Genome-wide analysis of hypothalamic gene expression in prenatally undernourished male rat offspring under high fat diet
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: christophe breton
PROVIDER: E-GEOD-43547 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Based on the developmental origin of health of disease hypothesis, we previously showed that prenatal 70% maternal food restriction (FR30) predisposes the offspring to development of pathologies in adulthood. In the present study, we focused on the hypothalamus gene expression profile of standard and high fat (HF)-fed FR30 adult offspring.
2013-01-17 | GSE43547 | GEO
Project description:Based on the developmental origin of health of disease hypothesis, we previously showed that prenatal 70% maternal food restriction (FR30) predisposes the offspring to development of pathologies in adulthood. In the present study, we focused on the liver gene expression profile of standard and high fat (HF)-fed FR30 adult offspring.
2019-07-12 | GSE134149 | GEO
Project description:Mammary gland (MG) de novo lipogenesis contributes significantly to milk fat in animals but little is known in humans. We hypothesized that de novo lipogenesis, as reflected by incorporation of 13C carbons from [U-13C]glucose into fatty acids (FAs) and glycerol in triglycerides (TG), will be greater: a. in milk than plasma TG, b. during a high carbohydrate (H-CHO) diet than high fat (H-FAT) diet and c. during feeding than fasting. Healthy lactating women were studied on two isocaloric, isonitrogenous diets. On one occasion subjects received diets containing H-FAT or H-CHO diet for 1 week. Incorporation of 13C from infused [U-13C]glucose into FAs and glycerol was measured using GC/MS methodology and gene expression using RNA isolated from breast milk fat globule (MFG). Incorporation of 13C2 into milk FAs, increased with increased chain length of the FAs from C2:0 to C12:0 but progressively declined in C14:0 and C16:0 and was not detected in FAs >C16. During feeding, regardless of diets, enrichment of 13C2 in milk FA and 13C3 in milk glycerol were ~3 and ~7 fold higher compared to plasma FA and glycerol, respectively. Following an overnight fast during H-CHO and H-FAT diets study periods, 25% and 6%, respectively, of medium chain FAs (MCFAs, C6-C12) were derived from glucose but increased to 75% and 25% with feeding. The expression of genes involved in FA or glycerol synthesis pathways was unchanged regardless of diet or fast-fed conditions. Conclusions: The human MG is capable of de novo lipogenesis, of primarily MCFAs and glycerol, which is influenced by the macro-nutrient composition of the maternal diet. On day 7 of consumption of each of the two diets milk samples collected from 7 healthy, lean, exclusively breastfeeding women following an overnight fast and feeding conditions [7 x 2 x 2 = 28 samples] were processed for isotope enrichments and RNA isolation from the milk fat globules. The total RNA was utilized for microarray analyses.
2014-05-19 | E-GEOD-51874 | biostudies-arrayexpress
Project description:Gaining understanding of common complex diseases and their treatments are the main drivers for life sciences. As we show here, comprehensive protein set analyses offer new opportunities to decipher functional molecular networks of diseases and assess the efficacy and side-effects of treatments in vivo. Using mass spectrometry, we quantitatively detected several thousands of proteins and observed significant changes in protein pathways that were (dys-) regulated in diet-induced obesity mice. Analysis of the expression and post-translational modifications of proteins in various peripheral metabolic target tissues including adipose, heart, and liver tissue generated functional insights in the regulation of cell and tissue homeostasis during high-fat diet feeding and medication with two antidiabetic compounds. Protein set analyses singled out pathways for functional characterization, and indicated, for example, early-on potential cardiovascular complication of the diabetes drug rosiglitazone. In vivo protein set detection can provide new avenues for monitoring complex disease processes, and for evaluating preclinical drug candidates. Male C57BL/6 mice (age 6 wks) were fed for 12 weeks with high-fat diet (HFD) and than distributed into 3 groups. Mice were than fed over 3 weeks with HFD without compound ('HFD'), HFD with 4 mg/kg/d rosiglitazone ('HFD_RSG') or with 100 mg/kg/d amorfrutin 1 ('HFD_A1'). In parallel, mice were fed for 15 weeks with low-fat diet (LFD) as healthy control subjects. In addition, a group of mice was treated with 37 mg/kg/d amorfrutin 1 during the whole 15 weeks of HFD feeding ('HFD+A1prev'). Finally, visceral white adipose tissue (WAT) was harvested and RNA extracted. --> 2-4 biological replicates (2 mice per each replicate, RNA of 2 mice always pooled).
