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OBJECTIVE -To assess the 24-h glucose levels in a group of nondiabetic, nonobese pregnant women and to verify the presence of correlations between maternal glucose levels and sonographic parameters of fetal growth. RESEARCH DESIGN AND METHODS -A total of 66Caucasian nonobese pregnant women with normal glucose challenge tests (GCT) enrolled in the study; from this population, we selected 51 women who delivered term (from 37 to 42 weeks completed) live-born infants without evidence of congenital malformations. The women were requested to have three main meals and to perform daily glucose profiles fortnightly from 28 -38 weeks without modifying their lifestyle or following any dietary restriction. All subjects were taught how to monitor their blood glucose by using a reflectance meter. Fetal biometry was evaluated by ultrasound scan according to standard methodology at 22, 28, 32, and 36 weeks of pregnancy.RESULTS -The overall daily mean glucose level during the third trimester was 74.7 Ϯ 5.2 mg/dl. Daily mean glucose values increased between 28 (71.9 Ϯ 5.7 mg/dl) and 38 (78.3 Ϯ 5.4 mg/dl) weeks of pregnancy. We found a significant positive correlation at 28 weeks between 1-h postprandial glucose values and fetal abdominal circumference (AC). At 32 weeks, we documented positive correlations between fetal AC and maternal blood glucose levels 1 h after breakfast, 1 and 2 h after lunch, and 1 and 2 h after dinner. At 36 weeks, there was a positive correlation between fetal AC and 1-and 2-h postprandial blood glucose levels. In addition, there was a negative correlation between head-abdominal circumference ratio and 1-h postprandial blood glucose values.CONCLUSIONS -This longitudinal study first provides a contribution toward the definition of normoglycemia in nondiabetic, nonobese pregnant women; moreover, it reveals significant correlations of postprandial blood glucose levels with the growth of insulin-sensitive fetal tissues and, in particular, between 1-h postprandial blood glucose values and fetal AC. Diabetes Care 24:1319 -1323, 2001T he complex phenomenon of fetal growth has been thoroughly investigated over past decades (1) but still remains to be fully understood. We know that maternal glucose is one of the most important factors of influence (1,2), and Reece et al. (3) showed that normoglycemia in pregnancy is associated with normal levels of other nutrients, such as amino acids and lipids. For this reason, glycemia is the single maternal metabolic parameter routinely assessed in diabetic pregnancies. Indeed, the criteria for metabolic control and therapeutic strategies of diabetes in pregnancy are based almost exclusively on maternal glucose levels (2). Although there is overwhelming evidence that good perinatal outcomes can be achieved in diabetic pregnancies only with the normalization of maternal glucose values (4 -6), there is no clear definition of normoglycemia in nondiabetic pregnancies. In fact, a very limited number of studies have been performed thus far in the attempt to define maternal glucose l...

