Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA178006 | ENA |
REPOSITORIES: ENA
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Project description:Aside from the perinatal complications associated with low birth weight, individuals born with intra-uterine growth restriction suffer from chronic diseases late in life that ultimately lead to a shortened lifespan. These late life metabolic sequelae of low birth weight include obesity and metabolic syndrome, diabetes mellitus, cardiovascular disease, hypertension, stroke, dyslipidemia, and non-alcoholic fatty liver disease/steatohepatitis. Animal models employing perinatal calorie restriction recapitulate the observations made in humans. Interestingly, if continued calorie restriction is employed post-natally the late life sequelae of intra-uterine growth restriction are ameliorated. These observations linking both fetal and early post natal growth to later health is now termed the developmental origins of health and disease. To further our understanding of the mechanism of how early growth affects late life health we have employed Affymetrix microarray-based expression profiling to characterize hepatic gene expression in a rat model of maternal semi-nutrient restriction. In these experiments we have limited maternal calorie intake to 50% of normal so as to create 3 groups of animals: Control (Con) male offspring born to mothers who were fed normally throughout gestation and lactation; intra-uterine calorie restricted male offspring (IUCR) born to mothers who had 50% restriction of calories from e11 to e21; and combined intra-uterine and post-natal calorie restriction (IPCR) male offspring who were born to mothers who received calorie restriction during both fetal growth (e11 to e21) and post-natally (p1-p21). Livers were collected at p21(day 21 of life) for Con and IPCR groups (IUCR withheld owing to ‘catch up” growth), and at p450 (day 450 of life) for Con, IUCR, and IPCR. The profiling data reveals clear alteration of circadian cycling at P21, and subtle changes for circadian gene expression at p450. In addition, a clear transcriptional response is found during active calorie restriction at p21 but an absence of a transcriptional response late in life at p450. Transcritional studies have been performed using Affymetrix Rat Gene 1.0 arrays for the following treatment groups, with each group run in triplicate (each replicate from separate littermates): Day 21 Control, Day 21 IPCR, Day 450 Con, Day 450 IUCR, Day 450 IPCR
2014-06-01 | E-GEOD-41709 | biostudies-arrayexpress
Project description:Aside from the perinatal complications associated with low birth weight, individuals born with intra-uterine growth restriction suffer from chronic diseases late in life that ultimately lead to a shortened lifespan. These late life metabolic sequelae of low birth weight include obesity and metabolic syndrome, diabetes mellitus, cardiovascular disease, hypertension, stroke, dyslipidemia, and non-alcoholic fatty liver disease/steatohepatitis. Animal models employing perinatal calorie restriction recapitulate the observations made in humans. Interestingly, if continued calorie restriction is employed post-natally the late life sequelae of intra-uterine growth restriction are ameliorated. These observations linking both fetal and early post natal growth to later health is now termed the developmental origins of health and disease. To further our understanding of the mechanism of how early growth affects late life health we have employed Affymetrix microarray-based expression profiling to characterize hepatic gene expression in a rat model of maternal semi-nutrient restriction. In these experiments we have limited maternal calorie intake to 50% of normal so as to create 3 groups of animals: Control (Con) male offspring born to mothers who were fed normally throughout gestation and lactation; intra-uterine calorie restricted male offspring (IUCR) born to mothers who had 50% restriction of calories from e11 to e21; and combined intra-uterine and post-natal calorie restriction (IPCR) male offspring who were born to mothers who received calorie restriction during both fetal growth (e11 to e21) and post-natally (p1-p21). Livers were collected at p21(day 21 of life) for Con and IPCR groups (IUCR withheld owing to ‘catch up” growth), and at p450 (day 450 of life) for Con, IUCR, and IPCR. The profiling data reveals clear alteration of circadian cycling at P21, and subtle changes for circadian gene expression at p450. In addition, a clear transcriptional response is found during active calorie restriction at p21 but an absence of a transcriptional response late in life at p450.
2014-06-01 | GSE41709 | GEO
Project description:Perinatal nutritional imbalances may have long-lasting consequences on health and disease, increasing risk of obesity, insulin resistance, type 2 diabetes or cardiovascular disease. This idea has been conceptualized in the Developmental Origins of Health and Disease Hypothesis (DOHaD). In addition, there is evidence that such early-programmed phenotypes can be transmitted to the following generation(s). It is proposed that, environmentally induced, transmission of disease risk is mediated by epigenetic mechanisms. The aim of this study was to determine whether patterns of gene expression in the first generation offspring are also present in the following generation offspring, via the paternal lineage. Paternal transmission of patterns of gene expression strongly suggest epigenetic inheritance of disease risk. Liver tissue was obtained from the follwing experimental groups: a) control male mice, b) adult male mice previously exposed to 50% caloric restriction in utero (IUGR), c) adult male mice overfed during lactation (ON), d) adult male offspring from control mice, e) adult male offspring from IUGR mice and f) adult male offspring from ON mice.RNA was extracted and processed for further hybridization on Affymetrix microarrays (GeneChip Mouse Genome 430 2.0 (Affymetrix, Santa Clara, CA)).
