Maternal low birth weight and gestational hyperglycemia.

We aimed to investigate whether birth weight could predict the subsequent risk of gestational diabetes and impaired glucose tolerance. Consecutive women with a singleton pregnancy and gestational diabetes (n = 50), impaired glucose tolerance (n = 50) and normoglycemia (n = 200) were included in the study. Birth data were collected from original hospital records of the women. Women with gestational hyperglycemia were significantly older and heavier than those with normoglycemia. Maternal birth weights significantly declined for each class of glucose tolerance (3389 +/- 644; 3184 +/- 583 and 3077 +/- 661, respectively for women with normoglycemia, impaired glucose tolerance and gestational diabetes). After adjustment for age, gestational age and weight gain, maternal diabetes, and pre-pregnancy body mass index, maternal birth weight was negatively related to impaired glucose tolerance (OR 0.88, 95% CI 0.81-0.97) and to gestational diabetes (OR 0.82, 95% CI 0.74-0.91) in a multiple logistic regression model. These findings suggest that women with low birth weight constitute a group at increased risk for both gestational impaired glucose tolerance and diabetes.     

Placental vanadium in gestational diabetes mellitus

Although many studies in animal models and in cell cultures have shown that vanadate has insulin-like effects, it has not been studied in human diabetes mellitus. In this study the levels of vanadium in human placentae from 23 pregnancies complicated by gestational diabetes mellitus were compared with 18 uncomplicated non-diabetic pregnancies closely matched for maternal age, gravidity, and gestational age. Using the unpaired Student's t-test, the mid-disc placental levels in gestational diabetes (7.62 +/- 1.29 micrograms/g dry weight) were significantly lower (p less than 0.05) than controls (8.73 +/- 1.85 micrograms/g dry weight). These findings appear to be independent of placental size and birthweight. When these data were analyzed according to treatment, the vanadium levels in insulin-treated cases (8.07 +/- 1.32 micrograms/g dry weight) were not significantly different from the matched controls (8.84 +/- 1.69 micrograms/dry weight); the levels in noninsulin treated cases (7.08 +/- 1.25 micrograms/g dry weight), however, were significantly (p less than 0.005) lower than controls (8.99 +/- 1.96 micrograms/g dry weight). It is interesting to speculate that there may be increased binding of vanadium to maternal tissues in human diabetes mellitus when insulin is deficient.     

Placental pathology in women with type 1 diabetes and in a control group with normal and large-for-gestational-age infants

Unexplained intra-uterine fetal death is still a problem in diabetic pregnancies, especially in those with an LGA-infant. We hypothesized that in these pregnancies impaired placental function, in terms of abnormal placental weight and/or abnormal placental histology, may account for this phenomenon. To test this hypothesis, we assessed the relative placental weight and scored several histological abnormalities in 34 AGA- and 24 LGA-placentae of type 1 diabetic women and in 22 AGA- and 16 LGA-placentae of control women. Relative placental weight was comparable in the LGA-diabetic cases and in the control groups, but was significantly higher in the AGA-diabetic subgroup. Histological abnormalities such as the presence of nucleated fetal red blood cells, fibrinoid necrosis, villous immaturity and chorangiosis were observed more often in the diabetic placentae compared with the control placentae. These differences in histology were particularly observed when we compared both AGA-groups. LGA-control placentae showed a high incidence of histological abnormalities, almost comparable to the diabetic placentae. Only fibrinoid necrosis was significantly more common in the LGA-diabetic placentae. Three of the four cases of perinatal death/asphyxia in the diabetic group concerned an LGA-infant with a relative low placental weight. In conclusion, placentae of women with type 1 diabetes showed several abnormalities that can be associated with impaired functioning. The difference between AGA- and LGA-diabetic placentae was related to relative placental weight and our data suggest that an increase in relative weight may protect the fetus from asphyxia. Placentae from LGA-non-diabetic women showed several similarities to those of women with diabetes.     

