Maternal Fasting Glucose Research Articles

Increased fetal adiposity: A very sensitive marker of abnormal in utero development

Objective Because offspring of women with gestational diabetes mellitus have an increased risk of obesity and diabetes mellitus as young adults, our purpose was to characterize body composition at birth in infants of women with gestational diabetes mellitus and normal glucose tolerance. Study design One hundred ninety-five infants of women with gestational diabetes mellitus and 220 infants of women with normal glucose tolerance had anthropometric measurements and total body electrical conductivity body composition evaluations at birth. Parental demographic, anthropometric, medical and family history data, and diagnostic glucose values were used to develop a stepwise regression model that related to fetal growth and body composition. Results There was no significant difference in birth weight (gestational diabetes mellitus [3398±550 g] vs normal glucose tolerance [3337±549 g], P = .26) or fat-free mass (gestational diabetes mellitus [2962±405 g] vs normal glucose tolerance [2975±408 g], P = .74) between groups. However, infants of women with gestational diabetes mellitus had significantly greater skinfold measures ( P = .0001) and fat mass (gestational diabetes mellitus [436±206 g] vs normal glucose tolerance [362±198 g], P = .0002) compared with infants of women with normal glucose tolerance. In the gestational diabetes mellitus group, although gestational age had the strongest correlation with birth weight and fat-free mass, fasting glucose level had the strongest correlation with neonatal adiposity. Conclusion Infants of women with gestational diabetes mellitus, even when they are average weight for gestational age, have increased body fat compared with infants of women with normal glucose tolerance. Maternal fasting glucose level was the strongest predictor of fat mass in infants of women with gestational diabetes mellitus. This increase in body fat may be a significant risk factor for obesity in early childhood and possibly in later life.

Effect of betamethasone on maternal glucose

Objective: To determine the effect of single and multiple betamethasone courses on maternal fasting and postprandial glucose values. Study design: A prospective cohort study was performed in women receiving betamethasone at 24–34 weeks' gestation. Fasting and 1-h postprandial capillary glucose values were obtained daily following betamethasone therapy for hospitalized patients. A control group comprised outpatients who underwent weekly fasting and postprandial assessments for 3 weeks. Fasting and 1-h postprandial capillary glucose values were compared between control and betamethasone patients using an unpaired t test. Results: Thirty-five women received a single course of therapy, 19 received multiple courses and 28 served as controls. Mean fasting glucose values for control patients fell within a narrow range of 81.6 ± 10.3 to 82.2 ± 6.4 mg/dl for weeks 1–3. Of women receiving betamethasone, 59% of fasting glucose values were greater than 90 mg/dl as compared to 16% of control fasting values (p < 0.001, χ2 test). Mean 1-h postprandial values for control women ranged from 107.7 ± 15.1 to 112.3 ± 20.0 mg/dl for weeks 1-3. Mean 1-h postprandial glucose values were ≤ 140 mg/dl following one, two or three courses of betamethasone therapy. Conclusions: Betamethasone resulted in an acute increase in fasting glucose following a single course of betamethasone, whereas two or more courses of therapy resulted in a continuous elevation of fasting glucose values. One-hour postprandial values were not clinically abnormal.

Relationship of neonatal body composition to maternal glucose control in women with gestational diabetes mellitus

Objective: To determine whether neonatal fat mass, which may be a better estimate of fetal overgrowth, is correlated with maternal fasting, preprandial and/or postprandial glucose values in womenwith gestational diabetes mellitus (GDM).Study Design: Women with GDM and no other medical or obstetric problems, and their infants, were the subjects of this study. Portable reflectance meterswere used by all participants for self-monitoring of blood glucose levels. Average fasting, preprandial, 2-h postprandial and bedtime glucose values were determined for each subject. Neonatal body compositionwas obtained by total body electric conductivity and/or anthropometric measurements within 48 h after delivery.Results: Eighteen women with their infants participated in this study. The age(mean ± SD) of the mothers was 28.0 ± 5.7 years. Nine were treated with diet and nine with diet and insulin. An average of 40 fasting (84 ± 13 mg/dl), 50 preprandial (87 ± 14mg/dl), 80 2-h postprandial (106 ± 19 mg/dl) and 17 bedtime (104 ± 19 mg/dl) glucose values were obtained from each subject. The average gestational age of the infants at birth was 38.3 ±1.3 weeks with a mean weight of 3356 ± 526 g. Three infants were > 4 kg and seven infants were > 90th centile for gestational age. The strongest correlation with neonatal fat mass was maternalfasting glucose level (r = 0.71, p < 0.01). Neonatal fat mass was not found to be significantly correlated with any other mean glucose value. Additionally, the infant's per cent body fat(r = 0.71, p < 0.01), sum of skinfold thicknesses (r = 0.70, p < 0.01), fat-free mass (r = 0.50, p < 0.05), and weight (r = 0.61, p < 0.01) were also found to becorrelated with maternal fasting glucose level. No other maternal glucose measurements were correlated with either birth weight or estimates of fat free mass.Conclusion: Maternal fasting glucoselevels correlated best with neonatal fat mass and other estimates of neonatal body composition.

