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Microarray and qPCR Analysis of Mitochondrial Metabolism Activation during Prenatal and Early Postnatal Development in Rats and Humans with Emphasis on CoQ10 Biosynthesis

ABSTRACT: During the mammalian ontogenesis, a rapid switch from glycolytic metabolism to oxidative phosphorylation must proceed during postnatal adaptation to extra-uterine conditions. It was proposed that in the course of intra-uterine fetal development, expression changes proceed to cover all metabolic demands all along this critical and extremely fast period. Using microarray techniques, quantitative PCR, enzyme activities’ and coenzyme Q content measurements, we describe perinatal mitochondrial metabolism acceleration in rat liver and skeletal muscle between the 16th day of gestation and the first days of life and possible correlation with results in human. Out of 1546 mitochondrial genes, 72% and 53% were significantly changed in liver and skeletal muscle, respectively. The most important expression shift occurred in the liver at least two days before parturition. We used microarrays to detail the orchestration of gene expression underlying perinatal metabolic shift and identified up- and down-regulated genes during this process.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE131012 | GEO | 2021/05/10

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

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Microarray and qPCR Analysis of Mitochondrial Metabolism Activation during Prenatal and Early Postnatal Development in Rats and Humans with Emphasis on CoQ10 Biosynthesis

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