Maternal plasma leptin levels and their relationship to insulin and glucose in gestational-onset diabetes

To investigate the changes in leptin levels and the relationship between this substance and insulin and glucose in pregnant women with gestational-onset diabetes, we measured plasma leptin levels in the maternal peripheral vein of 17 healthy and 17 diabetic women at 29 and 33 weeks of gestation. We also correlated maternal plasma leptin levels in diabetic women with fasting plasma insulin levels and plasma glucose levels obtained 1 h after oral administration of 50 g of glucose. Maternal serum leptin levels in women with gestational diabetes (mean +/- SD 16.52 +/- 5.07 ng/ml, range 10.84-27.4 ng/ml) were significantly higher (p < 0.001) than those found in uncomplicated pregnancies (10.61 +/- 1.47 ng/ml, range 7.28-13.4 ng/ml). A positive correlation was found between maternal serum leptin levels and glycosylated haemoglobin values in diabetic pregnant women (r = 0.94, p < 0.001). A positive correlation was also found between maternal leptin concentrations and fasting serum insulin levels, as well as between leptin concentrations and plasma glucose levels obtained 1 h after the administration of 50 g of glucose in women with gestational diabetes (r = 0.84, p < 0.001, and r = 0.92, p < 0.001, respectively). We conclude that leptin levels are elevated in pregnant women with gestational diabetes, and its metabolism depends on insulin levels and the severity of diabetes.     

Fetal pancreatic function in infants of diabetic and rhesus-isoimmunized women

OBJECTIVE: To measure insulin and glucagon concentrations in amniotic fluid (AF) collected near term in basal conditions and after an arginine test in diabetic, rhesus-isoimmunized, and control pregnant women. METHODS: At baseline, AF was collected from 44 diabetic, 32 rhesus-isoimmunized, and 27 control pregnant women in late pregnancy. Fifty-two diabetic, six rhesus-isoimmunized, and nine control pregnant women had amniocentesis 2 hours after arginine infusion (30 g intravenous/30 minutes) at 33-36 weeks. RESULTS: Baseline AF glucose concentrations were significantly greater in diabetic women than the other conditions, and they related to the gestational age in the women with hemolytic disease of the newborn. Insulin and glucagon AF content of isoimmunized pregnancies overlapped controls, whereas insulin and insulin/glucagon molar ratios were significantly higher, and glucagon values lower, in diabetic pregnancies compared with isoimmunized and control pregnancies. In isoimmunized pregnancies, the AF concentrations of glucose, insulin, and glucagon were correlated with gestational age (less than 34, 34 weeks or more). The samples collected after arginine infusion, compared with those collected at baseline, showed significantly greater insulin and insulin/glucagon molar ratio values in diabetic (28 +/- 5 versus 11 +/- 1 microU/mL, P = .001; 29.4 +/- 1.7 versus 12.0 +/- 2.8, P = .001) and in Rh pregnant women (18 +/- 6 versus 7.7 +/- 0.7 microU/mL, P = .001; 30 +/- 9 versus 3.4 +/- 0.4 I/G, P = .001), whereas no significant difference was observed in the controls. CONCLUSION: Basal islet hormone concentrations in AF are modified by maternal diabetes and further influenced by arginine administration. Arginine produces an AF response that is similar in pregnancies complicated by diabetes mellitus and rhesus-isoimmunization, despite different (hyperglycemia and euglycemia) maternal blood glucose levels.     

Comparison of immunoreactive gonadotropin-releasing hormone and human chorionic gonadotropin in term placentas from normal women and those with insulin-dependent and gestational diabetes

We measured prohormone gonadotropin-releasing hormone (high-molecular-weight gonadotropin-releasing hormone), gonadotropin-releasing hormone and human chorionic gonadotropin concentrations in term placentas from normal women and those with insulin-dependent and gestational diabetes. The placental immunoreactive gonadotropin-releasing hormone levels were significantly higher in normal tissues than in tissues from insulin-dependent and gestational diabetes (p less than 0.01). When compared with diabetic placental extracts, normal tissue also had more stored prohormone immunoreactive gonadotropin-releasing hormone. Whereas there were no consistent differences in placental human chorionic gonadotropin concentrations in normal tissues and tissues from insulin-dependent and gestational diabetes, there was a significant correlation between gonadotropin-releasing hormone and human chorionic gonadotropin concentrations in normal samples (r = 0.57, p less than 0.05), which was abolished when the diabetic tissue was included in the analysis. These data suggest that differences in high-molecular-weight gonadotropin-releasing hormone and gonadotropin-releasing hormone concentrations in term placentas from normal versus diabetic mothers may be due to enhanced processing of the prohormone and increased release of the decapeptide in diabetic pregnancy.     