Effect of betamethasone on maternal glucose

Objective: To determine the effect of single and multiple betamethasone courses on maternal fasting and postprandial glucose values.Study design: A prospective cohort study was performedin women receiving betamethasone at 24–34 weeks' gestation. Fasting and 1-h postprandial capillary glucose values were obtained daily following betamethasone therapy for hospitalized patients. A controlgroup comprised outpatients who underwent weekly fasting and postprandial assessments for 3 weeks. Fasting and 1-h postprandial capillary glucose values were compared between control and betamethasone patientsusing an unpaired t test.Results: Thirty-five women received a single course of therapy, 19 received multiple courses and 28 served as controls. Mean fasting glucose values for controlpatients fell within a narrow range of 81.6 ± 10.3 to 82.2 ± 6.4 mg/dl for weeks 1–3. Of women receiving betamethasone, 59% of fasting glucose values were greater than 90 mg/dl as comparedto 16% of control fasting values (p < 0.001, χ2 test). Mean 1-h postprandial values for control women ranged from 107.7 ± 15.1 to 112.3 ± 20.0 mg/dl for weeks 1-3.Mean 1-h postprandial glucose values were ≤ 140 mg/dl following one, two or three courses of betamethasone therapy.Conclusions: Betamethasone resulted in an acute increase in fasting glucosefollowing a single course of betamethasone, whereas two or more courses of therapy resulted in a continuous elevation of fasting glucose values. One-hour postprandial values were not clinically abnormal.

Patterns of congenital anomalies and relationship to initial maternal fasting glucose levels in pregnancies complicated by type 2 and gestational diabetes

Objectives: We sought to determine the types of congenital anomalies affecting infants of women with gestational diabetes mellitus or type 2 diabetes and to examine the relationship between those malformation types and measures of initial glycemia of women at entry into prenatal care with type 2 diabetes or at time of diagnosis in women with gestational diabetes mellitus. Study Design: A total of 4180 pregnancies complicated by gestational diabetes mellitus (n = 3764) or type 2 diabetes (n = 416) that were delivered after 20 weeks of gestation were reviewed for the presence of congenital malformations diagnosed before hospital discharge. Anomalies were categorized as being absent, minor, major, genetic syndromes, or aneuploidies. Major anomalies were further categorized by the number and type of affected organ systems. In addition to maternal clinical and historical parameters, the initial fasting serum glucose either from the diagnostic glucose tolerance test (gestational diabetes mellitus) or at entry to prenatal care (type 2 diabetes) and the initial glycosylated hemoglobin before insulin therapy were examined for a relationship to anomalies. Results: The initial fasting serum glucose and glycosylated hemoglobin levels were significantly higher in pregnancies with major (n = 143) and minor (n = 112) anomalies and genetic syndromes (n = 9) compared with pregnancies with no anomalies (n = 3895). Of those pregnancies with major anomalies, the most commonly affected organ systems were the cardiac (37.6%), musculoskeletal (14.7%), and central nervous systems (9.8%) and anomalies involving multiple organ systems (16%). There was no increased predominance of any specific organ system involvement seen with increasing fasting serum glucose levels in pregnancies with major congenital anomalies. Pregnancies with major anomalies affecting multiple organ systems had significantly higher initial fasting serum glucose levels (166 ± 64 mg/dL) compared with pregnancies in which one organ system was affected (141 ± 55 mg/dL, P < .04) or no organ systems were affected (115 ± 38 mg/dL, P < .0001). Conclusion: Congenital anomalies in offspring of women with gestational and type 2 diabetes affect the same organ systems that have been previously described in pregnancies complicated by type 1 diabetes. Increasing hyperglycemia at diagnosis or presentation for care was associated with an increasing risk of anomalies in general and with anomalies involving multiple organ systems without a preferential increase in involvement of specific organ system. (Am J Obstet Gynecol 2000;182:313-20.)

Gestational diabetes: risk or myth?

