The influence of obesity and diabetes on the prevalence of macrosomia.

How can the scientific literature provide unbiased conclusions if it represents a biased sample of available studies? Publication bias refers to phenomena arising from bias in submitting, reviewing, accepting and publishing scientific results. Direct and indirect methods for investigating publication bias are now readily available, but indirect methods are generally open to alternative interpretations. Publication bias distorts attempts to review a scientific field quantitatively if the likelihood of locating completed studies depends on the strength or direction of the findings of quantitative studies. It is the responsibility of researchers, reviewers and editors to address issues of bias to ensure the existence of an unbiased literature.

/pdf/testing-and-adjusting-for-publication-bias-3ot2zal1jr.pdf

Testing and adjusting for publication bias

Complex though integrated hormonal and metabolic changes characterize pregnancy. In the face of progressive decline in insulin action, glucose homeostasis is maintained through a compensatory increase in insulin secretion. This switches energy production from carbohydrates to lipids, making glucose readily available to the fetus. This precise and entangled hormonal and metabolic condition can, however, be disrupted and diabetic hyperglycemia can develop (gestational diabetes). The increase in plasma glucose level is believed to confer significant risk of complications to both the mother and the fetus and the newborn. Moreover, exposition of fetal tissues to the diabetic maternal environment can translate into an increased risk for development of diabetes and/or the metabolic syndrome in the adult life. In women with previous gestational diabetes, the risk of developing type 2 diabetes is greatly enhanced, to the point that GDM represents an early stage in the natural history of type 2 diabetes. In these women, accurate follow-up and prevention strategies are needed to reduce the subsequent development of overt diabetes. This paper will review current knowledge on the modifications occurring in normal pregnancy, while outlining the mechanisms. In this paper, we will review the changes of intermediary metabolism occurring during pregnancy. In particular, we will outline the mechanisms responsible for gestational diabetes; the link between these alterations and associated maternal and neonatal morbidity will be examined.

Intermediate metabolism in normal pregnancy and in gestational diabetes

The known and unknown of leptin in pregnancy

Objective. To determine a precise estimate for the contribution of maternal obesity to macrosomia. Data Sources. The search strategy included database searches in 2011 of PubMed, Medline (In-Process & Other Non-Indexed Citations and Ovid Medline, 1950–2011), and EMBASE Classic + EMBASE. Appropriate search terms were used for each database. Reference lists of retrieved articles and review articles were cross-referenced. Methods of Study Selection. All studies that examined the relationship between maternal obesity (BMI ≥30 kg/m2) (pregravid or at 1st prenatal visit) and fetal macrosomia (birth weight ≥4000 g, ≥4500 g, or ≥90th percentile) were considered for inclusion. Tabulation, Integration, and Results. Data regarding the outcomes of interest and study quality were independently extracted by two reviewers. Results from the meta-analysis showed that maternal obesity is associated with fetal overgrowth, defined as birth weight ≥ 4000 g (OR 2.17, 95% CI 1.92, 2.45), birth weight ≥4500 g (OR 2.77,95% CI 2.22, 3.45), and birth weight ≥90% ile for gestational age (OR 2.42, 95% CI 2.16, 2.72). Conclusion. Maternal obesity appears to play a significant role in the development of fetal overgrowth. There is a critical need for effective personal and public health initiatives designed to decrease prepregnancy weight and optimize gestational weight gain.

/pdf/maternal-obesity-and-occurrence-of-fetal-macrosomia-a-4aequ7guis.pdf

Maternal obesity and occurrence of fetal macrosomia: a systematic review and meta-analysis.

