ABSTRACT
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.
Subject(s)
Human Umbilical Vein Endothelial Cells/metabolism , Lipid Metabolism/genetics , Mothers , Obesity/genetics , Pregnancy Complications/genetics , Umbilical Cord/cytology , Adult , Cohort Studies , Female , Fetal Development , Gene Expression Profiling , Gene Expression Regulation , Humans , Infant , Inflammation/physiopathology , Maternal Nutritional Physiological Phenomena/physiology , Mitochondria/metabolism , Obesity/metabolism , Obesity/pathology , Obesity/prevention & control , Pregnancy , Pregnancy Complications/metabolism , Pregnancy Complications/pathology , Prenatal Exposure Delayed EffectsABSTRACT
OBJECTIVES: This report is the first release of multistate data for selected items exclusive to the 2003 revision of the U.S. Standard Certificate of Live Birth. Included is information for prepregnancy body mass index, smoking and quitting smoking in the 3 months prior to pregnancy, receipt of food from the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) during pregnancy, pregnancy resulting from infertility treatment, source of payment for delivery, and maternal morbidities. METHODS: Descriptive statistics are presented for 100% of 2011 births to residents of the 36 states, the District of Columbia (D.C.), and Puerto Rico that had implemented the revised birth certificate by January 1, 2011. This reporting area is not a random sample, and results are not generalizable to the United States as a whole. RESULTS: The 3,267,934 births to residents of the 36-state and D.C. reporting area represented 83% of all 2011 U.S. births. Levels of prepregnancy obesity ranged from 18.0% in Utah to 28.6% in South Carolina. Hispanic women were the least likely to smoke in the 3 months prior to pregnancy and were the most likely to quit smoking prior to pregnancy. Women under age 20 were more than twice as likely to receive WIC food during pregnancy as women aged 35 and over in nearly all states and D.C. The percentage of births resulting from infertility treatment ranged from 0.3% in New Mexico to over 3.5% in Maryland and Utah. The percentage of deliveries covered by Medicaid ranged from 28.8% in North Dakota to 64.2% in Louisiana.