095801_2.fastq.gz | Fastqsanger.gz | |||
| SRR31095802_1.fastq.gz | Fastqsanger.gz |
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Project description:Long-term consumption of erythritol, a widely used sugar substitute, has been associated with increased risks of thrombosis and cardiometabolic diseases. In this study, we investigated the effects and mechanisms of allulose in mitigating these risks compared to erythritol using the clusterProfiler tool. Since a high-fat diet (HFD) is known to enhance platelet aggregation, we compared the pathways related to these processes between groups of mice treated with allulose and those treated with erythritol. While erythritol exacerbated HFD-induced increased platelet aggregation, allulose treatment significantly reduced it. The groups consisted of a normal diet group (ND, with 10% of calories derived from fat), a high-fat diet group (HFD, with 40% of calories from fat), a high-fat diet with 5% allulose supplementation (ALLU), and a high-fat diet with 5% erythritol supplementation (ERY).
2024-10-28 | GSE280173 | GEO
Project description:MuRF1 is an E3 ubiquitin ligase known to play a role in skeletal muscle atrophy. Our objectives in this study were to gain further insight into the roles MuRF1 plays in skeletal muscle and to determine if this is influenced by sex and/or consumption of a high fat diet. To address these objectives we used RNA sequencing to analyze the transcriptome of gastrocnemius muscle from 30 week old, MuRF1 knockout (-/-) and wild type, male and female mice fed a chow or high fat diet (HFD).
2021-12-01 | GSE179163 | GEO
Project description:Metabolic disorders, such as obesity and type 2 diabetes, are major public health concerns worldwide. Dietary interventions, such as tea consumption, have been suggested as an effective strategy to prevent and treat metabolic disorders. White adipose tissue, as the main energy storage organ in mammals, plays a critical role in the regulation of whole-body metabolism. Recent studies have shown that the microenvironmental cell composition and metabolic network of white adipose tissue can be modulated by dietary factors, including tea consumption. However, the underlying mechanisms and the effects of tea consumption on white adipose tissue in the context of high-fat diet-induced metabolic disorders are not fully understood. Therefore, this study aimed to investigate the effects of tea consumption on the microenvironmental cell composition and metabolic network of white adipose tissue in high-fat diet-fed mice.
2023-12-11 | GSE235473 | GEO
Project description:Background: Post-menopausal obesity is an established risk factor for breast cancer. Consumption of diets high in fat is known to be highly correlated with obesity. In this, we sought to evaluate the interaction(s) between high fat diet, weight gain and mammary carcinogenesis using an obese-resistant and obese-prone rat model with direct correlates to human disease. Methods: Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly. Results: The DMBA-treated OR rats on the 39% safflower diet had significantly greater incidence of ductal carcinoma-in-situ (DCIS) lesions and significantly greater DCIS multiplicity than DMBA-treated OR rats on the 10% safflower diet. These differences were not seen in the OP strain. Gene expression analysis of mammary ductal epithelium from OR rats on the high fat diet showed significant upregulation of proliferation-related genes compared to those consuming the low fat safflower diet. Again, these differences were not seen in the OP strain. Conclusion: Our findings indicate that consumption of high fat safflower diet enhances mammary carcinogenesis in an OR rat strain through increased proliferation of mammary epithelium at the time of exposure, but not in the OP rat strain. Thus, the diet-induced increase in sensitivity was strain-specific and independent of weight gain or obesity level. Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly.
2010-09-25 | E-GEOD-21150 | biostudies-arrayexpress
Project description:The objective of the experiment was to dissect the effects of a high-fat diet on juvenile adipose tissue gene expression under conditions of excess calorie intake versus normal calorie intake in comparison to a standard low-fat diet. For this purpose juvenile mice were fed (A) a standard low-fat diet (CD), (B) a high-fat diet ad libitum (excess calorie intake) (HFD) and (C) a high-fat diet with calorie consumption restricted to the calorie consumption of the CD diet (R-HFD). RNA expression was profiled after 1 week of feeding in the periuterine fat depot.
