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Genome-wide analysis of hypothalamic gene expression in prenatally undernourished male rat offspring under high fat diet

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE43547 | GEO | 2013/01/17

SECONDARY ACCESSION(S): PRJNA186681

REPOSITORIES: GEO

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Genome-wide analysis of hypothalamic gene expression in prenatally undernourished male rat offspring under high fat diet

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. Total RNA obtained from isolated hypothalami of control standard and high fat-fed adult offspring compared to prenatally undernourished (FR30) counterparts.

2013-01-17 | E-GEOD-43547 | biostudies-arrayexpress

Genome-wide analysis of liver gene expression in prenatally undernourished male rat offspring under high-fat diet

2019-07-12 | GSE134149 | GEO

DNA Methylation profile in hypothalamus for mouse offspring with maternal high fat (HF), low protein (LP) and control (CO) diets

Project description:To investigate the materal dietary effects (HF, LP) on affecting DNA methylations in the mouse offspring hypothalamus.

2019-01-01 | GSE79619 | GEO

Maternal dietary fat during lactation shapes single nucleus transcriptomic profile of postnatal offspring hypothalamus in a sexually dimorphic manner in mice

Project description:Maternal overnutrition during pregnancy/or lactation predisposes offspring obesity and related metabolic syndromes in later life. Hypothalamus is the highest heterogeneous brain region located at the base of the brain that is critical to the regulation of the energy homeostasis.We investigated how the maternal programming shapes the single-nucleus transcriptomic landscapes in postnatal day15 offspring hypothalamus in a sex-specific manner.

2024-02-18 | GSE217677 | GEO

Alterations in hepatic gene expression and DNA methylation as underlying mechanisms of disturbed metabolism in adult mouse offspring after exposure to a prenatal high fat diet

Project description:Exposure to a prenatal high fat (HF) diet leads to an impaired metabolic phenotype in mouse offspring. The underlying mechanisms, however, are not yet fully understood. Therefore, this study investigated whether the impaired metabolic phenotype could have been mediated through altered hepatic DNA methylation and gene expression. In this study, both parent mice received a HF or low fat (LF) diet before and during pregnancy, and throughout lactation, after which offspring was weaned onto a HF diet. Previous work showed that at 12 weeks of age, the offspring displayed postprandial hypertriglyceridemia, which related to an impaired clearance of lipids from the blood into the liver after a HF meal. To study the mechanisms underlying the impaired metabolic phenotype after prenatal exposure to a HF diet, hepatic genome-wide gene expression was studied using whole transcript microarrays. In addition, hepatic DNA methylation of selected genes was assessed by bisulphite pyrosequencing.

2019-06-24 | GSE123009 | GEO

Prenatal maternal vitamin D deficiency sex-dependently programs adipose tissue metabolism and energy homeostasis in offspring

Project description:In utero environment is crucial to ensure normal development of the fetus and to program metabolic health throughout the life. Beside macronutrients, the role of micronutrients, including vitamin D, begins to be explore. The aim of this study was to decipher the impact of maternal vitamin D deficiency (VDD), in normal and high-fat (HF) diet context, on adipose tissue metabolism and energy homeostasis in offspring, considering sex-specific responses. Body weight, energy expenditure, and spontaneous activity was differential impacted in juvenile male and female offspring born from VDD mice. In adulthood, a HF diet combined with maternal VDD disrupted glucose homeostasis and adiposity in male offspring but not in females. Such phenotypes were associated to different transcriptomic profiles in adipose tissue, which could be related to differential modulation of plasma 17b-estradiol concentrations. Thus, maternal VDD sex-dependently modulated metabolic fate of the offspring, especially when associated with HF diet in adulthood.

2022-06-22 | GSE206372 | GEO

Aberrant DNA methylation of hypothalamic angiotensin receptor in prenatal-programmed hypertension

Project description:Malnutrition during pregnancy, which causes prenatal exposure to excessive glucocorticoid, induces adverse metabolic programming leading to hypertension in offspring. Pregnant rats receiving a low-protein diet exhibited moderate downregulation of 11-beta-dehydrogenase isozyme 2, which inactivates corticosterone, in the placenta, resulting in prenatal exposure to excessive corticosterone. In offspring of pregnant rats receiving a low-protein diet or dexamethasone, mRNA expression of angiotensin receptor type 1a (Agtr1a) in the paraventricular nucleus (PVN) of the hypothalamus was upregulated, concurrent with reduced expression of DNA methyltransferase 3a (Dnmt3a), reduced binding of DNMT3a to the Agtr1a promoter, and DNA demethylation, suggesting hypothalamic Agtr1a expression is epigenetically modulated by excess glucocorticoid. Dexamethasone treatment of PVN cells downregulated DNMT3a while upregulating Agtr1a, and decreased DNMT3a binding and DNA demethylation at the Agtr1a promoter. Consistent with Agtr1a upregulation in the hypothalamus, salt loading increased BP in both types of offspring. Even without dexamethasone treatment, hypothalamic neuron-specific DNMT3a-deficient mice, in which Agtr1a was upregulated, exhibited salt-induced BP elevation. By contrast, dexamethasone-treated Agtr1a-deficient mice failed to show salt-induced BP elevation, despite reduced expression of DNMT3a. Thus, epigenetic modulation of hypothalamic angiotensin signaling contributes to salt-sensitive hypertension induced by prenatal glucocorticoid excess in offspring of mothers that are malnourished during pregnancy.