2013-09-05 | E-GEOD-38855 | biostudies-arrayexpress
Project description:The present study aimed to examine the effect of high-fat diet prior to pregnancy on the liver of mouse offspring. Female C57BL/6J mice were fed a normal chow (15.2% fat by energy) (CTR and CTR-PP groups) or a high-fat chow (31.2% fat by energy) (HFD and HFD-PP groups) for 3−4 weeks and then mated with male C57BL/6J mice fed normal chow. Some mothers continued on the same diet until pups reached 21 days of age (CTR and HFD), and others were fed the different chows from gestational day 0 (CTR-PP and HFD-PP) to determine the effects of a high-fat diet during the pre-pregnancy period in HFD-PP/CTR and HFD/CTR-PP comparisons. RNA sample was taken from liver of 3-week-old mouse prenatally received high-fat diet prior to pregnancy, during pregnancy and lactation, or through prior to and during pregnancy and lactation, while control RNA was taken from control counterpart prenatally received normal diet alone. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
2013-06-18 | E-GEOD-48014 | biostudies-arrayexpress
Project description:Gaining understanding of common complex diseases and their treatments are the main drivers for life sciences. As we show here, comprehensive protein set analyses offer new opportunities to decipher functional molecular networks of diseases and assess the efficacy and side-effects of treatments in vivo. Using mass spectrometry, we quantitatively detected several thousands of proteins and observed significant changes in protein pathways that were (dys-) regulated in diet-induced obesity mice. Analysis of the expression and post-translational modifications of proteins in various peripheral metabolic target tissues including adipose, heart, and liver tissue generated functional insights in the regulation of cell and tissue homeostasis during high-fat diet feeding and medication with two antidiabetic compounds. Protein set analyses singled out pathways for functional characterization, and indicated, for example, early-on potential cardiovascular complication of the diabetes drug rosiglitazone. In vivo protein set detection can provide new avenues for monitoring complex disease processes, and for evaluating preclinical drug candidates. Male C57BL/6 mice (age 6 wks) were fed for 12 weeks with high-fat diet (HFD) and than distributed into 3 groups. Mice were than fed over 3 weeks with HFD without compound ('HFD'), HFD with 4 mg/kg/d rosiglitazone ('HFD_RSG') or with 100 mg/kg/d amorfrutin 1 ('HFD_A1'). In parallel [GSE38854; Liver B], mice were fed for 15 weeks with low-fat diet (LFD) as healthy control subjects. In addition, a group of mice was treated with 37 mg/kg/d amorfrutin 1 during the whole 15 weeks of HFD feeding ('HFD+A1prev'). Finally, LIVER tissue was harvested and RNA extracted. --> 3-4 biological replicates (2 mice per each replicate, RNA of 2 mice always pooled). liver_HFD_*A and _*B samples are from the same biological source material, but the cRNA preparation and hybridization to Illumina arrays were performed at different days (i.e. technical repeats).
2013-09-05 | E-GEOD-38853 | biostudies-arrayexpress
Project description:Gaining understanding of common complex diseases and their treatments are the main drivers for life sciences. As we show here, comprehensive protein set analyses offer new opportunities to decipher functional molecular networks of diseases and assess the efficacy and side-effects of treatments in vivo. Using mass spectrometry, we quantitatively detected several thousands of proteins and observed significant changes in protein pathways that were (dys-) regulated in diet-induced obesity mice. Analysis of the expression and post-translational modifications of proteins in various peripheral metabolic target tissues including adipose, heart, and liver tissue generated functional insights in the regulation of cell and tissue homeostasis during high-fat diet feeding and medication with two antidiabetic compounds. Protein set analyses singled out pathways for functional characterization, and indicated, for example, early-on potential cardiovascular complication of the diabetes drug rosiglitazone. In vivo protein set detection can provide new avenues for monitoring complex disease processes, and for evaluating preclinical drug candidates. Male C57BL/6 mice (age 6 wks) were fed for 12 weeks with high-fat diet (HFD) and than distributed into 3 groups. Mice were than fed over 3 weeks with HFD without compound ('HFD'), HFD with 4 mg/kg/d rosiglitazone ('HFD_RSG') or with 100 mg/kg/d amorfrutin 1 ('HFD_A1') [GSE38853; Liver A]. In parallel, mice were fed for 15 weeks with low-fat diet (LFD) as healthy control subjects. In addition, a group of mice was treated with 37 mg/kg/d amorfrutin 1 during the whole 15 weeks of HFD feeding ('HFD+A1prev'). Finally, LIVER tissue was harvested and RNA extracted. --> 3-4 biological replicates (2 mice per each replicate, RNA of 2 mice always pooled). liver_HFD_*A and _*B samples are from the same biological source material, but the cRNA preparation and hybridization to Illumina arrays were performed at different days (i.e. technical repeats).
