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Early alterations in glucose homeostasis increase the risk of developing insulin resistance (IR) and obesity later in life. The study aimed to ascertain the peripheral blood levels of hormones that controlling glucose homeostasis and inflammatory factors that are correlated with IR and fetal outcomes in small-for-gestational-age (SGA) infants born to mothers with gestational diabetes mellitus (GDM).This cohort study included a total of 90 SGA infants born to mothers with GDM (Compared with SGA infants born to mothers without GDM, the levels of low-density lipoprotein-cholesterol (LDL-C), GH, and fibrinogen were significantly higher in the SGA infants born to mothers with GDM (Altered biomarkers of IR were observed among SGA infants born to mothers with GDM, suggesting that these infants were more prone to develop IR after birth.

We studied the demographic and clinical characteristic, risk factors, outcomes of full-term small-for-gestational-age (SGA) infants born to mothers with gestational diabetes mellitus (GDM) in China. A retrospective case-control study that included 1981 SGA infants was conducted; the demographic and clinical data between SGA infants born to mothers with and without GDM were compared. Of 383 SGA infants born to mothers with GDM, 221 (57.7%) were female, and the incidence of these infants was 1 in 155 live births. The risk of SGA siblings (RR, 1.88; 95% CI, [1.23–2.86]), low 1- and 5-min Apgar scores (RR,2.04 and 4.21; 95%CI [1.05–4.00] and [1.05–16.89], respectively), early thrombocytopenia (RR, 3.39; 95%CI, [1.33–8.64]), hypoglycemia(RR, 2.49; 95%CI, [1.55–3.98]), and hypoxic-ischemic encephalopathy (RR,5.61; 95%CI, [1.25–25.18]) were increased in SGA infants born to mothers with GDM compared to SGA infants born to mothers without GDM. SGA girls born to mothers with GDM had a significantly higher ratio of catch-up growth (CUG) (RR, 1.73; 95%CI, [1.18–2.54]) in the first year of life. These results show that genetic factors may be one of the etiologies of SGA infants born to mothers with GDM; and these infants have more adverse perinatal outcomes compared to SGA infants born to mothers without GDM. SGA girls born to mothers with GDM had accelerated CUG in the first year of life.

The aim of the present study was to investigate the association of neonatal necrotizing enterocolitis (NEC) with myeloid differentiation-(MD-2) and GM2 activator protein (GM2A) genetic polymorphisms. Gene resequencing of the MD-2 and GM2A gene exons was performed on 42 neonates, diagnosed with NEC (NEC group), as well as in the rs11465996 locus, located in the MD-2 gene promoter region. The aim was to detect the genetic polymorphisms present in the neonates with NEC and compare the functional polymorphic loci with 83 neonates without NEC (control group), who had been born during the same period. A polymorphic locus with abnormal frequency was detected in the exon region of the MD-2 gene. In the NEC group, the frequency of genotypes carrying the low frequency allele (G) in the rs11465996 locus (MD-2 promoter region) was significantly higher compared with the control group (χ(2)=4.388, P=0.036). Furthermore, the frequencies of genotypes carrying the low frequency A and C alleles in the rs1048719 (GM2A gene exon 1) and rs2075783 loci (GM2A intron), respectively, were significantly higher in the NEC group compared with the control group (χ(2)=4.316, P=0.038; and χ(2)=13.717, P=0.000, respectively). In addition, the rs11465996 polymorphism in the MD-2 gene promoter region was found to be associated with the severity of NEC. Furthermore, the rs2075783 polymorphism in the GM2A gene exon 1 and the rs1048719 polymorphism in the intron region of this gene, were associated with the occurrence of NEC. The present study demonstrated that gene polymorphisms of MD-2 and GM2A were associated with the occurrence or severity of NEC; however, further in-depth exploration is required to clarify the associations between genetic predispositions to polymorphisms, and NEC.

