Expression data from third instar Drosophila larvae offspring from maternal control or high-sucrose fed diets
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE33989 | GEO | 2011/11/30
SECONDARY ACCESSION(S): PRJNA150609
REPOSITORIES: GEO
Similar Datasets
Project description:Maternal obesity and diabetes is associated with increased risk of obesity and diabetes in offspring. We generated a model of maternal caloric excess in Drosophila and noted altered body composition in offspring from females fed a high-sucrose diet. To gain insight into the mechanisms underlying this response, we profiled gene expression in mid-third instar larvae (mid-L3) offspring from either control or high-sucrose fed females. All offspring were raised on control food. We used microarrays to detail the response of Drosophila larvae to maternal high calorie diet Virgin female w1118 flies were fed control (0.15M) or high (1M) sucrose food for 7 days, mated with male w1118 flies such that all embryos were laid on control food. Mid-L3 larvae were selected for RNA extraction and hybridization on Affymetrix microarrays. Mid-L3 were selected as L2, aged overnight until early L3, then transferred to fresh control food for 12 more hours before selection.
2011-11-30 | E-GEOD-33989 | biostudies-arrayexpress
Project description:Maternal obesity can program metabolic syndrome in offspring but the mechanisms are not well characterized. Moreover, the consequences of maternal overnutrition in the absence of frank obesity remain poorly understood. This study aimed to determine the effects of maternal consumption of a high fat-sucrose diet on the skeletal muscle metabolic and transcriptional profiles of adult offspring. Female Sprague Dawley rats were fed either a diet rich in saturated fat and sucrose (HFD, 23.5% fat, 20% sucrose wt/wt) or a standard chow diet (NFD, 7% fat, 10% sucrose w/w) for the 3 weeks prior to mating and throughout pregnancy and lactation. Although maternal weights were not different between groups at conception or weaning, HFD dams were ~22% heavier than chow fed dams from mid-pregnancy until 4 days post-partum. Adult male offspring of HFD dams were not heavier than controls but demonstrated features of insulin resistance including elevated plasma insulin concentration (+40%, P<0.05). Next Generation mRNA Sequencing was used to identify differentially expressed genes in the soleus muscle of offspring, and Gene Set Enrichment Analysis (GSEA) to detect coordinated changes that are characteristic of a biological function. GSEA identified 15 pathways enriched for up-regulated genes, including cytokine signaling (P<0.005), starch and sucrose metabolism (P<0.017), and inflammatory response (P<0.024). A further 8 pathways were significantly enriched for down-regulated genes including oxidative phosphorylation (P<0.004) and electron transport (P<0.022). Western blots confirmed a ~60% reduction in the phosphorylation of the insulin signaling protein Akt (P<0.05) and ~70% reduction in mitochondrial complexes II (P<0.05) and V expression (P<0.05). On a normal diet, offspring of HFD dams developed an insulin resistant phenotype, with transcriptional evidence of muscle cytokine activation, inflammation and mitochondrial dysfunction. These data indicate that maternal overnutrition, even in the absence of pre-pregnancy obesity can promote metabolic dysregulation and predispose offspring to type 2 diabetes. Messenger RNA profile of skeletal muscle of male offspring from female Sprague Dawley rats fed either a diet rich in saturated fat and sucrose (HFD, 23.5% fat, 20% sucrose wt/wt) or a standard chow diet (NFD, 7% fat, 10% sucrose w/w) for the 3 weeks prior to mating and throughout pregnancy and lactation. There were 5 HFD samples compared to 6 NFD control samples.
2013-08-13 | E-GEOD-49797 | biostudies-arrayexpress
Project description:Maternal obesity can program metabolic syndrome in offspring but the mechanisms are not well characterized. Moreover, the consequences of maternal overnutrition in the absence of frank obesity remain poorly understood. This study aimed to determine the effects of maternal consumption of a high fat-sucrose diet on the skeletal muscle metabolic and transcriptional profiles of adult offspring. Female Sprague Dawley rats were fed either a diet rich in saturated fat and sucrose (HFD, 23.5% fat, 20% sucrose wt/wt) or a standard chow diet (NFD, 7% fat, 10% sucrose w/w) for the 3 weeks prior to mating and throughout pregnancy and lactation. Although maternal weights were not different between groups at conception or weaning, HFD dams were ~22% heavier than chow fed dams from mid-pregnancy until 4 days post-partum. Adult male offspring of HFD dams were not heavier than controls but demonstrated features of insulin resistance including elevated plasma insulin concentration (+40%, P<0.05). Next Generation mRNA Sequencing was used to identify differentially expressed genes in the soleus muscle of offspring, and Gene Set Enrichment Analysis (GSEA) to detect coordinated changes that are characteristic of a biological function. GSEA identified 15 pathways enriched for up-regulated genes, including cytokine signaling (P<0.005), starch and sucrose metabolism (P<0.017), and inflammatory response (P<0.024). A further 8 pathways were significantly enriched for down-regulated genes including oxidative phosphorylation (P<0.004) and electron transport (P<0.022). Western blots confirmed a ~60% reduction in the phosphorylation of the insulin signaling protein Akt (P<0.05) and ~70% reduction in mitochondrial complexes II (P<0.05) and V expression (P<0.05). On a normal diet, offspring of HFD dams developed an insulin resistant phenotype, with transcriptional evidence of muscle cytokine activation, inflammation and mitochondrial dysfunction. These data indicate that maternal overnutrition, even in the absence of pre-pregnancy obesity can promote metabolic dysregulation and predispose offspring to type 2 diabetes.