Leptin can be considered as a peripheral signal which informs the centers about the mass of energy stores. Studies done on the human adult population have demonstrated that degree of adiposity and insulin levels play a major role as determinants of leptin circulating levels. The aim of this study was to evaluate which factors may influence leptin levels at birth. We examined the role played by baby size and by the metabolic environment the fetus was exposed to during pregnancy. We considered 85 newborns from normal (n = 60), gestational (GDM, n = 17) and pregestational (IDDM = 8) diabetes mellitus mothers. At delivery, blood was taken from the umbilical cord vein. Babies from normal and GDM mothers were subdivided into AGA (appropriate for gestational age) and LGA (large for gestational age). There was no difference in leptin levels between babies from normal or GDM mothers belonging to the same weight category, but leptin levels were always higher in LGA than in AGA newborns, and highly correlated with birth weight (r = 0.34, P = 0.001). Moreover, IDDM mothers gave birth to newborns with significantly higher levels of leptin and insulin when compared with normal and GDM mothers. Diabetes of both GDM and IDDM mothers was clinically well controlled (HbA1c was 4.0 and 7.2, respectively). The correlation between leptin and insulin was significant only when newborns from IDDM mothers were included in the regression analysis (r = 0.39, P = 0.0002). Our results suggest that degree of adiposity is one of the main regulators of leptin concentration in the human newborn and that babies exposed to an altered, though clinically controlled, metabolic environment, as in IDDM mothers, have increased levels of leptin.

Plasma leptin levels in newborns from normal and diabetic mothers.

OBJECTIVE : To evaluate in a selected population the clinical characteristics (time of diagnosis, different treatment, metabolic parameters, etc.) of gestational diabetes in relation to prepregnancy body mass index (BMI) and the influence of BMI on neonatal outcome. DESIGN : This study was retrospectively led using a computerized data system for all deliveries that occurred at the Departments of Obstetrics and Gynecology of the University of Pisa (Italy) from 1 January 1987 to 31 December 1992. SUBJECTS : 93 women with GDM and 110 control subjects divided into three groups according to their pre-pregnancy BMI : normal weight (Nw), overweight (Ow) and obese (Ob). MEASUREMENTS : Time of diagnosis, mode of treatment and metabolic control of GDM ; time and mode of delivery, neonatal outcome (macrosomia, respiratory distress syndrome, hyperbilirubinemia, hypoglycemia, polycythemia, hypocalcemia). RESULTS : GDM was diagnosed earlier in Ow and Ob than in Nw (p 0.01) with prepregnancy BMI in both groups. The body weight increase during pregnancy was not associated with neonatal macrosomia. CONCLUSIONS : The degree of overweight is associated with an earlier diagnosis of GDM ; prepregnancy BMI is more predictive of macrosomia than weight gain, both in control and GDM women ; GDM seems to play the most important role in increasing the possibility of the occurrence of macrosomia.

Neonatal outcome and obstetric complications in women with gestational diabetes: effects of maternal body mass index.

This retrospective study investigates the clinical characteristics of gestational diabetes mellitus (GDM) (time of diagnosis, different treatment, metabolic parameters, etc.) in relation to prepregnancy body mass index (BMI) and the influence of BMI on neonatal outcome. 93 GDM women and 110 control subjects were divided into three groups in relation to their prepregnancy BMI: normalweight (Nw), overweight (Ow) and obese (Ob). GDM was diagnosed significantly (p < 0.01) earlier in Ow and Ob than in Nw. Preterm deliveries and cesarean sections resulted significantly (p < 0.01) increased in all BMI categories of GDM respect to matched controls. Prevalence of neonatal macrosomia was higher in GDM patients (44.6%) compared with normal controls (15.4%) and correlated (p < 0.01) with prepregnancy BMI in both groups. Nevertheless in each BMI category the prevalence of macrosomia was significantly higher in GDM patients. The body weight increase during pregnancy was not associated with neonatal macrosomia. This study shows that prepregnancy BMI is an important risk factor for GDM and is predictive for macrosomia specially in women suffering from GDM.

Gestational diabetes: clinical characteristics and birth weight.

590 Biological and in-silico characterization of pyrazole and pyrazolone derivatives: Identifies novel anti-skin cancer, antioxidant and tyrosinase inhibitory agents

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Plasma leptin levels in newborns from normal and diabetic mothers.

Neonatal outcome and obstetric complications in women with gestational diabetes: effects of maternal body mass index.

Gestational diabetes: clinical characteristics and birth weight.

590 Biological and in-silico characterization of pyrazole and pyrazolone derivatives: Identifies novel anti-skin cancer, antioxidant and tyrosinase inhibitory agents