Periprostatic fat gene expression in male mouse diet induced obesity and calorie restriction study
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PROVIDER: PRJNA508408 | ENA |
REPOSITORIES: ENA
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Project description:Obesity is associated with an increased incidence of high grade prostate cancer (PC) and worse prognosis for PC patients. Recently, we showed in men that obesity-related periprostatic white adipose tissue (WAT) inflammation, characterized by macrophages surrounding dead or dying adipocytes forming crown-like structures, was associated with high grade PC. Possibly, interventions that suppress periprostatic WAT inflammation will improve outcomes for men with PC. We found that supplemental 17β-estradiol (E2) could decrease periprostatic WAT inflammation in obese male mice in association with reduction in weight and calorie consumption. Here, we tested the hypothesis that calorie restriction alone would have similar effects on periprostatic WAT inflammation in obese male mice. To test this hypothesis, male mice were fed high fat diet to induce obesity and then switched to a 30% caloric restriction diet for an addition 7 weeks until sacrifice. LFD fed mice and mice fed HFD ad libitum serve as controls.
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2014-04-30 | GSE56025 | 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 Total mRNA was extracted from mouse colon tissue that was flash frozen immediately after euthaniasia. A total of 6 colons per the three groups were used for microarray analysis. Briefly, 5 ug of RNA were biotin labeled and hybridized to OSU-CCC microRNA microarrays version 4.0. We then analyzed differences in expression with BRB Array.
2014-04-30 | E-GEOD-56025 | 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. 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:Caloric restriction is a robust intervention to increase life span. Giving less food (CR), or allowing free access to diluted diet with indigestible components (CD) are two methods to impose restriction. CD does not generate the same lifespan effect as CR. We compared responses of C57BL/6 mice to equivalent levels of CR and CD. Our study calorie restriction and calorie two restriction methods different effect on hypothamic gene expression pattern, RNA-seq was performed using hypothalamus of mice with 2 methods treatment as well as control group.
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Project description:Obesity, a major risk factor for chronic diseases, is related to dsyfunctional adipose tissue signaling. First human trials suggest benefits of intermittent calorie restriction diet (ICR) in chronic disease prevention that may exceed those of continuous calorie restriction diet (CCR), even at equal net calorie intake. The effect of intermittent calorie restriction on adipose tissue signaling has not been investigated to date. Thus we initiated a randomized controlled trial to analyze the effect of ICR (eu-caloric diet on five days and two days per week with energy restriction of 75%), CCR (daily energy restriction of 20%) and a control group on subcutaneous adipose tissue (SAT) gene expression. 150 overweight or obese non-smoking adults (50 per group, 50% women) were randomly asiged to one of the study arms. SAT biopsies were taken before and after the 12 week intervention phase.
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Project description:Calorie restriction and calorie dilution have different impacts on body fat, metabolism, behavior and hypothalamic gene expression
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Project description:Calorie restriction (CR) has been shown to extend life- and health-span in model species. For most humans, a life-long CR diet is too arduous to adhere to. The aim of this study was to explore whether weekly intermittent CR can 1) provide long-term beneficial effects and 2) counteract diet-induced obesity in male aging mice. In this study, we have exposed C57Bl/6J mice for 24 months to an intermittent (INT) diet, alternating weekly between CR of a control diet and ad libitum moderate-fat (MF) feeding. This weekly intermittent CR significantly counteracted the adverse effects of the MF diet on mortality, body weight and liver health markers in male 24-month-old mice. Hepatic gene expression profiles of INT-exposed animals appeared much more comparable to CR than to MF-exposed mice. At 12 months of age, a subgroup of MF-exposed mice was transferred to the INT diet. Gene expression profiles in the liver of the 24-month-old diet switch mice were highly similar to the INT-exposed mice. However, a small subset of genes was consistently changed by the MF diet during the first phase of life. Weekly intermittent CR largely, but not completely, reversed adverse effects caused by a MF diet.
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