2019-04-09 | E-MTAB-7755 | biostudies-arrayexpress
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:Background: Post-menopausal obesity is an established risk factor for breast cancer. Consumption of diets high in fat is known to be highly correlated with obesity. In this, we sought to evaluate the interaction(s) between high fat diet, weight gain and mammary carcinogenesis using an obese-resistant and obese-prone rat model with direct correlates to human disease. Methods: Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly. Results: The DMBA-treated OR rats on the 39% safflower diet had significantly greater incidence of ductal carcinoma-in-situ (DCIS) lesions and significantly greater DCIS multiplicity than DMBA-treated OR rats on the 10% safflower diet. These differences were not seen in the OP strain. Gene expression analysis of mammary ductal epithelium from OR rats on the high fat diet showed significant upregulation of proliferation-related genes compared to those consuming the low fat safflower diet. Again, these differences were not seen in the OP strain. Conclusion: Our findings indicate that consumption of high fat safflower diet enhances mammary carcinogenesis in an OR rat strain through increased proliferation of mammary epithelium at the time of exposure, but not in the OP rat strain. Thus, the diet-induced increase in sensitivity was strain-specific and independent of weight gain or obesity level.
2010-09-25 | GSE21150 | GEO
Project description:ackground/Objectives: The aim of the current study was to elucidate the effects of long-term supplementation with D-allulose on obesity and associated comorbidities by analyzing transcriptional and metabolic responses. Subjects/Methods: C57BL/6J mice were divided into three groups and fed a normal diet, high-fat diet (HFD), or high-fat + 5% (w/w) D-allulose diet for 16 weeks. Results: Body weight and body fat mass were significantly decreased in HFD-fed with D-allulose supplemented mice and their levels were similar to that of the normal diet. Also, major symptoms of obesity, such as high plasma lipid profiles and cytokine levels, were attenuated by D-allulose supplementation. D-allulose supplement induced the alteration of mRNA expression in epididymal white adipose tissue (eWAT) and hepatic tissue. D-allulose normalized mRNA expression related lipid metabolism in eWAT and hepatic tissue. In Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway mapper analyses, D-allulose supplementation were down regulated the “cytokine-cytokinereceptor interaction”, “chemokinesignaling pathway”, “MAPK signaling pathway”and“toll-like receptor signaling pathway” in eWAT and hepatic tissue.
2019-09-13 | GSE137365 | GEO
Project description:Hepatic gene expression variations and sex-differences due to high-fat diet consumption using the Collaborative Cross mouse model
2019-12-10 | GSE126490 | GEO
Project description:The increasing consumption of high-fat western foods combined with a lack of exercise is a major contributor to the burden of obesity in humans. Aerobic exercise such as running is known to provide metabolic benefits, but how the over-consumption of a high fat diet (HFD) and exercise interact is not well characterized at the molecular level. Here, we examined the plasma proteome in mice for the effects of aerobic exercise as both a treatment and as a preventative regime for animals on either HFD or a healthy control diet. This analysis detected large changes in the plasma proteome induced by the HFD intervention, such as increased abundance of SERPINA7, ALDOB, APOE, and down-regulation of SERPINA1E, CFD (adipsin), LIFR. Some of these changes were only significantly reverted using aerobic exercise as a preventative measure, but not as a treatment regime. To determine if either the intensity, or duration, of exercise influenced the outcome, we compared high-intensity interval training (HIIT) and endurance running. Endurance running slightly outperformed HIIT exercise, but overall both provided similar reversion in abundance of plasma proteins modulated by the high-fat diet including SERPINA7, APOE, SERPINA1E, and CFD. Finally, we compared the changes induced by over-consumption of HFD to previous data from mice fed an isocaloric high saturated fat (SFA) or polyunsaturated fat (PUFA) diet. This identified several common changes including increased APOC2 and APOE, but also highlighted changes specific for either over-consumption of HFD (ALDOB, SERPINA7, CFD), SFA-based diets (SERPINA1E), or PUFA-based diets (Haptoglobin - Hp). Together, these data highlight the importance of early intervention with exercise to revert HFD-induced phenotypes and suggest some of the molecular mechanisms leading to the changes in the plasma proteome generated by high fat diet consumption in both mice and humans.
2020-11-02 | PXD018561 | Pride