Abstract-Certain similarities between preeclampsia and insulin resistance syndrome suggest a possible link between the 2 diseases. The aim of our study was to evaluate 3 insulin sensitivity (IS) indexes (fasting homeostasis model assessment IS [IS HOMA ], quantitative insulin sensitivity check index [IS QUICKI ], and oral glucose IS [OGIS]) early and late in pregnancy in a large number of normotensive pregnant women with a normal glucose tolerance and to test the ability of these indexes to predict the risk of subsequent preeclampsia. In all, 829 pregnant women were tested with a 75-g, 2-hour oral glucose load in 2 periods of pregnancy: early (16 to 20 weeks) and late (26 to 30 weeks). In early and late pregnancy, respectively, IS HOMA was 1.23Ϯ0.05 and 1.44Ϯ0.05 (PϽ0.01), IS QUICKI was 0.40Ϯ0.002 and 0.38Ϯ0.002 (PϽ0.01), and OGIS was 457Ϯ2.4 mL min Ϫ1 m Ϫ2 and 445Ϯ2.2 (PϽ0.001), all confirming the reduction in insulin sensitivity during pregnancy. Preeclampsia developed in 6.4% of the pregnant women and correlated positively with the 75th centile of IS HOMA (Pϭ0.001), with a sensitivity of 79% in the early and 83% in the late period and a specificity of 97% in both. IS QUICKI Ͻ25th centile was also related with preeclampsia (Pϭ0.001), with a sensitivity of 85% in the early and 88% in the late period and a specificity of 97% in both. Judging from our findings, IS HOMA and IS QUICKI are simple tests that can pinpoint impaired insulin sensitivity early in the pregnancy. Given their high sensitivity and specificity, these indexes could be useful in predicting the development of preeclampsia in early pregnancy, before the disease become clinically evident. Key Words: pregnancy Ⅲ metabolism Ⅲ insulin Ⅲ insulin resistance Ⅲ hypertension, pregnancy Ⅲ preeclampsia N ormal pregnancy can be considered as a state of insulin resistance, and fasting insulin concentrations double during the course of gestation. Insulin resistance peaks in the 3rd trimester and rapidly returns to prepregnancy levels after delivery. 1 The reasons for this insulin resistance in normal pregnancy are not well known, although it has been suggested that placental hormones, such as lactogen, cortisol, progesterone, and estrogen, 2 and tumor necrosis factor ␣ 3 may be responsible.A number of standard clinical procedures are available for evaluating maternal insulin sensitivity during pregnancy, such as the euglycemic-hyperinsulinemic clamp, the oral and intravenous glucose tolerance tests (OGTT and IVGTT, respectively), and various derivations of fasting glucose and insulin levels, 1,4 including the fasting homeostasis model assessment insulin sensitivity index (IS HOMA ) 5 and the quantitative insulin sensitivity check index [IS QUICKI ]. 6 The oral glucose insulin sensitivity index (OGIS), for instance, is a widely used index of dynamic insulin sensitivity by assessing glucose clearance during an OGTT. 7 Preeclampsia is a complication of late pregnancy characterized mainly by hypertension and proteinuria. 8 It is a major cause of perinatal and ma...

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Objective: Insulin sensitivity and secretion during early and late pregnancy were assessed in women with normal glucose tolerance and gestational diabetes mellitus (GDM). Research Design and Methods:The oral glucose tolerance test (OGTT) was performed in 903 women at 16 -20th gestational week, of whom 37 had GDM (GDM1 group), and 859 repeated the OGTT at wk 26 -30. At the second test, 55 had GDM (GDM2 group); the others remained normotolerant (ND group). Insulin sensitivity from OGTT (as quantitative insulin sensitivity check index and OGTT insulin sensitivity) and ␤-cell function (as the ratio of the areas under the insulin and glucose concentration curves, adjusted for insulin sensitivity) were assessed in both tests. Results:In early pregnancy the quantitative insulin sensitivity check index was not different in the three groups, whereas OGTT insulin sensitivity was lowest in GDM2, intermediate in GDM1, and highest in ND. In late pregnancy both indices were reduced in GDM compared with ND and lower than in early pregnancy. In early pregnancy GDM1, but not GDM2, had lower ␤-cell function than ND. During the late visit, GDM2 also showed impaired ␤-cell function compared with ND; furthermore, the adaptation to the increase to insulin resistance from early to late pregnancy was defective in GDM2. Conclusions:In early pregnancy insulin sensitivity, as assessed from the OGTT but not from fasting measurements, is impaired in women who developed GDM. ␤-Cell function impairment is evident only when GDM is manifest and is characterized by inappropriate adaptation to the pregnancy induced increase in insulin resistance. (J Clin Endocrinol Metab 93: 876 -880, 2008) N ormal pregnancy can be considered a state of insulin resistance because insulin sensitivity decreases in pregnancy, reaching its nadir in the third trimester and rapidly returning to prepregnancy levels after delivery (1-4). Although the specific mechanisms behind the progressive insulin resistance during pregnancy have not been completely clarified, an important contribution seems to come from the endocrine modifications characteristic of pregnancy, including the increase in estrogens, progesterone, human placental lactogen, cortisol, and TNF-␣ (5, 6). Both insulin resistance (7) and a defective insulin secretion and action (8, 9) also characterize gestational diabetes mellitus (GDM).The euglycemic glucose clamp, the "gold standard" for assessing insulin sensitivity, has been used in pregnancy, but the test is complex, so most of the studies were performed on a small number of patients (1-3). Studies on insulin secretion, which usually simply evaluated the area under the concentration curve (1, 2), only rarely also using the glucose clamp (9), have involved a small number of patients, who were obese in most cases (1, 9). Evaluation of insulin sensitivity and secretion in large numbers Abbreviations: AUC, Area under the curve; AUC glu , area under the glucose concentration curve; AUC ins , area under the insulin concentration curve; AUCR, area under the curv...

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