Foetal and placental weights in relation to maternal characteristics in gestational diabetes

An increased placental weight has been reported in pregnancies complicated with gestational diabetes (GDM). We have analysed foetal (F) and placental weight (P) and foetal length in 143 consecutive normal (N) and 132 GDM pregnancies in relation to type of treatment and to a number of maternal variables. All N pregnancies had a negative oral glucose challenge test at 24-28 weeks. GDM was diagnosed at 28-32 weeks by a 100-gm, 3-h oral glucose tolerance test (OGTT). Treatment was diet (D: n=82) or diet plus insulin (D+I: n=50) according to self-monitoring of blood glucose. A significant difference was observed between N and GDM pregnancies for maternal age (N=30.6+/-5.38 years; GDM=33.2+/-4.53 years; P< 0.001), pre-pregnancy weight (N=58.2+/-8.0 kg; GDM=63.0+/-12.9 kg; P< 0.001) and BMI (N= 21.9+/-2.63; GDM=24.4+/-4.71;P< 0.001). Foetal weight became significantly higher in the GDM group (N=3274.2+/-296.0 g; GDM=3287.1+/-474.1g; P< 0.05) once correction was made for the significant difference in gestational age between the two groups (N=39.4+/-1.17 weeks; GDM=38.8+/-1.39 weeks; P< 0.001). Significantly higher placental weights (N=561.87+/-91.0 g; GDM=592.2+/-115.8 g;P< 0.01) and significantly lower F/P weight ratios were found in GDM pregnancies (N=5.96+/-1.02; GDM=5.69+/-1.13; P< 0.05).In GDM pregnancies a significantly negative correlation was found between the OGTT response and weights of foetus and placentae at delivery, suggesting that both foetal and placental growth are affected by maternal insulin resistance.     

Hemodynamic changes in underweight pregnant women.

Twelve normal-weight and 12 underweight women were compared to test whether fetal growth retardation in underweight gravidas is related to inadequate maternal hemodynamic adjustments. Plasma volume (+/- standard error) was 3227 +/- 103 mL in normal-weight and 2731 +/- 84 mL in underweight women (P less than .002). Cardiac output was 6340 +/- 167 mL/minute in controls and 5689 +/- 213 mL/minute in underweight women (P less than .03). Total peripheral vascular resistance was lower in controls than in underweight subjects (1025 +/- 31 versus 1198 +/- 58 dyne/second/cm5). Mean birth weight was 2837 +/- 125 g in underweight women and 3362 +/- 106 g in controls (P less than .005). Similarly, placental weight was reduced in the underweight group. All infants delivered by control mothers had a normal birth weight, whereas six infants from underweight gravidas were growth-retarded. In all cases combined, maternal plasma volume correlated significantly with both birth weight (r = 0.6, P less than .002) and placental weight (r = 0.56, P less than .01); total peripheral vascular resistance also correlated significantly and inversely with newborn weight and placental weight. Cardiac output correlated only with placental weight (r = 0.54, P less than .02). These results are consistent with the hypothesis that underweight mothers are at higher risk of fetal growth retardation because of a smaller plasma volume and lower cardiac output.     

Excessive gestational weight gain in women with gestational and pregestational diabetes

We sought to determine the frequency of excessive gestational weight gain (GWG) and its impact on perinatal outcomes in women with gestational (GDM) and pregestational diabetes mellitus (DM). A retrospective cohort of diabetic women was studied. GWG was categorized by the 2009 Institute of Medicine guidelines. Perinatal outcomes were compared between those women with and without excessive GWG. There were 153 women who met study criteria. There was no difference in excessive GWG between women with GDM and pregestational DM (44.4% versus 38.5%, P?=?0.51) or based on White's class ( P?=?0.17). After adjusting for confounders, excessive GWG was not associated with an increased rate of adverse perinatal outcomes (odds ratio 1.49, 95% confidence interval 0.56 to 2.35) and had similar associations with both pregestational DM and GDM. Although excessive GWG was common in our diabetic population, it was not associated with an increased rate of adverse perinatal outcomes.     