2013-08-13 | GSE49797 | GEO
Project description:Chronic Kidney Disease (CKD), a global health burden, is strongly associated with age-related renal function decline, hypertension and diabetes, frequent consequences of obesity. Despite extensive studies the mechanisms determining susceptibility to CKD remain elusive. Clinical evidence together with prior studies from our group showed that perinatal metabolic disorders after maternal obesity adversely affect kidney structure and function throughout life. Since obesity and aging processes converge in similar pathways we tested if perinatal obesity induced by High-Fat Diet (HFD)-fed female mice sensitizes aging-associated mechanism in kidneys of newborn mice. Tissue from the kidney cortex and the kidney medulla was collected from offspring of control or HFD-fed mice.
2022-12-31 | E-MTAB-10954 | biostudies-arrayexpress
Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers.
2013-02-01 | GSE43323 | GEO
Project description:Background: Epidemiological studies suggest an association between maternal obesity and adverse neurodevelopmental outcomes in offspring. Objective: To compare the global proteomic portrait in the cerebral cortex between mice born to mothers on a high-fat or control diet who themselves were fed a high-fat or control diet. Methods: Male mice born to dams fed a control (C) or high fat (H) diet four weeks before conception and during gestation and lactation were assigned to either C or H diet at weaning. Mice (n=24) were sacrificed at 19-weeks and their cerebral cortices were pooled into 8 samples and analysed using an iTRAQ based 2D LC-MS methodology. Results: A total of 6,695 proteins were identified and fully quantified (q<0.01). Approximately 10% of these proteins demonstrated a minimum of one Standard Deviation of regulation across all biological replicates in at least one of the experimental groups (CH, HC, HH) relative to the control (CC). Principal component analysis and hierarchical clustering analysis showed that mice clustered based on the diet of the mother and not their current diet. In silico bioinformatics analysis revealed that maternal high-fat diet was significantly associated with response to hypoxia/oxidative stress and apoptosis in the cerebral cortex of the adult offspring. Conclusion: Maternal high-fat diet was associated with distinct endophenotypic changes of the adult mouse cerebral cortex independent of the diet of the offspring. The identified modulated proteins could represent novel therapeutic targets for the prevention of neuropathological features resulting from maternal obesity.
2018-01-29 | PXD001540 | Pride
Project description:In rainbow trout (Oncorhynchus mykiss), the effect of a paternal and a maternal "high carbohydrate/low protein" diet was assessed on progeny. To this purpose, two-year old males and females rainbow trout were fed either a control diet or a "high carbohydrate/low protein" diet for an entire reproductive cycle for females and for 5 months for males. Crossed-fertilizations were carried out in order to obtain 4 groups of offspring. Offspring were fed with a commercial diet until they reached a market size. At this stage, hepatic transcriptomes were compared to detect any impact of the parental diet on offspring metabolism.
2021-08-16 | GSE169001 | GEO
Project description:In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS. To better understand the mechanisms contributing to metabolic dysfunction in obesity-induced diabetes, we used microarrays to comprehensively profile gene expression livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db) DBA/2J females were mated to C57BL/6 males carrying leptin receptor deficiency (db/+) and, F1 (db/+) offspring were interbred to produce F2 mice. Offspring deficient in leptin receptor (db/db) were fed on a chow diet until 5 weeks or 12 weeks of age and then euthanized for collection of liver tissue for RNA profiling along with other diabetes-related phenotypes.
2011-12-29 | E-GEOD-30140 | biostudies-arrayexpress
Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers. Fetal hearts were collected from baboon fetuses born to obese and lean mothers, total RNA was isolated, and fetal cardiac miRNA were sequenced and profiled
2013-02-01 | E-GEOD-43323 | biostudies-arrayexpress
Project description:Aims: Epidemiological and animal studies have shown that maternal diet can influence metabolism in adult offspring. However, the molecular mechanisms underlying these changes remain poorly understood. Here, we aim to explore phenotypes induced by maternal obesity in a mouse model and examine gene expression and epigenetic alterations in adulthood induced by maternal diet. Methods: We analyzed genetically identical male mice born from dams fed a high- or low-fat diet throughout pregnancy and until day 21 postpartum. After weaning, half of the males of each group were fed a high-fat diet, the other half a low-fat diet. We first characterized the genome-wide gene expression patterns of six tissues of adult offspring - liver, pancreas, white adipose, brain, muscle and heart [GSE40903] . We then measured DNA methylation patterns in liver at selected loci and throughout the genome. Results: Maternal diet had a significant effect on the body weight of the offspring when they are fed an obesogenic diet after weaning. Our analyses showed that maternal diet had a pervasive effect on gene expression, with a pronounced effect in liver where it affected many genes involved in inflammation, cholesterol synthesis and RXR activation. Maternal diet had no detectable effect on DNA methylation in the liver. Conclusions: Overall, our findings highlighted the persistent influence of maternal diet on adult tissue regulation and suggested that the transcriptional changes were unlikely to be caused by DNA methylation differences in adult liver. Methylation is compared between nine week old animals fed a common diet as adults, but derived from mothers fed different diets.
2014-03-04 | E-GEOD-52266 | biostudies-arrayexpress