Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial
S M R Costa1,2,3, E Isganaitis2,3, T J Matthews2
1Universidade Federal de Pernambuco, Recife, Pernambuco, Brazil.
Insights
Maternal obesity alters infant umbilical vein endothelial cells (HUVEC) gene expression, particularly in mitochondrial and lipid metabolism pathways. This suggests prenatal factors influence offspring obesity risk through metabolic programming.
Area of Science:
- Endocrinology
- Metabolomics
- Genomics
Background:
- Maternal obesity is a significant risk factor for childhood obesity.
- The underlying molecular mechanisms linking maternal obesity to offspring obesity risk are not fully understood.
Purpose of the Study:
- To investigate the hypothesis that primary umbilical vein endothelial cells (HUVEC) from infants of overweight and obese mothers exhibit transcriptional patterns indicative of offspring obesity risk.
- To explore the molecular underpinnings of how maternal obesity influences fetal development and metabolic programming.
Main Methods:
- An observational cohort study involving 13 lean and 24 overweight-obese women.
- Isolation of primary HUVEC and analysis of gene expression using Affymetrix Primeview arrays.
- Analysis of cord blood lipidome and levels of hormones and adipokines.
Main Results:
- 142 transcripts were differentially expressed in HUVEC from infants of overweight-obese mothers (FDR<0.05).
- Pathway analysis indicated negative correlation between maternal BMI and genes involved in mitochondrial and lipid metabolism (FDR<0.05).
- Infants of overweight-obese mothers showed significantly increased levels of total free fatty acids, palmitate, and stearate in cord blood.
Conclusions:
- Prenatal exposure to maternal obesity induces alterations in HUVEC gene expression related to mitochondrial and lipid metabolism.
- These transcriptomic changes may reflect developmentally programmed differences in oxidative and lipid metabolism, contributing to offspring obesity risk.
Background/Objectives:
Maternal obesity increases risk for childhood obesity, but molecular mechanisms are not well understood. We hypothesized that primary umbilical vein endothelial cells (HUVEC) from infants of overweight and obese mothers would harbor transcriptional patterns reflecting offspring obesity risk.
Subjects/Methods:
In this observational cohort study, we recruited 13 lean (pre-pregnancy body mass index (BMI) <25.0 kg m-2) and 24 overweight-obese ('ov-ob', BMI⩾25.0 kg m-2) women. We isolated primary HUVEC, and analyzed both gene expression (Primeview, Affymetrix) and cord blood levels of hormones and adipokines.
Results:
A total of 142 transcripts were differentially expressed in HUVEC from infants of overweight-obese mothers (false discovery rate, FDR<0.05). Pathway analysis revealed that genes involved in mitochondrial and lipid metabolism were negatively correlated with maternal BMI (FDR<0.05). To test whether these transcriptomic patterns were associated with distinct nutrient exposures in the setting of maternal obesity, we analyzed the cord blood lipidome and noted significant increases in the levels of total free fatty acids (lean: 95.5±37.1 μg ml-1, ov-ob: 124.1±46.0 μg ml-1, P=0.049), palmitate (lean: 34.5±12.7 μg ml-1, ov-ob: 46.3±18.4 μg ml-1, P=0.03) and stearate (lean: 20.8±8.2 μg ml-1, ov-ob: 29.7±17.2 μg ml-1, P=0.04), in infants of overweight-obese mothers.
Conclusions:
Prenatal exposure to maternal obesity alters HUVEC expression of genes involved in mitochondrial and lipid metabolism, potentially reflecting developmentally programmed differences in oxidative and lipid metabolism.
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