Relation between placental morphometry and fetal growth]

Forty-eight placentae of full term infants, 21 placentae from appropriate for gestational age infants (AGA) and 27 placentae from small for gestational age infants (SGA) were measured by morphometric technic using the automatic image analyzer, in order to find out the extent of fetomaternal exchange which determines the transfer of oxygen and nutrition from mother to fetus and fetal growth. The results of measurement correlated well both with infant birth weight and placental weight. They demonstrated striking quantitative differences when the placentae of SGA were compared with those of AGA. The placenta weights in the group of SGA were notably less than those in the group of AGA. It seems that low birth weight relates to low functional tissue mass of placenta. This reduction of functional tissue is accompanied by diminution of the area for exchange between mother and fetus, both at the villous surface area and at fetal capillary surface area. Thus, the ability of transferring oxygen and nutrition from mother to fetus is curtailed. The results show that the rate of fetal growth is limited by placental function as well as its weight.     

Perinatal complications in women with gestational diabetes mellitus

BACKGROUND: The aim of the study was to examine the outcome of the pregnancy and neonatal period in 1) women with gestational diabetes mellitus and non-diabetic pregnant women, and 2) in women with early and late diagnosis of gestational diabetes mellitus. METHODS: Included were 327 women with gestational diabetes mellitus and 295 non-diabetic women, who were screened with a 75 g oral glucose tolerance test because of risk factors for gestational diabetes. Women with gestational diabetes mellitus were treated with low-caloric diet and insulin when appropriate, while women in the control group received routine antenatal care. RESULTS: Gestational age at delivery was significantly lower in the group with gestational diabetes mellitus, both when considering all deliveries (39.1+/-1.7 weeks versus 39.8+/-2.0 weeks, p<0.05) and only those with spontaneous onset of labor (38.8+/-2.0 weeks versus 40.0+/-1.6 weeks, p<0.05). The frequency of macrosomia was increased, although not statistically significant (8% vs. 2%, p=0.07), and the rate of admission to the neonatal ward was significantly increased (18% vs. 9%, p<0.05) in the group with gestational diabetes. Women with early diagnosis of gestational diabetes mellitus had a significantly increased need for insulin treatment during pregnancy (36% vs. 9% p<0.05) and a significantly higher occurrence of diabetes mellitus at follow-up from two months until three years postpartum. CONCLUSIONS: This study of women with gestational diabetes mellitus and non-diabetic pregnant women showed that gestational diabetes mellitus was associated with a significantly lower gestational age at delivery and an increased rate of admission to the neonatal ward. Women diagnosed with GDM before 20 weeks of gestation had an increased need for insulin treatment during pregnancy and a high risk of subsequent overt DM, compared with women diagnosed with GDM later in pregnancy.     

Reference values for the weight of freshly delivered term placentas and for placental weight-birth weight ratios

BACKGROUND: There is evidence for a correlation between placental weight and future chronic disease, notably hypertension and diabetes. However, there are no reference scales for placentas that are readily weighed in the delivery room. METHODS: This cross-sectional study generated reference values for the weight of freshly delivered untrimmed placentas, and placental weight-birth weight (pw/bw) ratios from a database of 11,141 uncomplicated singleton term pregnancies (37-42 weeks). The data analysis followed stringent validated and state of the art methodological recommendations. A regression model was fitted to estimate the mean and standard deviation for placental weight and pw/bw ratios at each week of gestational age. RESULTS: Reference scales, percentile tables and regression equations are presented for placental weights according to the mode of delivery and for pw/bw ratios. Mean placental weight from vaginal deliveries was 76 g lighter than from Caesarean sections (545+/-107 g versus 621+/-139 g, respectively, P<0.05). Mean placental weight increased by 60 g from 37 to 42 weeks irrespective of the mode of delivery. The pw/bw ratio decreased from 17.6 to 15.6 between 37 and 42 weeks. CONCLUSION: For the first time, reference values for freshly delivered term placental weights depending on the mode of delivery were generated. In the light of growing evidence for a correlation of placental weight with chronic diseases in later life, these values provide the possibility to judge placentas at site for abnormalities in weight and to estimate the potential risks for chronic diseases in later life.     

