Neurodevelopmental outcome at 1 year in offspring of women with gestational diabetes mellitus.

OBJECTIVE: To study the metabolic derangements in the second half of pregnancy caused by gestational diabetes mellitus(GDM), on the short term neurodevelopment of infants. DESIGN: A prospective cohort study of 555 mother-child pairs were recruited, which included 177 GDM patients and 378 pregnant women with normal glucose tolerance as controls. Clinical and demographic characteristics were obtained at enrollment, birth and follow-up. Neurodevelopment was examined with the Bayley Scales of Infant Development V.1 mental development index (MDI) and psychomotor development index (PDI). Fatty acids (FA) were analyzed by gas chromatography mass spectrometry (GC-MS). RESULTS: Statistically significant differences were found between the two groups in fasting plasma glucose (FPG) and triglyceride (TG). The scores of MDI and PDI of control group were higher than those of GDM group. The regression analysis showed that maternal age and saturated fatty acid (SFA) were independently associated with lower scores on the MDI whereas gestational age and docosahexaenoic acid (DHA) were associated with higher scores; in addition, lower scores on the PDI were associated with FPG and neonatal weigh associated with higher scores. CONCLUSION: SFA, DHA and FPG as indicators of lipid metabolism were associated with neurodevelopmental outcome at 1 year in offspring of women with gestational diabetes mellitus. Control the level of blood glucose and lipid during pregnancy and the appropriate supplementation of DHA during pregnancy in the second half of pregnancy may be beneficial to the neurodevelopment of infants.

Excessive weight gain during pregnancy and risk of macrosomia: a meta-analysis.

PURPOSE: This meta-analysis aimed to estimate the relation between excessive gestational weight gain and macrosomia. METHODS: We performed a meta-analysis by searching PubMed, EMBASE and the Cochrane library for English-language literature from inception to 1 October 2014. Studies assessing the relationship between excessive gestational weight gain and macrosomia were included. Characteristics including study design, country, sample size, definition of macrosomia, adjusted odds ratios, CIs and adjustment factors were extracted independently by two reviewers. Summary odds ratios were calculated by using a random-effects model meta-analysis. RESULTS: 15 relevant articles were eligible for the meta-analysis. Incorporated by random-effect model before the heterogeneity tests, the value of OR was 2.35 (95 % CI: 1.95, 2.85). Stratified analysis showed no differences regarding different study design, definition of macrosomia and location of study. There was no indication of a publication bias either from the result of Egger's test (P = 0.572) or Begg's test (P = 0.572). CONCLUSIONS: Our meta-analysis indicated that excessive gestational weight gain might increase the risk of macrosomia.

Is gestational diabetes mellitus an independent risk factor for macrosomia: a meta-analysis?

PURPOSE: The aim of our meta-analysis was to explore whether gestational diabetes mellitus (GDM) is an independent risk factor for macrosomia or not. METHODS: Three databases were systematically reviewed and reference lists of relevant articles were checked. Meta-analysis of published epidemiological studies (cohort and case-control studies) comparing whether GDM was associated with macrosomia. Calculations of pooled estimates were conducted in random-effect models. Heterogeneity was tested by using Chi square test and I (2) statistics. Publication bias was estimated from Egger's test (linear regression method) and Begg's test (rank correlation method). RESULTS: Twelve studies met the inclusion criteria, including five cohort studies and seven case-control studies. The meta-analysis showed that GDM was associated with macrosomia independent of other risk factors. The adjusted odds ratio was 1.71, 95% CI (1.52, 1.94) in random-effect model, stratified analyses showed no differences regarding different study design, quality grade, definition of macrosomia, location of study and number of confounding factors adjusted for. There was no indication of a publication bias either from the result of Egger's test or Begg's test. CONCLUSION: Our findings indicate that GDM should be considered as an independent risk factor for newborn macrosomia. To adequately evaluate the clinical evolution of GDM need to be carefully assessed and monitored.

Downregulation of peroxisome proliferator-activated receptor gamma in the placenta correlates to hyperglycemia in offspring at young adulthood after exposure to gestational diabetes mellitus.

AIMS/INTRODUCTION: Children who are exposed to gestational diabetes mellitus (GDM) in utero are at high risk of developing related illnesses, such as type 2 diabetes mellitus in young adulthood, but the underlying mechanism and related predictive biomarkers are not known. MATERIALS AND METHODS: The present study identified the related biomarkers of hyperglycemia in young adults from the relationship between fetal blood glucose and placental lipid transporters at messenger ribonucleic acid (mRNA) and protein expression levels. We recruited patients from a prospective cohort, and determined the mRNA and protein levels of placental fatty acid transporters. Diet-induced mouse models of GDM were established, and the mRNA and protein levels of the same transporters in placentas were validated. RESULTS: Only the mRNA levels of peroxisome proliferator-activated receptor gamma correlated with the levels of neonatal blood glucose in GDM patients using linear regression and Spearman's correlation analyses (r = 0.774, P = 0.001). The mRNA levels of peroxisome proliferator-activated receptor gamma, matrix metalloproteinase-2 and fatty acid transport protein-6 correlated with blood glucose levels in mouse offspring (r = 0.82, P = 0.001, r = 0.737, P = 0.006 and r = -0.891, P = 0.001, respectively) at young adulthood using the same analyses. Notably, we observed significantly higher blood glucose levels in GDM offspring at 12 weeks-of-age compared with the control and rosiglitazone-supplemented groups (P < 0.05). CONCLUSIONS: The downregulation of peroxisome proliferator-activated receptor gamma in the placenta might predict hyperglycemia in offspring at young adulthood.