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P M Catalano

Publications and source records attributed to P M Catalano.

At least 19 recordsLinked to original sources

The short- and long-term implications of maternal obesity on the mother and her offspring.

Obesity's increasing prevalence has reached epidemic proportions in the USA, with close to one-third of the adult population affected in 2000. Additionally, there is increasing prevalence of obesity in other industrialised areas of the world such as Europe. Of potentially more concern is the potential risks associated with obesity and related metabolic complications in the developing world. The maternal, fetal, peripartum and neonatal complications of obesity in pregnancy have far-reaching implications for both mother and offspring. Of alarming interest is the increasing rate of obesity among adolescents and the cycle of obesity in future generations it portends. The purpose in this review is to briefly review the maternal perinatal morbidities associated with maternal pregravid obesity. Additionally, we will review evidence of both short- and long-term effect of maternal obesity on the in utero environment as it relates to fetal growth, neonatal body composition and adolescent obesity.

Birth Weight↗

Adiponectin in human pregnancy: implications for regulation of glucose and lipid metabolism.

AIMS/HYPOTHESIS: Adiponectin is upregulated during adipogenesis and downregulated in insulin-resistant states. The mechanism(s) governing the re-arrangements from adipogenesis to facilitated lipolysis during pregnancy are unknown. Our purpose was to analyse the role of adiponectin relative to the metabolic changes in human pregnancy. SUBJECTS, MATERIALS AND METHODS: Lean women (BMI <25 kg/m(2)) were evaluated longitudinally before conception, and in early (12-14 weeks) and late (34-36 weeks) pregnancy. Insulin sensitivity was measured using the glucose clamp technique. Venous blood and subcutaneous adipose tissue biopsies were obtained at each time point. RESULTS: Adiponectin concentrations were lower in the third trimester than in the pregravid condition (9.9+/-1.4 vs 13.5+/-1.8 microg/ml). The hypoadiponectinaemia was reflected by a 2.5-fold decrease in white adipose tissue adiponectin mRNA. These changes were associated with a 25% increase in fat mass (23.7+/-2.9 vs 18.9+/-2.9 kg). Insulin infusion decreased high molecular weight adiponectin complexes in pregravid women (9.9+/-0.6 vs 6.2+/-0.06) and the suppressive effect of insulin was lost during pregnancy. The pregnancy-mediated changes in adiponectin were strongly correlated with basal insulin levels and insulin sensitivity (p<0.0001). The relationship between adiponectin and insulin sensitivity was related to the decreased insulin regulation of glucose utilisation (r=0.55, p<0.001) but not of endogenous hepatic glucose production. CONCLUSIONS/INTERPRETATION: These data demonstrate that pregnancy is associated with adiponectin changes in lean women. Hypoadiponectinaemia is reflected by a lower amount of high molecular weight adiponectin and by the ratio of high to low molecular weight multimers. The adiponectin changes relate to decreased insulin sensitivity of glucose disposal rather than alterations of lipid metabolism.

Adiponectin↗

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 women with 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 meters were 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 composition was 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 +/- 14 mg/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 3,356 +/- 526 g. Three infants were > 4 kg and seven infants were > 90th centile for gestational age. The strongest correlation with neonatal fat mass was maternal fasting 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 be correlated 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 glucose levels correlated best with neonatal fat mass and other estimates of neonatal body composition.

Adult↗

Fetal macrosomia and maternal weight gain during pregnancy.

BACKGROUND: To calculate an adjusted maternal weight gain during pregnancy including infant and placental weights to the actual weight gain and secondarily examine its influence on the occurrence of fetal macrosomia. METHODS: The corrected weight gain was calculated as follows: maternal body weight at the last prenatal visit - (pregravid body weight + birth weight + placental weight) in 259 women (65 with type 1 diabetes, 69 with gestational diabetes mellitus, and 125 controls). RESULTS: Although weight gain was greater in non obese normal glucose tolerant and type 1 diabetic mothers of macrosomic infants, the difference was no longer significant when using corrected maternal weight gain. The correlation between birth weight and maternal weight gain decreased when using this index. CONCLUSION: The corrected weight gain is a better estimate of true accretion of maternal weight. Our results suggest that recommendations for weight gain during pregnancy should take this index into account.