Pregnancy outcome after age 50

OBJECTIVE: To evaluate pregnancy complications occurring after age 50. METHODS: We compared the pregnancy outcomes of women aged 50-64 years with those aged 45-49 years and with the general population. RESULTS: During 5 years from January 1, 1999, to June 30, 2004, 123 women aged 45 years and older gave birth. Fifty-five percent were nulliparous, 24 of 123 were aged 50-64 years, and 99 of 123 women were aged 45-49 years. All women older than age 50 conceived via in vitro fertilization with oocyte donation. For these 123 women, the overall mean gestational age at delivery was 37.6+/-2.6 weeks. The mean birth weight was 2,684+/-754 g, significantly lower than the general population, and the incidences of multifetal pregnancies, diabetes, and hypertension were high. Women aged 50 years and older were more likely to be hospitalized during pregnancy than women younger than 50 years (63% versus 22%, P<.001). Neonatal outcome was generally good. Women aged 50 years and older gave birth to significantly more low birth weight babies than those younger than age 50 years (61% versus 32%, P=.002). Gestational age and birth weight were both significantly lower for singletons and multiples in women older than age 50 years compared with those younger than age 50 years (gestational age of singletons 36.9 versus 38.4 weeks, P=.005; birth weight of singletons 2,694 versus 3,027 g, P=.019; gestational age of multiples 35.1 versus 36.4 weeks, P=.01; birth weight of multiples 1,976 versus 2,310 g, P=.038, respectively). CONCLUSION: Pregnant women aged 50-64 years have increased risks of preterm birth, low birth weight babies, diabetes mellitus, hypertension, and hospitalization. LEVEL OF EVIDENCE: II-2.     

Human placental lactogen and pregnancy-specific β1-glycoprotein in pregnant diabetic women

Summary. Serum placental lactogen (hPL) and pregnancy-specific β₁ glycoprotein (SP₁) concentrations were measured in 16 insulin-dependent pregnant diabetic women and in 16 non-diabetic control subjects matched for placental weight. hPL concentrations were found to be significantly higher in diabetics with placental weight >90th centile compared with those in (i) non-diabetic controls with placental weight >90th centile and (ii) diabetics with placental weights <90th centile. SP_l concentrations were higher in both diabetic groups compared with those in their respective nondiabetic controls, but no difference existed between the two diabetic groups. In the control subjects infant birthweights were lower in the women with small placentae, but no such difference was observed between the two diabetic groups.     

Maternal low birth weight and gestational hyperglycemia

We aimed to investigate whether birth weight could predict the subsequent risk of gestational diabetes and impaired glucose tolerance. Consecutive women with a singleton pregnancy and gestational diabetes (n = 50) ,impaired glucose tolerance (n = 50) and normoglycemia (n = 200) were included in the study. Birth data were collected from original hospital records of the women. Women with gestational hyperglycemia were significantly older and heavier than those with normoglycemia. Maternal birth weights significantly declined for each class of glucose tolerance (3389 ± 644; 3184 ± 583 and 3077 ± 661 ,respectively for women with normoglycemia ,impaired glucose tolerance and gestational diabetes). After adjustment for age ,gestational age and weight gain ,maternal diabetes ,and pre-pregnancy body mass index ,maternal birth weight was negatively related to impaired glucose tolerance (OR 0.88 ,95% CI 0.81-0.97) and to gestational diabetes (OR 0.82 ,95% CI 0.74-0.91) in a multiple logistic regression model. These findings suggest that women with low birth weight constitute a group at increased risk for both gestational impaired glucose tolerance and diabetes.     

