Hypothalamic transcriptome of Spraque Dawley rat at postnatal day 10 exposed to maternal high fat diet or control diet
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE107324 | GEO | 2017/12/01
SECONDARY ACCESSION(S): PRJNA419761
REPOSITORIES: GEO
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Project description:Hypothalamic transcriptome of Spraque Dawley rat at postnatal day 10 exposed to maternal high fat diet or control diet
| PRJNA419761 | ENA
Project description:Maternal consumption of a high fat diet during early development has been shown to impact the formation of hypothalamic neurocircuitry, thereby contributing to imbalances in appetite and energy homeostasis and increasing the risk of obesity in subsequent generations. Early in postnatal life, the neuronal projections responsible for energy homeostasis develop in response to appetite-related peptides such as leptin. To date, no study characterises the genome-wide transcriptional changes that occur in response to exposure to high fat diet during this critical window. We explored the effects of maternal high fat diet consumption on hypothalamic gene expression in Sprague Dawley rat offspring at postnatal day 10. RNA-sequencing enabled discovery of differentially expressed genes between offspring of dams fed a high fat diet and offspring of control diet fed dams. Female high fat diet offspring displayed altered expression of 86 genes (adjusted P-value<0.05), including genes coding for proteins of the extra cellular matrix, particularly Collagen 1a1 (Col1a1), Col1a2, Col3a1, and the imprinted Insulin-like growth factor 2 (Igf2) gene. Male high fat diet offspring showed significant changes in collagen genes (Col1a1 and Col3a1) and significant upregulation of two genes involved in regulation of dopamine availability in the brain, tyrosine hydroxylase (Th) and dopamine reuptake transporter Slc6a3 (also known as Dat1). Transcriptional changes were accompanied by increased body weight, body fat and body length in the high fat diet offspring, as well as altered blood glucose and plasma leptin. Transcriptional changes identified in the hypothalamus of offspring of high fat diet mothers could alter neuronal projection formation during early development leading to abnormalities in the neuronal circuitry controlling appetite in later life, hence priming offspring to the development of obesity.
| S-EPMC5730210 | biostudies-literature
Project description:To identify novel neurocircuits activated upon short-term HFD feeding, we employed phosphoribotrap-profiling, which allows for the unbiased identification of alterations in neuronal activation via immunoprecipitation of phosphorylated S6 ribosomal protein-tagged ribosomes from hypothalamic extracts of mice exposed to either 3 days of normal chow diet or HFD-feeding. We have analyzed mRNA selectively expressed in hypothalamic cells activated by a either normal chow diet (NCD)-feeding for 3 days or high fat diet (HFD)-feeding for 3 days. 10-week-old male C57/BL6N mice were put either on a normal chow diet or a high fat diet for 3 days. Afterwards, mice were sacrificed by cervical dislocation. The hypothalamus was rapidly dissected using a stainless steel brain matrix and immediately frozen in liquid nitrogen. Hypothalamic tissues were pooled (8 per IP).
2020-04-16 | GSE137737 | GEO
Project description:The consumption of a 60% high fat diet leads to increased body weight and the development of the metabolic syndrome. We analyzed hypothalamic samples of WT mice as it has been previously shown that the hypothalamus plays a crucial role in the regulation of energy homeostasis. We used microarrays to detail the global programme of gene expression affected by the consumption of a high fat diet specifically in the hypothalamus of WT mice.
2019-05-01 | GSE127056 | GEO
Project description:A number of studies have proposed that excess food intake, particularly of high fat diets arise due dysregulation of homeostatic mechanisms regulating neuroendocrine control of appetite and energy balance. Current dogma suggests high fat diets invoke hypothalamic inflammation which reduces hypothalamic sensitivity to metabolic and hormonal cues of conveying peripheral status of energy balance, such as leptin and insulin. A hypothesis for the mechanism leading to hypothalamic inflammation is based on high fat diet mediated changes in gut microbiota which are then proposed to increase circulating levels of lipopolysaccharide (LPS). This in turn activates a hypothalamic inflammatory response via the toll-like receptor (TLR4) and CD14. The aim of this study was to determine hypothalamic gene expression in response to long term feeding of a high fat diet, taking into account the importance of using a control diet with a similar composition and balanced for sucrose content.
2018-10-23 | E-MTAB-6929 | biostudies-arrayexpress
Project description:Expression data from hypothalamic samples of WT mice fed normal diet vs high fat diet
| PRJNA524141 | ENA
Project description:Fructose consumption has increased by over 25% since 1970, and excess consumption has deleterious metabolic effects. Additionally, fructose can alter hypothalamic pituitary adrenal axis function, potentially resulting in increased vulnerability to mood disorders. Adolescents are the greatest consumers of fructose and also at a critical period of development. Here, we examine the effects of consumption of a 55% fructose diet from weaning until adulthood on the hypothalamic transcriptome.
2015-03-25 | GSE56238 | GEO
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
Project description:We hypothesized that postnatal development of the vagina is impacted by early nutritional environment. Our objective was to determine if lipid profiles of vaginal swabs were different between postnatal gilts suckled by sow or fed milk replacer the first 48 h after birth, with or without a lard-based fat supplement. Gilts (>1.3 kg) were selected at birth across 8 litters and assigned to one of four treatments: 1) suckled by sow (S, n = 8); 2) suckled by sow plus administration of a fat supplement (SF, n = 5); 3) bottle-fed solely milk replacer (B, n = 8); or 4) bottle-fed solely milk replacer plus administration of a fat supplement (BF, n = 7). At 48 h postnatal, vaginal swabs of gilts were taken with a cytology brush, and lipids were extracted for analysis using multiple reaction monitoring (MRM)-profiling. Lipids extracted from serum collected at 48 h from gilts, milk collected at 24 h from sows, and milk replacer were also analyzed with MRM-profiling. Receiver operating characteristic curve analysis found 18 lipids recovered from vaginal swabs that highly distinguished between S and B gilts [area-under-the-curve (AUC) > 0.9], including phosphatidylethanolamine with 34 carbons and four unsaturations in the fatty acyl residues [PE (34:4)]. Twelve lipids from vaginal swabs highly correlated (r > 0.6; p < 0.01) with nutrition source. Lipids with greater abundance in milk replacer drove association. For example, mean intensity of PE (34:4) was 149-fold higher in milk replacer than colostrum. Consequently, PE (34:4) was found to have 1.6- and 2.12-fold higher levels in serum and vaginal swab samples (p < 0.001), respectively, of B gilts as compared to S gilts. Findings support that vaginal swabs can be used to noninvasively study effects of perinatal nutrition on tissue composition.
| S-EPMC6762109 | biostudies-literature
Project description:Maternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy.
| S-EPMC9189289 | biostudies-literature