High-fat and high-sucrose diet impairs female reproduction by altering ovarian transcriptomic and metabolic signatures
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PROVIDER: PRJNA1004213 | ENA |
REPOSITORIES: ENA
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Project description:Excessive energy intake in modern society has led to an epidemic surge in metabolic diseases, such as obesity and type 2 diabetes. These disorders pose profound threats to women’s reproductive health. However, the precise impact and underlying pathogenesis of energy excess on female reproduction remain unclear. In this study, we established an obese and hyperglycemic female mouse model induced by a high-fat and high-sucrose (HFHS) diet, mimicking the modern lifestyle of overnutrition. These mice displayed marked reproductive dysfunction, including elevated serum testosterone levels, irregular estrous cycles, and impaired folliculogenesis. Analysis of the ovarian metabolome of the HFHS mice revealed a pronounced disturbance in amino acid metabolism. Transcriptomic profiling of these ovaries identified dysregulated genes involved in steroid hormone biosynthesis and glucolipid metabolism. Further multi-omic analysis unveils aberrations in ovarian arginine biosynthesis metabolism induced by HFHS diet. Notably, comparisons between HFHS mice and a cohort of women with polycystic ovary syndrome (PCOS) identified analogous reproductive and metabolic signatures. Therefore, our results provide direct in vivo evidence for the detrimental effects of overnutrition on female reproduction and offer insights into the metabolic underpinnings of PCOS.
2024-02-26 | GSE240547 | GEO
Project description:BackgroundExcessive energy intake in modern society has led to an epidemic surge in metabolic diseases, such as obesity and type 2 diabetes, posing profound threats to women's reproductive health. However, the precise impact and underlying pathogenesis of energy excess on female reproduction remain unclear.MethodsWe established an obese and hyperglycemic female mouse model induced by a high-fat and high-sucrose (HFHS) diet, then reproductive phenotypes of these mice were evaluated by examing sexual hormones, estrous cycles, and ovarian morphologies. Transcriptomic and precise metabolomic analyses of the ovaries were performed to compare the molecular and metabolic changes in HFHS mice. Finally, orthogonal partial least squares discriminant analysis was performed to compare the similarities of traits between HFHS mice and women with polycystic ovary syndrome (PCOS).ResultsThe HFHS mice displayed marked reproductive dysfunctions, including elevated serum testosterone and luteinizing hormone levels, irregular estrous cycles, and impaired folliculogenesis, mimicking the clinical manifestations of women with PCOS. Precise metabolomic overview suggested that HFHS diet disrupted amino acid metabolism in the ovaries of female mice. Additionally, transcriptional profiling revealed pronounced disturbances in ovarian steroid hormone biosynthesis and glucolipid metabolism in HFHS mice. Further multi-omics analyses unveiled prominent aberration in ovarian arginine biosynthesis pathway. Notably, comparisons between HFHS mice and a cohort of PCOS patients identified analogous reproductive and metabolic signatures.ConclusionsOur results provide direct in vivo evidence for the detrimental effects of overnutrition on female reproduction and offer insights into the metabolic underpinnings of PCOS.
| S-EPMC10860219 | biostudies-literature
Project description:Heart profiling in HMDP (high-fat/high-sucrose diet)
| PRJNA799591 | ENA
Project description:Expression Profiling In HMDP (high-fat/high-sucrose diet)
| PRJNA271822 | ENA
Project description:We report that maternal high-fat, high-sucrose diet during pregnancy affects metabolic disorders on the liver of offspring via DNA hypermethylation and hypomethylation.
2021-08-18 | GSE181760 | GEO
Project description:Two high-sucrose/low-oil mutants (FN0176450/2012CM7F040P06/SRX826343 and FN0176450/2012CM7F040P05/SRX826351) were identified in a soybean fast neutron population (Bolon et al. 2014). These mutant lines were then advanced to the M3:7 generation and compared to thier wild-type parent (M92-220-Long) using CGH to identify the causative region/gene associated with high-sucrose/low-oil.
2017-01-14 | GSE93411 | GEO
Project description:In order to study the heart disorder that the long term, high energy diet caused, Bama miniature pigs were fed a high-fat, high-sucrose diet for 23 months. These pigs developed symptoms of metabolic syndrome and showed cardiac steatosis and hypertrophy with a greatly increased heart weight (1.82-fold, P<0.05) and heart volume (1.60-fold, P<0.05) compared with the control pigs. To understand the molecular mechanisms of cardiac steatosis and hypertrophy, nine pig heart cRNA samples were hybridized to porcine GeneChips.
2015-10-31 | GSE67890 | GEO
Project description:High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver.
2015-09-01 | GSE47570 | GEO
Project description:Identify genes in the liver whose expression is under genetic regulation in the Hybrid Mouse Diversity Panel (HMDP). The HMDP comprises classical inbred and recombinant inbred wild type mice. The RMA values of genes were used for genome wide association as described in Parks et al Cell Metabolism 2015. These data are used to identify candidate genes at loci associated with obesity and dietary responsiveness. GWAS for expression of liver in inbred strains fed chow diet for 8 weeks followed by high-fat/high-sucrose diet 8 weeks
2015-01-08 | E-GEOD-64769 | biostudies-arrayexpress
Project description:DNA Methylation Status in Mouse Liver Affected by Maternal High-fat, High-sucrose diet
| PRJNA753308 | ENA