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Metabolomics profile of umbilical cord blood is associated with maternal pre-pregnant obesity in a perspective multi-ethnic cohort displaying health disparities

ABSTRACT: Maternal obesity has become a growing global health concern that impacts fetal health and subsequently predisposes the offspring to medical conditions later in life. However, the molecular link between abnormal fetal metabolomic profiles and maternal obesity has not yet been fully elucidated. In this study, we report new discoveries from the newborn cord blood metabolomes associated with a case-control maternal obesity cohort, collected from multi-ethnic populations in Hawaii, including rarely reported Native Hawaiian and other Pacific Islanders (NHPI). This cohort displays significant maternal obesity disparities by subjects’ residential area average income and health insurance. An elastic net penalized logistic regression model was constructed to associate cord blood metabolomics and demographic/physiological information to maternal obesity, with accuracy as high as 0.947. We identify 29 metabolites as early-life biomarkers manifesting intrauterine effect of maternal obesity.

ORGANISM(S): Human Homo Sapiens

TISSUE(S): Blood

DISEASE(S): Obesity

SUBMITTER: Lana Garmire

PROVIDER: ST001114 | MetabolomicsWorkbench | Thu Mar 08 00:00:00 GMT 2018

REPOSITORIES: MetabolomicsWorkbench

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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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Metabolomics profile of umbilical cord blood is associated with maternal pre-pregnant obesity in a perspective multi-ethnic cohort displaying health disparities

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