Adult↗

Maternal factors that determine neonatal size and body fat.

These data are a review of previously published data. Initially, body composition was estimated in 186 neonates. Fat- free mass (FFM), which constituted 86% of birth weight, accounted for 83% of the variance in birth weight; fat mass (FM), which constituted 14% of birth weight, accounted for 46% of the variance in birth weight. Male neonates were an average of 175 g heavier than females. FFM was greater among males compared with females (P = 0.0001). Using stepwise logistic regression, 29% of the variance in birth weight, 30% in FFM, and 17% in FM was accounted for. Independent variables included maternal height, pregravid weight, weight gain during pregnancy, education, parity, paternal height and weight, neonatal sex, and gestational age. Including maternal insulin sensitivity explained 48% of the variance in birth weight, 53% in FFM, and 46% in FM. There was a positive correlation between weight gain and birth weight in control subjects but a negative correlation in subjects with gestational diabetes mellitus. Lastly, the roles of insulin, insulin-like growth factors, and leptin were examined in relation to fetoplacental growth and body composition. The assessment of fetal/neonatal body composition may improve the understanding of the effect of differential factors on fetal growth. Factors associated with accretion of fetal adipose tissue in late gestation are less well understood compared with birth weight and FFM. Additional studies of maternal glucose and lipid metabolism are needed to better evaluate fetal growth.

Adipose Tissue↗

Nutrient intake and hypertensive disorders of pregnancy: Evidence from a large prospective cohort.

OBJECTIVE: The objective of this analysis was to prospectively determine the effects of nutrient intakes on the incidences of preeclampsia and pregnancy-associated hypertension among women enrolled in the Calcium for Preeclampsia Prevention study. STUDY DESIGN: This was a prospective observational cohort study of women in a randomized clinical trial that included women seeking prenatal care at university medical centers and affiliated clinics and hospitals in 5 US communities. A total of 4589 nulliparous women were recruited between 13 and 21 weeks' gestation. Preeclampsia and pregnancy-associated hypertension were the main outcome measures. RESULTS: Preeclampsia was noted in 326 (7.6%) of the 4314 women with known pregnancy outcomes followed up until > or =20 weeks' gestation, and pregnancy-associated hypertension was noted in 747 (17.3%). As previously reported, there was no significant difference in these outcomes between cohorts randomly assigned to supplementation with calcium or placebo. By means of logistic regression a baseline risk model was constructed for preeclampsia and pregnancy-associated hypertension. After adjustment for treatment and clinical site, body mass index >26 kg/m(2) and race were significantly associated with an increased risk of preeclampsia. Body mass index > or =35 kg/m(2), race, and never smoking were significantly associated with an increased risk of pregnancy-associated hypertension. After adjustment for baseline risks, none of the 28 nutritional factors analyzed were significantly related to either preeclampsia or pregnancy-associated hypertension. CONCLUSION: We found no evidence in this study for a significant association of hypertensive disorders of pregnancy with any of the 23 nutrients measured.

Body Mass Index↗

Ethnicity, nutrition, and birth outcomes in nulliparous women.

OBJECTIVE: Ethnic differences in birth outcomes are well established, but it is not clear whether differences in nutrition may partly explain unaccounted differences in birth outcomes. Our purpose was to evaluate the relationship of nutrition to ethnic differences in birth outcomes. STUDY DESIGN: This was a multicenter, prospective study of 4589 healthy nulliparous women who were enrolled in the Calcium for Preeclampsia Prevention trial conducted from 1992 to 1995. Main outcome measures were birth weight, gestational age at delivery, preterm birth, and small for gestational age birth after the data were controlled for maternal characteristics and intake of total calories, protein, carbohydrate, fat, and 13 vitamin and mineral constituents that were obtained from a 24-hour recall at 13 to 21 weeks' gestation. RESULTS: Black and non-Hispanic white women differed significantly in birth outcomes, with odds ratios of 2.06 (95% confidence interval, 1.48-2.86) for small for gestational age and 1.38 (95% confidence interval, 0.98-1.95) for preterm birth, after adjustment for maternal characteristics. These odds ratios were hardly changed by the further adjustment for all nutritional variables, even though there were substantial nutritional differences between black and white women. Differences in birth outcomes between Hispanic and non-Hispanic white women were small. Hispanic women who spoke only Spanish were better nourished than those Hispanic women who spoke English, but this had only a modest effect on birth outcomes. CONCLUSION: Nutritional variation among women in the United States does not appear to have a significant role in the explanation of ethnic differences in birth outcomes.