2015-02-01 | E-GEOD-55304 | biostudies-arrayexpress
Project description:Background: Poor nutrition during development programs kidney function. No studies on postnatal consequences of decreased perinatal nutrition exist in nonhuman primates (NHP) for translation to human renal disease. Our baboon model of moderate maternal nutrient restriction (MNR) produces intrauterine growth restricted (IUGR) and programs renal fetal phenotype. We hypothesized that the IUGR phenotype persists postnatally influencing responses to a high-fat, high-carbohydrate, high-salt (HFCS) diet. Methods: Pregnant baboons ate chow Control (CON) or 70% of control intake (MNR) from 0.16 gestation through lactation. MNR offspring were IUGR at birth. At weaning, all offspring, (control and IUGR females and males n=3/group) ate chow. At ~3.5 years age, blood, urine, and kidney biopsies were collected before and after a 7-week high HFCS diet challenge. Kidney function, unbiased kidney gene expression, and untargeted urine metabolomics were evaluated. Results: IUGR female and male kidney transcriptome and urine metabolome differed from CON at 3.5 years, prior to HFCS. After the challenge, we observed sex-specific and fetal exposure-specific responses in urine creatinine, urine metabolites, and renal signaling pathways. Conclusions: We previously showed mTOR signaling dysregulation in IUGR fetal kidneys. Before HFCS, gene expression analysis indicated that dysregulation persists postnatally in IUGR females. IUGR male offspring response to HFCS showed uncoordinated signaling pathway responses suggestive of proximal tubule injury. To our knowledge, this is the first study comparing CON and IUGR postnatal juvenile NHP and the impact of fetal and postnatal life caloric mismatch. Perinatal history needs to be taken into account when assessing renal disease risk.
2022-12-01 | GSE149895 | GEO
Project description:Intrauterine growth restriction (IUGR) impairs fetal growth and development, perturbs nutrient metabolism, and increases the risk of developing diseases in the postnatal life. However, the underlying mechanisms by which IUGR affects fetuses remain incompletely understood. Here, we applied high-throughput proteomics approach and biochemical analysis to investigate the impact of IUGR on fetal liver.
2016-03-15 | PXD003524 | Pride
Project description:Calorie restriction (CR) extends lifespan by modulating the mechanisms involved in aging. We quantified the hepatic proteome of male C57BL/6 mice exposed to graded levels of CR (0% to 40% CR) for three months, and evaluated which signaling pathways were most affected.
2023-10-24 | PXD033436 | Pride
Project description:Analysis of glucose and Lipid metabolism in male and female offspring after protein restriction of the mother Male offspring showed features of metabolic syndrome after receiving a high fat diet, regardless of the diet of the dam. Glucose and lipid metabolism in male offspring was unaltered. Insulin sensitivity and hepatic fatty acid storage in female offspring of low-protein-fed dams changed in such a way that it resembled the male pattern of insulin sensitivity and hepatic fatty acid storage. Microarray analysis on hepatic gene expression patterns confirmed these findings. We therefore conclude that in mice, maternal protein restriction does not change the response of glucose and fatty acid metabolism to a high fat diet in male offspring, but does program metabolism in female offspring in such a way that it resembles male metabolism. Our findings might have implications for potential future gender-specific treatment of the features of metabolic diseases.
2012-02-08 | GSE15940 | GEO
Project description:Analysis of glucose and Lipid metabolism in male and female offspring after protein restriction of the mother Male offspring showed features of metabolic syndrome after receiving a high fat diet, regardless of the diet of the dam. Glucose and lipid metabolism in male offspring was unaltered. Insulin sensitivity and hepatic fatty acid storage in female offspring of low-protein-fed dams changed in such a way that it resembled the male pattern of insulin sensitivity and hepatic fatty acid storage. Microarray analysis on hepatic gene expression patterns confirmed these findings. We therefore conclude that in mice, maternal protein restriction does not change the response of glucose and fatty acid metabolism to a high fat diet in male offspring, but does program metabolism in female offspring in such a way that it resembles male metabolism. Our findings might have implications for potential future gender-specific treatment of the features of metabolic diseases. Total RNA obtained from liver (16 samples per gender) were compared in the different groups. In total, 4 groups per gender, each group consisting of 4 biological replicates.
2012-02-08 | E-GEOD-15940 | biostudies-arrayexpress
Project description:Intrauterine growth restriction (IUGR) is associated with increased risk of cardiometabolic disease later in life and have been shown to affects female and male offspring differently, but the mechanisms remain unclear. The purpose of this study was to identify proteomic differences and metabolic risk markers in IUGR from male and female neonates when compare with appropriate for gestational age (AGA) that will provide a better understanding of IUGR pathogenesis and its associated risks. Our result revealed alterations in IUGR cord plasma proteomes with most of the enriched proteins implicated in peroxisome pathways. This effect was evident in females but not in males. Furthermore, we observed that catalase activity, peroxisome enzyme, was significantly increased in females (P<0.05) but unchanged in males. Finally, we identified risk proteins associated with obesity, type-2 diabetes, and glucose intolerance such as EGF containing fibulin extracellular matrix protein 1, proprotein convertase subtilisin/kexin type 9 (PCSK9) and transforming growth factor beta receptor 3 (TGFBR3) proteins unique to females while coagulation factor IX (C9) and retinol binding protein 4 (RBP4) are for males. Our data reveal that IUGR may display sexual dimorphism which may be associated with differences in lifelong risk for cardiometabolic disease between males and females.
2023-09-22 | PXD045578 | Pride
Project description:Intrauterine growth restriction (IUGR) is associated with increased relative liver weight at birth, hepatic function decline, and a higher risk for chronic liver and cardiovascular diseases in adults. Precise mechanisms of early developmental plasticity to intervene in poor fetal programming and adult disease remain largely elusive and warrant extensive research. Selecting natural piglets’ model of IUGR, using the liver as a readout and combining previous transcriptome findings, a map of cellular landscape was created to reveal a sex-dependent manner in IUGR-induced hepatic injury and its long-term functional repercussions.Here, we show data on the transcriptional profiles of 41,969 high-quality cells from normal birthweight (NBWs) and IUGR piglets (IUGRs) from hepatic tissue and demonstrated strong homology with human using human-derived liver single-cell dataset. We discovered that male liver was much more severely damaged and inflammation by IUGR than female liver at the one-week postnatal node.
2024-01-31 | GSE222949 | GEO