The state and future of pediatric research-an introductory overview : The state and future of pediatric research series.

This is an introduction to an article series devoted to the current state and future of pediatric research. The role of public-private partnerships, influencing factors, challenges, and recent trends in pediatric research are described, with emphasis on funding, drug and device development, physician-scientist training, and diversity. Potential solutions and advocacy opportunities are discussed.

Explaining the Black-White Disparity in Preterm Birth: A Consensus Statement From a Multi-Disciplinary Scientific Work Group Convened by the March of Dimes.

In 2017-2019, the March of Dimes convened a workgroup with biomedical, clinical, and epidemiologic expertise to review knowledge of the causes of the persistent Black-White disparity in preterm birth (PTB). Multiple databases were searched to identify hypothesized causes examined in peer-reviewed literature, 33 hypothesized causes were reviewed for whether they plausibly affect PTB and either occur more/less frequently and/or have a larger/smaller effect size among Black women vs. White women.

Making the case for pediatric research: a life-cycle approach and the return on investment.

There is unmistakable evidence of increased NIH funding for pediatric and perinatal research, but there is much work to be done. To further promote NIH-funded pediatric and perinatal research, we advocate for a life-cycle approach in which the return on the investment continues over the lifespan. Although elected policymakers have short-time horizons, pediatric and perinatal researchers must provide novel evidence and theoretical arguments demonstrating the long-term health benefits for the adults of tomorrow by improving the health of our current pediatric populations.

The Term Newborn: Hypoglycemia.

This review provides an update on neonatal hypoglycemia in the term infant, including discussion of glucose metabolism, definitions of hypoglycemia, identification of infants commonly at risk, and the screening, treatment, and potential neurologic outcomes of postnatal hypoglycemia. Neonatal hypoglycemia is a common metabolic condition that continues to plague clinicians because there is no clear relationship between low glucose concentrations or their duration that determines adverse neurologic outcomes. However, severely low, prolonged, recurrent low glucose concentrations in infants who also have marked symptoms such as seizures, flaccid hypotonia with apnea, and coma clearly are associated with permanent brain damage.

Adiponectin Promotes Maternal β-Cell Expansion Through Placental Lactogen Expression.

Hypoadiponectinemia is a risk factor of gestational diabetes mellitus (GDM). Our previous study reported that adiponectin gene knockout mice ( ) develop GDM due to insulin insufficiency. The main objective of this study was to elucidate the underlying mechanism through which adiponectin controls islet expansion during pregnancy.

Concentrating human milk: an innovative point-of-care device designed to increase human milk feeding options for preterm infants.

Objective: The purpose of this study was to determine whether a point-of-care osmotic device concentrates important human milk (HM) nutrients to support feeding neonates requiring high-nutrient, low-volume feedings.

Study Design: Raw and pasteurized HM samples were concentrated to determine the effects of time and temperature on concentration. Concentrated samples were compared with matched baseline samples to measure changes in selected nutrient concentrations.

Effects of chronic hyperinsulinemia on metabolic pathways and insulin signaling in the fetal liver.

The effect of chronic of hyperinsulinemia in the fetal liver is poorly understood. Here, we produced hyperinsulinemia with euglycemia for ∼8 days in fetal sheep [hyperinsulinemic (INS)] at 0.9 gestation.

A Chronic Fetal Leucine Infusion Potentiates Fetal Insulin Secretion and Increases Pancreatic Islet Size, Vascularity, and β Cells in Late-Gestation Sheep.

Background: Infusion of a complete amino acid mixture into normal late-gestation fetal sheep potentiates glucose-stimulated insulin secretion (GSIS). Leucine acutely stimulates insulin secretion in late-gestation fetal sheep and isolated fetal sheep islets in vitro.

Objectives: We hypothesized that a 9-d leucine infusion would potentiate GSIS in fetal sheep.

"Extrauterine growth restriction" and "postnatal growth failure" are misnomers for preterm infants.

Preterm infants are increasingly diagnosed as having "extrauterine growth restriction" (EUGR) or "postnatal growth failure" (PGF). Usually EUGR/PGF is diagnosed when weight is <10th percentile at either discharge or 36-40 weeks postmenstrual age. The reasons why the phrases EUGR/PGF are unhelpful include, they: (i) are not predictive of adverse outcome; (ii) are based only on weight without any consideration of head or length growth, proportionality, body composition, or genetic potential; (iii) ignore normal postnatal weight loss; (iv) are usually assessed prior to growth slowing of the reference fetus, around 36-40 weeks, and (v) are usually based on an arbitrary statistical growth percentile cut-off.

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle.

Key Points: Previous studies in fetuses with intrauterine growth restriction (IUGR) have shown that adrenergic dysregulation was associated with low insulin concentrations and greater insulin sensitivity. Although whole-body glucose clearance is normal, 1-month-old lambs with IUGR at birth have higher rates of hindlimb glucose uptake, which may compensate for myocyte deficiencies in glucose oxidation. Impaired glucose-stimulated insulin secretion in IUGR lambs is due to lower intra-islet insulin availability and not from glucose sensing.

Skeletal muscle amino acid uptake is lower and alanine production is greater in late gestation intrauterine growth-restricted fetal sheep hindlimb.

In a sheep model of intrauterine growth restriction (IUGR) produced from placental insufficiency, late gestation fetuses had smaller skeletal muscle mass, myofiber area, and slower muscle protein accretion rates compared with normally growing fetuses. We hypothesized that IUGR fetal muscle develops adaptations that divert amino acids (AAs) from protein accretion and activate pathways that conserve substrates for other organs. We placed hindlimb arterial and venous catheters into late gestation IUGR ( = 10) and control (CON, = 8) fetal sheep and included an external iliac artery flow probe to measure hindlimb AA uptake rates.

Prolonged Prepregnant Maternal High-Fat Feeding Reduces Fetal and Neonatal Blood Glucose Concentrations by Enhancing Fetal β-Cell Development in C57BL/6 Mice.

The main objective of this study was to investigate the effect of maternal obesity on offspring's glucose metabolism during the perinatal period. Maternal obesity was established by feeding C57BL/6 mice with a high-fat (HF) diet before or during pregnancy. Our results showed that prolonged prepregnant HF feeding but not HF feeding during pregnancy significantly reduced fetal and neonatal blood glucose concentrations.

Sustained hypoxemia in late gestation potentiates hepatic gluconeogenic gene expression but does not activate glucose production in the ovine fetus.

Fetal hypoxemia is associated with pregnancy conditions that cause an early activation of fetal glucose production. However, the independent role of hypoxemia to activate this pathway is not well understood. We hypothesized that fetal hypoxemia would activate fetal glucose production by decreasing umbilical glucose uptake and increasing counter-regulatory hormone concentrations.