Maternal Malnutrition and Elevated Disease Risk in Offspring.

US populations have seen dramatic increases in the prevalence of chronic disease over the past three generations. Rapid increases in type 2 diabetes and obesity have occurred in all the states but have been particularly striking in the Deep South. These increases have contributed to decreases in life expectancy and to painful elevations in health care costs.

Perinatal Stressors and Consequences for Neonates with Critical Congenital Heart Disease.

Introduction: The prenatal diagnosis of congenital heart disease (CHD) is a traumatic event that can cause expectant parents to experience anxiety, depression, and toxic stress. Prenatal exposure to stress may impact neonatal postoperative outcomes. In addition, expectant parents may have other psychosocial stressors that may compound maternal stress.

Thyroid hormone increases fatty acid use in fetal ovine cardiac myocytes.

Cardiac metabolic substrate preference shifts at parturition from carbohydrates to fatty acids. We hypothesized that thyroid hormone (T ) and palmitic acid (PA) stimulate fetal cardiomyocyte oxidative metabolism capacity. T was infused into fetal sheep to a target of 1.

Development of a novel Guinea Pig model producing transgenerational endothelial transcriptional changes driven by maternal food restriction and a second metabolic insult of high fat diet.

Developmental programming of chronic adverse cardiovascular health outcomes has been studied both using numerous human populations and an array of animal models. However, the mechanisms that produce transgenerational effects have been difficult to study due to a lack of developmentally relevant models. As such, how increased disease risk is carried to the second generation has been poorly studied.

Maturation of lipid metabolism in the fetal and newborn sheep heart.

At birth, the fetus experiences a dramatic change in environment that is accompanied by a shift in myocardial fuel preference from lactate and glucose in fetal life to fatty acid oxidation after birth. We hypothesized that fatty acid metabolic machinery would mature during fetal life in preparation for this extreme metabolic transformation at birth. We quantified the pre- (94-day and 135-day gestation, term ∼147 days) and postnatal (5 ± 4 days postnatal) gene expression and protein levels for fatty acid transporters and enzymes in hearts from a precocial species, the sheep.

Sex-specific impact of maternal obesity on fetal placental macrophages and cord blood triglycerides.

Introduction: Maternal obesity is associated with increased risk of offspring obesity and cardiometabolic disease. Altered fetoplacental immune programming is a potential candidate mechanism. Differences in fetal placental macrophages, or Hofbauer cells (HBCs), have been observed in maternal obesity, and lipid metabolism is a key function of resident macrophages that may be deranged in inflammation/immune activation.

Augmenting workload drives T-tubule assembly in developing cardiomyocytes.

Contraction of cardiomyocytes is initiated at subcellular elements called dyads, where L-type Ca channels in t-tubules are located within close proximity to ryanodine receptors in the sarcoplasmic reticulum. While evidence from small rodents indicates that dyads are assembled gradually in the developing heart, it is unclear how this process occurs in large mammals. We presently examined dyadic formation in fetal and newborn sheep (Ovis aries), and the regulation of this process by fetal cardiac workload.

Vision for Improving Pregnancy Health: Innovation and the Future of Pregnancy Research.

Understanding, predicting, and preventing pregnancy disorders have been a major research target. Nonetheless, the lack of progress is illustrated by research results related to preeclampsia and other hypertensive pregnancy disorders. These remain a major cause of maternal and infant mortality worldwide.

Intrauterine growth restriction elevates circulating acylcarnitines and suppresses fatty acid metabolism genes in the fetal sheep heart.

At birth, the mammalian myocardium switches from using carbohydrates as the primary energy substrate to free fatty acids as the primary fuel. Thus, a compromised switch could jeopardize normal heart function in the neonate. Placental embolization in sheep is a reliable model of intrauterine growth restriction (IUGR).

Hyperglycemia and gestational diabetes suppress placental glycolysis and mitochondrial function and alter lipid processing.

The degree that maternal glycemia affects placental metabolism of trophoblast cell types [cytotrophoblast (CTB) and syncytiotrophoblast (SCT)] in pregnant persons with gestational diabetes mellitus (GDM) is unknown. We tested the hypotheses that (a) hyperglycemia suppresses the metabolic rates of CTB and SCT; and (b) low placental metabolic activity from GDM placentas is due to decreased oxygen consumption of CTB. Trophoblast cells isolated from GDM and non-GDM term placentas were cultured for 8-hour (CTB) and following syncytialization at 72-hour (SCT) in 5 mM of glucose or 25 mM of glucose.

Maternal dietary fat intake during pregnancy and newborn body composition.

Objective: Increased infant birth weight and adiposity are associated with an altered risk of adult chronic diseases. The objective was to investigate the association between maternal dietary fat intake during pregnancy and newborn adiposity.

Study Design: The study included 79 singleton pregnancies.

Exclusive Breastfeeding Rates at 6 Weeks Postpartum as a Function of Preconception Body Mass Index Are Not Impacted by Postpartum Obstetrical Practices or Routines.

Women with overweight/obesity have significantly lower rates of exclusive breastfeeding (EBF) at 6 weeks postpartum compared with women of normal weight. We sought to determine whether differences in Baby-Friendly Hospital Initiative (BFHI) adherence, obstetric practices, or social support explain these weight-related EBF disparities. One hundred forty-two healthy women who intended EBF (61 normal weight, 50 overweight, and 31 obese by preconception body mass index [BMI]) were enrolled in a cross-sectional study.

Social Determinants of Placental Health and Future Disease Risks for Babies.

Birthweight is a well-known predictor of adult-onset chronic disease. The placenta plays a necessary role in regulating fetal growth and determining birth size. Maternal stressors that affect placental function and prenatal growth include maternal overnutrition and undernutrition, toxic social stress, and exposure to toxic chemicals.

30th anniversary for the Developmental Origins of Endocrinology.

This special issue for the Journal of Endocrinology celebrates the 30th anniversary of David Barker's seminal findings that led to the scientific field of the Developmental Origins of Health and Disease (DOHaD). In 1989, Barker and colleagues reported that low birth weight and weight at one year, proxies for fetal growth restriction, were related to an individual's risk for developing hypertension and cardiovascular heart disease. Barker's initial epidemiological studies also demonstrated that low birth weight was predictive of later glucose intolerance, Type 2 Diabetes, and other metabolic-related diseases.

Down-regulation of MEIS1 promotes the maturation of oxidative phosphorylation in perinatal cardiomyocytes.

Fetal cardiomyocytes shift from glycolysis to oxidative phosphorylation around the time of birth. Myeloid ecotropic viral integration site 1 (MEIS1) is a transcription factor that promotes glycolysis in hematopoietic stem cells. We reasoned that MEIS1 could have a similar role in the developing heart.

Thyroid hormone receptor function in maturing ovine cardiomyocytes.

Key Points: Plasma thyroid hormone (tri-iodo-l-thyronine; T ) concentrations rise near the end of gestation and is known to inhibit proliferation and stimulate maturation of cardiomyocytes before birth. Thyroid hormone receptors are required for the action of thyroid hormone in fetal cardiomyocytes. Loss of thyroid hormone receptor (TR)α1 abolishes T signalling via extracellular signal-related kinase and Akt in fetal cardiomyocytes.