We investigated the effect of inactivated Bifidobacterium on the mRNA expression of TRAF6, GSK-3β, and microRNA-146a in lipopolysaccharide (LPS)-stimulated rat small intestinal epithelial cells (IEC-6s). IEC-6s were randomly divided into an LPS group, a culture supernatant group, and an inactivated bacteria group. After stimulation with LPS for 5 h, the three groups were treated as follows: the LPS group was cultured for 24 h with sterile saline; the culture supernatant group was cultured with Bifidobacterium (infantis strain) culture supernatant for 24 h; and the inactivated bacteria group was cultured with inactivated infantis Bifidobacterium for 24 h. Reverse transcription polymerase chain reaction was used to determine mRNA expression levels. The mRNA expression levels of TRAF-6 and GSK-3β in the culture supernatant group were lower, and microRNA-146a expression was higher, compared with the LPS group (t = 5.278, P = 0.000; t = 6.316, P = 0.000; t = 13.218, P = 0.000, respectively). GSK-3β mRNA expression in the inactivated bacteria group was lower than in the LPS group (t = 4.837, P = 0.000). There was no difference in the mRNA expression levels of TRAF-6 and microRNA-146a between the two groups (t = 0.732, P = 0.472 and t = 1.463, P = 0.164). Both the culture supernatant and the inactivated Bifidobacterium had a protective effect on LPS-stimulated IEC-6s. The protective effect of Bifidobacterium may be achieved through increased microRNA-146a by reducing levels of TRAF6 and GSK-3β; the protective effect of inactivated Bifidobacterium may be achieved by reducing levels of GSK-3β.

Background/Purpose Toll-like receptor (TLR)-4 and TLR-2 play an essential role in the pathogenesis of necrotizing enterocolitis (NEC). In this study, we investigated the protective effect of glutamine (Gln) in an NEC neonatal rat model, and the potential association with TLR-4 and TLR-2 expression in local intestinal tissues. Methods Preterm neonatal rats were randomly divided into 3 groups: normal control; NEC model; and NEC plus Gln intervention. NEC was induced by feeding with artificial milk substitutes, plus exposure to hypoxia and cold stress. All preterm rats were sacrificed at 3days after birth. The intestinal tissues were taken for pathological analysis. Protein and mRNA expression of TLR-2, TLR-4, and caspase-3 was examined by immunohistochemistry and real-time RT-PCR, respectively. Results Compared with the normal control, the NEC neonatal rats showed mucosal injury and upregulated mRNA and protein expression of TLR-2, TLR-4, and caspase-3 in ileum and colon. Gln intervention significantly reduced the mucosal injury and suppressed the upregulated expression of TLR-2, TLR-4, and caspace-3 in the ileum and colon of NEC neonatal rats. Conclusions Gln protects the intestinal tract of NEC neonatal rats, which may be associated with the reduction of TLR-2 and TLR-4 expression in intestines

Background Prader-Willi syndrome is a rare genetic abnormality that can be challenging to diagnose early, but for which early interventions improve prognosis. Methods To improve understanding of Prader–Willi syndrome in neonates in Asia, we retrospectively analyzed the clinical records of 20 affected newborns diagnosed in the Department of Neonatology, Guangzhou Women and Children’s Medical Center, Guangzhou, China from January 2007 to December 2014 and performed a review of the relevant literature. Results Fourteen boys and six girls presented with hypotonia, poor responsiveness, feeding difficulty, and infrequent, weak crying. Different from western patients, the 20 Asian patients exhibited at least five of the following typical features: prominent forehead, narrow face, almond-shaped eyes, small mouth, downturned mouth, thin upper lip, and micromandible. All 14 boys had a small scrotum, including nine with cryptorchidism. Diagnoses were made with microarray comparative genomic hybridization. All 20 infants required feeding tubes. Fifteen received swallowing training immediately after admission; the period of continuous tube feeding for these patients ranged from 8 to 22 days (mean, 14 ± 5.3 days). For the five patients who did not receive swallowing training, the period of continuous tube feeding ranged from 15 to 35 days (mean, 18 ± 4.3 days). Comprehensive care measures included: giving parents detailed health education and basic information about this disease, teaching skills to promote feeding and prevent suffocation, increasing children’s passive activity, providing nutrition management for normal development, and preventing excessive or inadequate nutrient intake. Conclusions Neonates with Prader–Willi syndrome in Asia have hypotonia, poor responsiveness, feeding difficulty, infrequent and weak crying, genital hypoplasia, and characteristic facial features. Recognition of the syndrome in neonates with confirmation by genetic testing is essential, because early diagnosis allows early intervention. Treatment measures including swallowing training can improve prognosis, prevent growth retardation and obesity, and elevate quality of life in individuals with Prader–Willi syndrome.