Adult↗

Clinically useful estimates of insulin sensitivity during pregnancy: validation studies in women with normal glucose tolerance and gestational diabetes mellitus.

OBJECTIVE: We examined whether selected indexes of insulin sensitivity derived from an oral glucose tolerance test (IS(OGTT)) or fasting glucose/insulin levels (IS(QUICKI) and IS(HOMA)) can be used to predict insulin sensitivity in women before and during pregnancy. RESEARCH DESIGN AND METHODS: A 2-h euglycemic-hyperinsulinemic clamp (5 mmol/l glucose, 40 mU. m(-2). min(-1) insulin) and a 120-min oral glucose tolerance test (75 g load pregravid, 100 g pregnant) were repeated on 15 women (10 with normal glucose tolerance [NGT] and 5 with gestational diabetes mellitus [GDM]) pregravid and during both early (12-14 weeks) and late (34-36 weeks) pregnancy. An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat-free mass and endogenous glucose production measured using [6,6(-2)H(2)]glucose. RESULTS: Univariate analysis using combined groups and periods of pregnancy resulted in significant correlations between IS(CLAMP) and IS(OGTT) (r(2) = 0.74, P < 0.0001), IS(QUICKI) (r(2) = 0.64, P < 0.0001), and IS(HOMA) (r(2) = 0.53, P < 0.0001). The IS(OGTT) provided a significantly better correlation (P < 0.0001) than either IS(QUICKI) or IS(HOMA.) Multivariate analysis showed a significant group effect (P < 0.0003) on the prediction model, and separate equations were developed for the NGT (r(2) = 0.64, P < 0.0001) and GDM (r(2) = 0.85, P < 0.0001) groups. When subdivided by period of pregnancy, the correlation between IS(CLAMP) and IS(OGTT) pregravid was r(2) = 0.63 (P = 0.0002), during early pregnancy was r(2) = 0.80 (P < 0.0001), and during late pregnancy was r(2) = 0.64 (P = 0.0002). CONCLUSIONS: Estimates of insulin sensitivity from the IS(OGTT) during pregnancy were significantly better than from fasting glucose and insulin values. However, separate prediction equations are necessary for pregnant women with NGT and women with GDM.

Analysis of Variance↗

Anthropometric estimation of maternal body composition in late gestation.

OBJECTIVE: To construct a model to estimate maternal body composition in late gestation using anthropometric measurements. METHODS: Twenty healthy pregnant women at 30 weeks' gestation had estimates of body composition using hydrodensitometry, with corrections for residual lung volume, and total body water using H(2)(18)O (development group). Total body water was estimated from (18)O abundances measured by gas-isotope-ratio mass spectrometry. Maternal age, height, weight, and seven skinfold sites were correlated with fat mass using stepwise regression analysis. The anthropometric model to estimate fat mass was then tested prospectively in a second group of 20 subjects and correlated with underwater weighing and total body water measurements (validation group). Statistical analysis used chi(2), paired t and Wilcoxon sign-rank tests. RESULTS: There were no statistically significant differences in maternal demographics between groups. The fat mass of development group subjects using underwater weighing and total body water was 22.7 +/- 7.6 kg. Using the development group, a model was derived that explained 91% of the variance in fat mass by underwater weighing and total body water using maternal weight and triceps, subscapular, and suprailiac skinfolds (r(2) = 0.91, P <.001). When tested prospectively in the validation group, the correlation remained statistically significant (r(2) = 0.89, P <.001). There was no statistically significant (P =.88) difference between the anthropometric estimates of fat mass and underwater weighing and total body water measurements (95% confidence interval -2.476, 2.748 kg of fat mass). CONCLUSION: This anthropometric model can be used to predict maternal fat mass in late gestation.