Placental ratio and anemia in third-trimester pregnancy

OBJECTIVE: To perform a prospective, observational study in a tertiary center to determine whether anemia (hemoglobin level < 10 g/dL) developing in the third trimester was associated with an increased placental weight/birth weight ratio (placental ratio) and whether the placental ratio correlated with the hemoglobin level at different periods and with other factors, such as gestational age and parity. STUDY DESIGN: A total of 476 nonanemic women with low-risk singleton pregnancies were recruited at their 28-30-week antenatal visit over a three-month period. Excluded from the final analysis were 20 women who delivered elsewhere and 19 found to be carriers of thalassemia traits due to their low mean cell volume. All women received standard obstetric care, and ferrous sulphate was prescribed for those who developed anemia. RESULTS: Anemia developed in 45 (10.3%) of the remaining 437 women. This group had significantly decreased red cell indices, gestational age (38.3 +/- 2.0 vs. 39.2 +/- 1.3 weeks, P = .004) and birth weight (3,082 +/- 416 vs. 3,220 +/- 411 g, P = .035) but no difference in placental weight (609 +/- 102 vs. 594 +/- 108 g), so the placental ratio was increased as compared with that in the control group (0.196 +/- 0.026 vs. 0.185 +/- 0.026, P = .002). Multiple regression analysis confirmed that the placental ratio correlated only with the last hemoglobin level (P = .041). CONCLUSION: Our results indicate that placental size increased relative to infant size in pregnancies complicated by anemia, but whether this phenomenon reflected actual placental hypertrophy or failure of fetal growth to keep up with placental growth remains to be determined.     

Clinical usefulness of estimation of serum fructosamine concentration as screening test for gestational diabetes

Serum fructosamine levels and fructosamine/protein ratios were measured in 100 pregnant women who underwent glucose tolerance tests because of clinical risk. Compared with normal pregnant women, the 13 study participants with gestational diabetes had higher fructosamine/protein levels (39 +/- 3.9 mumol/gm versus 37 +/- 3.2 mumol/gm, p less than 0.05), fasting serum glucose levels (107 +/- 13.7 mg/dl versus 82 +/- 8.6 mg/dl, p less than 0.001), and area under curve of glucose tolerance test (36 +/- 5 gm x min x dl-1 versus 22 +/- 3.6 gm x min x dl-1, p less than 0.001). The serum fructosamine levels were not significantly different between the two groups of participants (2.3 +/- 0.26 mmol/L versus 2.2 +/- 0.17 mmol/L); 10 of the 13 women with diabetes had a fructosamine/protein ratio within 2 SD of the mean of the groups of normal pregnant women. Spontaneous caloric intakes (r = 0.72, p less than 0.005) and the hospital mean daily capillary glucose levels during diabetic diet (r = 0.72, p less than 0.005) correlated better with the fructosamine/protein ratio than with fasting serum glucose levels (r = 0.58, p less than 0.05) and area under curve (r = 0.57, p less than 0.05). Consequently, serum fructosamine and fructosamine/protein ratio levels should be considered insensitive as a screening test in pregnant patients with clinical risk of gestational diabetes.     

The effect of gender and gestational diabetes mellitus on cord leptin concentration