As currently defined (5), gestational diabetes is associated with important perinatal and long-term health risks. Many of the risks increase, in relation to the severity of maternal hyperglycemia. For perinatal risks to infants, the relationship seems to be continuous. Maternal fasting glucose levels can be used to identify subsets of patients with very low and very high risks. The majority of pregnancies lie between these two extremes; and nonglucose measures, such as fetal ultrasound, can be used to enhance risk assessment, thereby minimizing over- and undertreatment of patients. The major long-term maternal risk is development of type 1 or type 2 diabetes, predominantly the latter. The risk increases continuously, in relation to maternal glycemia during and, especially, after pregnancy. Patients seem to have a B-cell defect that is characterized by maladaptation to insulin resistance. The B-cell defect is predictive of future diabetes, supporting the testing and clinical application of interventions that minimize insulin resistance to delay or prevent diabetes. Women with impaired glucose tolerance in the first few months postpartum are at particularly high risk for diabetes and should receive the most intensive education, intervention, and follow-up. Offspring of women with GDM are at increased risk for obesity and have an unexpectedly high prevalence of elevated glucose levels during childhood and adolescence. Both genetic and intrauterine environmental influences are likely to contribute to these abnormalities. Optimal strategies to detect and prevent the long-term risks to offspring remain to be established.

Impact of conceptus mass on glucose disposal rate in pregnant women

The impact of an increasing fetal and placental mass on maternal glucose disposal rate (GDR) was studied in 17 pregnant women. Eleven pregnancies were singleton pregnancies, five were twin and one was a triplet pregnancy. Both the maternal fasting glucose concentration [Glc] and the total fetal and placental weight (W) were significantly correlated with an increased maternal GDR. Glucose concentration and conceptus weight were interdependent. The multiple linear regression of glucose disposal rate on glucose concentration and total weight is given by GDR = -1.573 + 0.176W + 0.932[Glc] +/- 0.24, r2 = 0.52, P < 0.01. These data are utilized to estimate the glucose utilization rate of the human conceptus at a fasting glucose concentration of 3.9 mM with a range of 10-15 mg.kg-1.min-1. Maternal GDR increases with increasing glucose concentration at a rate similar to that reported for newborn infants, consistent with a high glucose utilization by the uterus.

Ovine Fetal Breathing and Swallowing Activity in Response to Plasma Glucose Changes

Fetal swallowing activity generally occurs simultaneously with fetal breathing movements (FBM) in sheep. The present study investigated the FBM and swallowing responses to altered fetal plasma glucose. Fetal lambs were chronically prepared with laryngeal, esophageal and diaphragm electromyogram (EMG) wires, an esophageal flow probe and vascular catheters. Beginning at 138 +/- 1 day, FBM and swallowing were monitored during control periods and in response to intravenous glucose infusions (14 mg/kg/min for 120 min) to fetuses of fed and fasted ewes. Glucose infusions to fetuses of fed ewes resulted in significant increases in fetal plasma glucose (21.2 +/- 0.7 to 40.5 +/- 1.9 mg/dl) and time breathing (46.2 +/- 6.3 to 60.0 +/- 9.5 min/2 h). In response to maternal fasting, fetal glucose levels (13.4 +/- 1.0 mg/dl) and time breathing (23.0 +/- 7.2 min/2 h) decreased significantly. Glucose infusion to fetuses of fasted ewes resulted in significant increases in time breathing (50.3 +/- 13.4 min/2 h) and diaphragmatic EMG activity (1,295 +/- 654 to 3,012 +/- 1,182 spikes/2 h). There was no change from basal levels of fetal EMG swallows (83.2 +/- 4.3 swallows/2 h) or esophageal flow (40.8 +/- 7.9 ml/2 h) in response to maternal fasting or fetal glucose infusions.

Postpartum testing for antecedent gestational diabetes

Gestational diabetes is a predictor of glucose intolerance in subsequent pregnancies and in the nongravid state. Many pregnant women are not tested for gestational diabetes, although they or their offspring may show signs suggestive of antecedent hyperglycemia. We examined the diagnostic utility of a postpartum (within 48 hours), 100 gm, oral glucose tolerance test and cord plasma glucose, cord plasma C-peptide, and 2-hour neonatal plasma glucose tests to detect antecedent gestational diabetes in women with documented gestational diabetes (n = 37) or with normal glucose tolerance test results late in the third trimester (n = 28). The 1-hour, 2-hour, and incremental 1-hour + 2-hour ([1-hour − fasting] + [2-hour − fasting]) glucose values of the postpartum glucose toelrance test showed significant differences between study participants with and without gestational diabetes (164 ± 30 versus 115 ± 22, 145 ± 31 versus 101 ± 21, and 153 ± 51 versus 67 ± 33 mg/dl, respectively, p < 0.025). Maternal fasting and 3-hour postpartum glucose tolerance test glucose, cord plasma glucose, cord plasma C-peptide, and 2-hour neonatal plasma glucose values showed no significant between-group differences. Receiver operating characteristic curve analyses for these tests indicated that the incremental 1-hour + 2-hour postpartum glucose tolerance test glucose values best sustain test specificity at the low test threshold values necessary for high test sensitivity. A threshold of 110 mg/dl for this test yielded a predicted specificity of 90% and sensitivity of 80% with regard to antecedent gestational diabetes.