Hepatic and Pancreatic Changes in Response to Prenatal Diet Restriction with Postnatal Exposure to a High Fat/high fructose Diet in the Adult Male and Female Rat Offspring
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE255675 | GEO | 2025/02/12
REPOSITORIES: GEO
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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:SCOPE: We investigated whether a novel dietary intervention consisting of an every-other-week calorie-restricted diet could prevent nonalcoholic fatty liver disease (NAFLD) development induced by a medium-fat (MF) diet. METHODS AND RESULTS: Nine-week-old male C57BL/6J mice received either a (i) control (C), (ii) 30E% calorie restricted (CR), (iii) MF (25E% fat), or (iv) intermittent (INT) diet, a diet alternating weekly between 40E% CR and an ad libitum MF diet until sacrifice at the age of 12 months. The metabolic, morphological, and molecular features of NAFLD were examined. The INT diet resulted in healthy metabolic and morphological features as displayed by the continuous CR diet: glucose tolerant, low hepatic triglyceride content, low plasma alanine aminotransferase. In contrast, the C- and MF-exposed mice with high body weight developed signs of NAFLD. However, the gene expression profiles of INT-exposed mice differed to those of CR-exposed mice and showed to be more similar with those of C- and MF-exposed mice with a comparable body weight. CONCLUSIONS: Our study reveals that the INT diet maintains metabolic health and reverses the adverse effects of the MF diet, thus effectively prevents the development of NAFLD in 12-month-old male C57BL/6J mice. Male C57Bl/6J mice were divided to 4 dietary intervention groups: Control (AIN-93W), 30% calorie restriction (CR; AIN-93W-CR), medium fat (MF; AIN-93W-MF; 25% energy from fat) and intermittent diet (INT; weekly alternating diet between AIN-93W-MF ad lib and 40% CR of AIN-93W). We performed various measurements on metabolic parameters and gene expression analysis on the liver. This entry represents the microarray data of the liver gene expression of each mouse.
2015-10-26 | E-GEOD-61233 | biostudies-arrayexpress
Project description:Background & Aims: In this study, we investigated metabolic and molecular effects of weekly intervening 30% calorie restriction on long term natural progression of non-alcoholic fatty liver disease (NAFLD), which was induced by a medium fat diet. Methods: Male C57BL/6J mice of 9 weeks old received either (1) a control (C), (2) a calorie restricted (CR), (3) a medium fat (MF; 25%fat) or (4) an intermittent diet (ID), a weekly alternating diet consisting of calorie restriction and medium fat diet ad libitum until sacrifice at the age of 12 months. Various metabolic and molecular features of the liver were examined. Results: The ID regimen improved the status of a range of metabolic parameters and showed no progression to NAFLD: proper glucose tolerance, low hepatic triglyceride content, low plasma alanine aminotransferase and no abnormalities in its liver morphological features; similarly to that of CR. In contrast, the metabolic parameters in a number of the C and MF animals indicated development of NAFLD and hepatic fibrosis, which was positively correlated with body weight. Despite the metabolic phenotypes similarity, the liver gene expression profile of ID-fed mice did not reflect that of CR mice and resembled more to C and MF-fed mice with similar low body weight. Conclusions: Our study reveals that ID is beneficial for metabolic health and prevents the development of NAFLD in mice, with a gene expression profile similar to C and MF diet in a body weight-dependent manner.
2018-05-09 | GSE53188 | GEO
Project description:SCOPE: We investigated whether a novel dietary intervention consisting of an every-other-week calorie-restricted diet could prevent nonalcoholic fatty liver disease (NAFLD) development induced by a medium-fat (MF) diet. METHODS AND RESULTS: Nine-week-old male C57BL/6J mice received either a (i) control (C), (ii) 30E% calorie restricted (CR), (iii) MF (25E% fat), or (iv) intermittent (INT) diet, a diet alternating weekly between 40E% CR and an ad libitum MF diet until sacrifice at the age of 12 months. The metabolic, morphological, and molecular features of NAFLD were examined. The INT diet resulted in healthy metabolic and morphological features as displayed by the continuous CR diet: glucose tolerant, low hepatic triglyceride content, low plasma alanine aminotransferase. In contrast, the C- and MF-exposed mice with high body weight developed signs of NAFLD. However, the gene expression profiles of INT-exposed mice differed to those of CR-exposed mice and showed to be more similar with those of C- and MF-exposed mice with a comparable body weight. CONCLUSIONS: Our study reveals that the INT diet maintains metabolic health and reverses the adverse effects of the MF diet, thus effectively prevents the development of NAFLD in 12-month-old male C57BL/6J mice.