OBJECTIVE: The purpose of this study was to determine the relationship of neonatal sex and gestational diabetes mellitus on cord leptin concentration and to determine whether cord leptin has a stronger correlation with fat mass compared with birth weight or lean body mass. We hypothesized that there are no significant differences in fetal leptin concentration between male and female or between neonates of mothers with gestational diabetes mellitus and control neonates, when adjusted for body composition. STUDY DESIGN: Cord blood leptin concentrations were measured in newborn infants of 78 women (44 control neonates and 34 gestational diabetes mellitus). Of the 78 neonates, 32 babies were female, and 46 babies were male. Birth weights were measured with a calibrated scale, and body compositions were measured by total body electrical conductivity. RESULTS: Estimated mean gestational age at delivery was 39.1 +/- 1.1 weeks for control neonates versus 38.6 +/- 1.3 weeks for neonates of mothers with gestational diabetes mellitus (P =.01). The fat mass for the control neonates and neonates of mothers with gestational diabetes mellitus was 0.36 +/- 0.15 kg versus 0.48 +/- 0.21 kg (P =.01); the percent body fat for the control neonates and neonates of mothers with gestational diabetes mellitus was 10.5% +/- 3.8% versus 13.2% +/- 4.3% (P =.006), respectively. There was no significant difference in cord leptin concentration between male and female neonates (16.0 +/- 13.8 ng/dL vs 12.7 +/- 12.8 ng/dL, P =.24). Cord leptin concentrations (18.1 +/- 16.2 ng/dL vs 10.9 +/- 9.5 ng/dL, P =.02) were significantly greater in neonates of mothers with gestational diabetes mellitus than in control neonates. In all subjects, cord leptin was significantly correlated with percent body fat (r = 0.51, P <.0001), fat mass (r = 0.49,P <.0001), and birth weight (r = 0.25, P =.03). After the adjustment for fat mass, there was no significant difference in cord leptin concentration between control neonates and neonates of mothers with gestational diabetes mellitus (P =.20), but there was a significant difference between male and female neonates (P =.04). However, when an adjustment was made for both fat mass and lean body mass, there was no longer a significant difference between male and female neonates (P =.12) CONCLUSION: The differences in cord leptin concentration between male and female neonates and between infants of women with gestational diabetes mellitus and control neonates are related to differences in body composition.     

Increased biological oxidation and reduced anti-oxidant enzyme activity in pre-eclamptic placentae

Oxidative stress occurs when cellular levels of reactive oxygen species exceed anti-oxidant capabilities and has been implicated in the pathogenesis of pre-eclampsia. In this study we have examined the tissue levels of endogenous anti-oxidant proteins (superoxide dismutase, glutathione peroxidase, thioredoxin reductase and thioredoxin) and the level of lipid and protein oxidation in placental samples from normal and pre-eclamptic pregnancies. Pre-eclamptic tissue homogenates demonstrated significantly increased levels of lipid peroxidation (20.68 +/- 7.811 microM protein versus 5.33 +/- 4.03 microM/mg protein, P < 0.001) and a trended increase in protein carbonyl concentration (248.1 +/- 97.71 units/mg protein versus 209.7 +/- 82.6 U/mg protein) when compared to controls. The levels and activities of the anti-oxidant proteins superoxide dismutase (2.48 +/- 0.6 U/mg protein versus 2.02 +/- 0.51 U/mg protein, P <0.02), thioredoxin reductase (19.25 +/- 9.81 U/mg protein versus 13.02 +/- 5.66 U/mg protein,P = 0.02), thioredoxin (107.00 +/- 18.11 ng/mg protein versus 91.12 +/- 21.18 ng/mg protein, P = 0.02) and glutathione peroxidase (17.33 +/- 6.63 mmol/min/mg protein versus 11.50 +/- 3.11 mmol/min/mg, P < 0.02) were all found to be significantly reduced when comparing pre-eclamptic placental tissue homogenates to gestational age-matched control placentae from non-pre-eclamptic pregnancies. The results of this study demonstrate a decreased enzymatic anti-oxidant capacity and increased oxidation in placental tissue from pre-eclamptic women, which may contribute to the pathogenesis of this complex disorder.     

Prophylactic insulin in the management of gestational diabetes

One hundred eight gestational diabetics were randomized to receive either diet alone or diet plus insulin (20 units NPH and 10 units regular) for glycemic control. Blood glucose levels were evaluated weekly in a high-risk clinic where medical and nutritional support and counseling were provided. Among 68 women successfully treated for a minimum of 6 weeks, the mean birth weight, macrosomia rate, and ponderal index were reduced significantly in the insulin-treated group. Insulin reduced birth weights significantly in women with a delivery weight of 200 lb or more (4060 +/- 342 versus 3397 +/- 640 g) and in those with a delivery weight less than 200 lb (3324 +/- 448 versus 3047 +/- 394 g). No patient with good glucose control and a maternal delivery weight under 200 lb had a newborn over 4000 g. Patients failing glycemic control were at greatest risk (30%) for fetal overgrowth whether initially receiving insulin or not. Maternal obesity or failure to achieve glycemic control should alert the clinician to a substantially increased risk of macrosomia.