Necrotizing enterocolitis (NEC) afflicts extremely low birth weight neonates, and probiotics reduces its incidence and severity. NO is involved in the pathogenesis of NEC, and caveolin-1 regulates NO signaling. We tested the hypothesis that intestinal caveolin-1 and NOS are deficient in formula-fed neonatal rats and that supplementation with "Florastar Kids" and/or galactooligosaccharides and fructo-oligosaccharides preserves caveolin-1 and NOS. At birth (P0), neonatal rat pups were maternally fed or hand-gavaged with or without supplemented formula. Samples from the terminal ileum were analyzed for total NO metabolites, growth factors, and gene expression of caveolin-1, NOS isoforms, and antioxidants. Our data showed that formula feeding with and without supplementation resulted in significant growth restriction. Despite suboptimal nutrition, growth factors involved in intestinal repair and regeneration were increased in the neonatal rat ileum. Caveolin-1, endothelial NOS, and neuronal NOS were simultaneously downregulated with formula feeding while inducible NOS was upregulated. Superoxide dismutase and glutathione peroxidase were up-regulated with supplementation. These data provide a probable mechanism for the benefits of supplemented formula for decreasing the severity of NEC by preserving the antioxidant systems. (Pediatr Res 67: 526-531, 2010)

IntroductionAllostatic load (AL) defines cardiometabolic, inflammatory, and neuroendocrine changes in the body in response to internal and external stressors. It is largely unknown whether gestational diabetes mellitus (GDM) alters maternal and fetal AL, which in turn affects GDM outcomes. Whether dietary intakes and quality can modify AL and thus influence GDM progression is also unknown.Research design and methodsIn this study, we recruited 35 GDM and 30 non-GDM women in gestational week 25–33. Fasting blood samples were collected at enrollment, and cord venous blood samples were collected at delivery for the measurement of a series of AL biomarkers to calculate the composite AL index. Three-day dietary recalls were conducted at enrollment.ResultsResults suggest that GDM women had 60% higher composite AL index scores (p value=0.01). Maternal AL index was associated with shorter duration of gestation (β=−0.33, p value=0.047) and higher fetal AL index (β=0.47, p value=0.006) after adjusting for GDM status. Dietary intake of monounsaturated fatty acids was negatively associated with maternal AL index (β=−0.20, p value=0.006). GDM women had lower total caloric intake and dietary glycemic load, yet their linolenic acid, vitamin C and E intakes were also decreased (all p value<0.05). These dietary differences were not related to birth outcomes measured.ConclusionsIn this study, GDM status and dietary intakes modify AL in this population. AL may serve as an indicator of GDM control. Future research on dietary interventions that can improve maternal AL markers during GDM is warranted.

Induction of IGF-I and EGF with moderate bowel integrity may represent a protective effect of probiotics against formula-induced inflammation. These data, taken collectively, suggest that probiotics may provide more beneficial effects on the developing large bowel than prebiotics and synbiotics.

Background: Maternal hyperglycemia influences childhood metabolic syndrome, including obesity and hyperglycemia. We tested the hypothesis that the maternal hyperglycemia influences growth factors in the fetal and pre-adolescent offspring. Methods: Hyperglycemia was induced in pregnant rats on embryonic day (E)16 using streptozocin followed by implantation with insulin or placebo pellets at embryonic day 18 (E18). Fetuses at E20 and pre-adolescent pups at postnatal day 14 (P14) were studied: (1) normal untreated controls (CTL) at E20; (2) hyperglycemic placebo-treated (HPT) at E20; (3) hyperglycemic insulin-treated (HIT) at E20; (4) CTL at P14; and (5) HIT at P14. Fetal and pre-adolescent growth factors were determined. Results: Biomarkers of hypoxia were elevated in the HPT group at E20. This group did not survive to term. Maternal insulin improved fetal survival despite lower fetal body weight at E20, however, at normal birth (postnatal day 0 (P0)) and at P14, body weights and blood glucose were higher than CTL. These high levels correlated with aberrant growth factors. Maternal hyperglycemia influenced glucose-6-phosphate dehydrogenase, glucagon, insulin, interleukin-10, and leptin genes. Conclusions: The impact of maternal hyperglycemia on pre-adolescent glucose and body weight was not a consequence of maternal overnutrition. This suggests an independent link which may affect offspring metabolic health in later life.

Thyroid diseases in children and adolescents include acquired or congenital conditions, including genetic disorders either isolated or part of a syndrome. Briefly, we will review the physiology and pathophysiology of the thyroid gland and its disorders. The aim of this chapter is to describe genetic abnormalities of the thyroid gland.

In this review, we describe genetic mutations affecting metabolic pathways of calcium and phosphorus homeostasis. Calcium and phosphorus homeostasis has tight hormonal regulation by three major hormones: vitamin D, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23). We describe the physiology and pathophysiology of disorders, their biochemical profile, clinical characteristics, diagnostics, and treatments.