2015-10-26 | GSE61233 | GEO
Project description:Paneth cells recide in the intestinal crypt bottom and are part of the innate immunity and of the intestinal stem cell niche. We used microarrays to detail the global changes in gene expression following reduced calorie intake. Mice were kept on ad libitum or calorie restricted (60% of calories of ad libitum) diets for 4-7 weeks and paneth cells were isolated using flowcytometry
2012-04-11 | E-GEOD-37209 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent form of hepatic disease and feeding mice a High-Fat, High-Caloric (HFHC) diet is a standard model of NAFLD. In order to better understand the genetic basis of NAFLD, we conducted an expression quantitative trait locus (eQTL) analysis of mice fed a HFHC diet. 265 (A/J × C57BL/6J) F2 male mice were fed a HFHC diet for 8 weeks. QTL analysis was utilized to identify genomic regions that regulate hepatic gene expression of Xbp1s and Socs3. We identified two overlapping loci for Xbp1 and Socs3 on Chr 1 (164.0-185.4 Mb and 174.4-190.5 Mb, respectively) and Chr 11 (41.1-73.1 Mb and 44.0-68.6 Mb, respectively), and an additional locus for Socs3 on Chr 12 (109.9-117.4 Mb). C57BL/6J-Chr 11A/J/ NaJ mice fed a HFHC diet manifested the A/J phenotype of increased Xbp1s and Socs3 gene expression (p<0.05), while C57BL/6J-Chr 1A/J/ NaJ mice retained the C57BL/6 phenotype. In addition, we replicated the eQTLs on Chr 1 and 12 (LOD scores ? 3.5) using mice from the BXD murine reference panel challenged with CCl4 to induce chronic liver injury and fibrosis. We have identified overlapping eQTLs for Xbp1 and Socs3 on Chr 1 and 11, and consomic mice confirmed that replacing the C57BL/6 with the A/J Chr 11 resulted in an A/J phenotype for Xbp1 and Socs3 gene expression. Identification of the genes for these eQTLs will lead to a better understanding of the genetic factors responsible for NAFLD and potentially other hepatic diseases. Liver samples from eight-week-old AJ and C57BL6J males fed a High Fat High Calorie diet.
2014-08-02 | E-GEOD-56987 | biostudies-arrayexpress
Project description:We performed a factorial experiment examining the effects of calorie restriction (CR) and exercise (EX) in mice. CR mice received 70% of calories but 100% of all other nutrients compared to AL mice. Food consumption, weight gain, and physical activity levels were recorded for 6 weeks. Diet and exercise treatments, both alone and in combination, had significant effects on body composition and levels of physical activity. Affymetrix oligo microarrays were used to determine global gene expression patterns in mammary gland total RNA. CR and EX had some overlapping but primarily unique effects on mammary gene expression, with CR affecting a much larger number of genes. The gene changes presented suggest that CR and EX influence mammary gland development and potentially carcinogenesis through distinct pathways. Keywords: 2 X 2 factorial mouse experiment; ad lib; calorie restriction; exercise; exercise + calorie restriction. Endpoints: body composition; bone density; gene expression in mammary gland
2008-12-24 | GSE14202 | GEO
Project description:In murine NAFL/NASH models, high-fat high-calorie fructose (HFHC) diet fed for 16 weeks induces hepatic steatosis, inflammatory cells infilatration and early stage fibrosis. In addition, HFHC diet 16 weeks but not 8 weeks is accompanied with weight gain and insulin resistance. The aim of this study is to determine the gene expression changes in mouse liver by HFHC diet for 8weeks.
2021-12-08 | GSE154426 | GEO
Project description:We analyzed the impact of calorie restriction and diet-induced obesity on expression of microRNAs in the mouse colon. For this analysis, data was LOESS normalized in R. Data was then imported into BRB Array for analysis. We identified microRNAs that were altered in response to calorie-restriction and diet-induced obesity
2014-04-30 | GSE56025 | GEO