2018-11-30 | GSE119235 | GEO

Female and Male C57Bl/6J Offspring Exposed to Maternal Obesogenic Diet Develop Altered Hypothalamic Energy Metabolism in Adulthood

Project description:Purpose: Study a cohort of C57Bl/6J dams, treated with a control or high-fat-high-sugar diet, and their adult offspring to explore potential hypothalamic mechanisms to explain the link between maternal and offspring obesity. Hypothalamic differential gene expression analysis was conducted following next-generation sequencing (NGS) and analyzed in Ingenuity Pathway Analysis. This methodology was supplementary to in vivo studies which characterized offspring metabolic phenotype. Methods: Total RNA was extracted from a subset of offspring hypothalamus tissue using a RNeasy Mini Kit (Qiagen, Germantown, MD). Tissues were homogenized in RLT buffer using mechanized syringe homogenization. RNA was assessed for purity and concentration using the NanoDrop (NanoDrop Technologies). Approximately 4ug of total RNA was used to generate cDNA by reverse transcription using a cDNA synthesis kit (Applied Biosystems, Carlsbad, CA). Results: There were 31,637 differentially expressed genes in adult OB offspring hypothalamus compared with control diet. Of the identified differentially expressed genes, there were 2510 differentially expressed genes that were significantly different between CON and OB offspring (Supplemental Table 3). In OB offspring, 65% of the identified differentially expressed genes were downregulated whereas 35% were upregulated. Conclusions: Collectively, data demonstrate that maternal obesity without diabetes is associated with adiposity and decreased hypothalamic energy production.

2022-04-13 | GSE200611 | GEO

Multi-omics data integration reveals sex-dependent hippocampal programming by maternal high-fat diet during lactation in adult mouse offspring

Project description:Early-life exposure to high-fat diet (HF) can program metabolic and cognitive alterations in adult offspring. Although the hippocampus plays a crucial role in memory and metabolic homeostasis, few studies reported the impact of maternal HF on this structure. We assessed the effects of maternal HF during lactation on physiological, metabolic and cognitive parameters in young adult offspring mice. To identify early-programming mechanisms in hippocampus, we developed a multi-omics strategy in male and female offspring. Maternal HF induced a transient increased body weight at weaning, a mild glucose intolerance only in 3-month-old male mice with no change in plasma metabolic parameters in adult male and female offspring. Behavioral alterations revealed by Barnes maze test were observed both in 6-month-old male and female mice. Multi-omics strategy unveiled sex-specific transcriptomic and proteomic modifications in the hippocampus of adult offspring. These studies, that were confirmed by regulon analysis, showing that, although genes whose expression was modified by maternal HF were different between sexes, the main pathways affected were similar with mitochondria and synapses as main hippocampal targets of maternal HF. The effects of maternal HF reported here may help to better characterize sex-dependent molecular pathways involved in cognitive disorders and neurodegenerative diseases.

2024-01-26 | PXD045639 | Pride

Effect of maternal exposure to dioxin on the pituitary and hypothalamic expression of genes in PND70 male pups

Project description:Our previous studies have revealed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 M-NM-<g/kg) at gestational day (GD) 15 reduces the pituitary synthesis of luteinizing hormone (LH) during late fetal and early postnatal period, leading to imprinting of defects in sexual behaviors at adulthood. However, it remains obscure how the attenuation of pituitary LH links to sexual immaturity. To address this issue, we firstly performed a DNA microarray analysis to identify the gene(s) responsible for dioxin-induced sexual immaturity, using the pituitary and hypothalamus of male pups, at the age of postnatal day (PND)70, born from TCDD-treated dams. Among the reduced genes, we focused on gonadotropin-releasing hormone (GnRH) in the hypothalamus, because of its role in sexual behaviors suggested so far. The present study strongly suggests that maternal exposure to TCDD fixes the status of the lowered expression of GnRH in the offspring by reducing steroidogenesis at perinatal stage, and this is the mechanism for the imprinting of defects in sexual behaviors at adulthood. Total RNA was isolated from the pituitary and hypothalamus of PND70 male pups born from the dams treated with TCDD (1 M-NM-<g/kg) or vehicle at GD15, using an RNeasy Mini Kit (QIAGEN). To identify the gene(s) the altered expression of which is fixed and linked to defects in sexual behaviors, the profile of gene expression was analyzed using the Illumina RatRef-12 Expression BeadChip. This series includes two dataset; hypothalamic and pituitary samples (each case; N=3x2). The normalization applied each dataset.

2013-08-21 | E-GEOD-48100 | biostudies-arrayexpress

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