2013-09-05 | E-GEOD-38854 | biostudies-arrayexpress
Project description:Gaining understanding of common complex diseases and their treatments are the main drivers for life sciences. As we show here, comprehensive protein set analyses offer new opportunities to decipher functional molecular networks of diseases and assess the efficacy and side-effects of treatments in vivo. Using mass spectrometry, we quantitatively detected several thousands of proteins and observed significant changes in protein pathways that were (dys-) regulated in diet-induced obesity mice. Analysis of the expression and post-translational modifications of proteins in various peripheral metabolic target tissues including adipose, heart, and liver tissue generated functional insights in the regulation of cell and tissue homeostasis during high-fat diet feeding and medication with two antidiabetic compounds. Protein set analyses singled out pathways for functional characterization, and indicated, for example, early-on potential cardiovascular complication of the diabetes drug rosiglitazone. In vivo protein set detection can provide new avenues for monitoring complex disease processes, and for evaluating preclinical drug candidates. Male C57BL/6 mice (age 6 wks) were fed for 12 weeks with high-fat diet (HFD) and than distributed into 3 groups. Mice were then fed over 3 weeks with HFD without compound ('HFD'), HFD with 4 mg/kg/d rosiglitazone ('HFD_RSG') or with 100 mg/kg/d amorfrutin 1 ('HFD_A1'). Finally, HEART tissue was harvested and RNA extracted. --> 3-4 biological replicates (2 mice per each replicate, RNA of 2 mice always pooled).
2013-09-05 | E-GEOD-38852 | biostudies-arrayexpress
Project description:Developmental programming is the concept that environmental factors during fetal growth can alter development, metabolism and physiology of an organism, thus diseases can be programmed by intrauterine influences. The fetal origin of health and disease hypothesis has received strong support from experimental studies in animals including livestock species. Using a sheep model, it has been shown that developmental changes of ewe offspring may be susceptible to maternal pregnancy bisphenol A (BPA) treatment. For example, prenatally BPA treated female offspring tended to have reduced birth weight. In this study we sought to identify gene expression differences in ewe offspring as a result of maternal pregnancy BPA treatment on a control or high-caloried diet. Samples of heart tissues were collected during the second breeding season, allowing us to examine gene expression changes in ewes prenatally treated with BPA and maturing under the different diets.
2017-01-29 | GSE77418 | GEO
Project description:PFAS are persistent man-made chemicals considered to be emerging pollutants, with PFOA, PFOS, and PFHxS having associations with liver toxicity and steatosis. PFOA, PFOS, and PFHxS can undergo placental/lactational transfer, however, little is known about the impact of PFAS mixtures during the developmental window, nor maternal diet on PFAS adverse effects. It was hypothesized that gestational/lactational PFAS exposure would alter the pup liver proteome. The work herein evaluated the liver proteome in offspring, identifying potential biochemical/signaling pathways altered via maternal PFAS exposure. Timed-pregnant CD-1 dams were fed a standard chow or 60% kcal high-fat diet. From GD1 until PND20, dams were orally gavaged daily with either 0.5% Tween 20, individual PFOA, PFOS, PFHxS at 1 mg/kg, or a mixture (1 mg/kg each, totaling 3 mg/kg). Livers were collected from PND21 offspring and SWATH-MS pro-teomics was performed. IPA analysis revealed disease and biological function pathways involved in liver damage, xenobiotics, and lipid regulation were modulated by PFAS exposure in the PND21 liver: lipid transport, storage, oxidation, and synthesis, xenobiotic metabolism and transport, liver damage and inflammation, and fatty acid metabolism, oxidation and transport. This indicates the pup liver proteome is altered via maternal exposure and predisposes the pup to metabolic dysfunctions.
2024-05-09 | PXD052106 | Pride