Adult↗

Pregnancy outcomes in healthy nulliparas who developed hypertension. Calcium for Preeclampsia Prevention Study Group.

OBJECTIVE: To determine maternal and perinatal outcomes in nulliparas with pregnancy-associated hypertension or preeclampsia. METHODS: We conducted (and reported elsewhere) a randomized, double-masked, placebo-controlled trial calcium supplementation of 4589 healthy nulliparas assigned at 13-21 weeks' gestation. This well-defined and characterized data set provided an opportunity to detail more precisely adverse maternal, fetal, and newborn outcomes in women who developed hypertension among a prospective series of healthy nulliparas. RESULTS: Of 4302 women observed to or beyond 20 weeks' gestation, 1073 (24.9%) developed mild or severe pregnancy-associated hypertension or preeclampsia. One hundred sixteen women of the 1073 with hypertension (10.8%) and 336 of the 3229 without hypertension (10.4%) were delivered before 37 weeks' gestation. Fetal and neonatal mortality were similar in those groups; however, selected maternal and newborn morbidities were significantly greater in women with hypertension. Significantly increased maternal morbidities included increased cesarean deliveries, abruptio placentae, and acute renal dysfunction; and significantly increased perinatal morbidities included respiratory distress syndrome, ventilatory support, and fetal growth restriction. Adverse outcomes were highest in women with severe pregnancy-associated hypertension or preeclampsia. CONCLUSION: Hypertension, especially severe hypertension, was associated with an appreciable increase in important maternal and perinatal morbidity but not perinatal mortality.

Adult↗

Vanadate enhances but does not normalize glucose transport and insulin receptor phosphorylation in skeletal muscle from obese women with gestational diabetes mellitus.

OBJECTIVE: We compared the insulin-mimetic effects of vanadate, a protein-tyrosine phosphatase inhibitor, with the effects of insulin on skeletal muscle glucose transport and insulin receptor and insulin receptor substrate 1 phosphorylation to test the hypothesis that protein-tyrosine phosphatases participate in pregnancy-induced insulin resistance. STUDY DESIGN: Skeletal muscle fiber strips were obtained from the rectus abdominis during cesarean delivery in 7 patients with gestational diabetes mellitus, 11 pregnant women with normal glucose tolerance (pregnant control group), and 11 nonpregnant women undergoing elective surgery (nonpregnant control group). Muscle tissues were incubated in vitro for 15 to 60 minutes with or without maximal insulin (100 nmol/L) or sodium vanadate (6 micromol/L). Insulin receptor and insulin receptor substrate 1 tyrosine phosphorylation were measured, as was 2-deoxyglucose transport. The levels of protein-tyrosine phosphatase 1B were measured by Western blot analysis. RESULTS: Vanadate stimulated maximal 2-deoxyglucose transport more than did insulin alone in all samples (P<.05), but the value was still less in muscle tissues from pregnant control subjects and patients with gestational diabetes mellitus (P<.05). In muscle tissues from pregnant control subjects vanadate increased tyrosine phosphorylation of the insulin receptor and insulin receptor substrate 1 to levels similar to those in muscle tissues from nonpregnant control subjects. In patients with gestational diabetes mellitus vanadate increased insulin receptor and insulin receptor substrate 1 tyrosine phosphorylation, but these values remained less than in muscle tissues from nonpregnant control subjects (P<.05). Protein-tyrosine phosphatase 1B levels were not significantly different in skeletal muscles from each group. CONCLUSION: Vanadate did not restore normal glucose transport activity during pregnancy complicated by gestational diabetes mellitus, which indicates that decreased glucose uptake is probably not caused by impaired tyrosine phosphorylation events alone. Increased serine kinase activity and impaired glucose transporter 4 translocation probably contribute to insulin signaling abnormalities associated with pregnancy, especially in patients with gestational diabetes mellitus.

Biological Transport↗

Should the definition of preeclampsia include a rise in diastolic blood pressure of >/=15 mm Hg to a level <90 mm Hg in association with proteinuria?

OBJECTIVE: This study was undertaken to compare baseline characteristics and pregnancy outcomes between normotensive women who did and those who did not have a rise in diastolic blood pressure of >/=15 mm Hg in association with proteinuria. STUDY DESIGN: We studied 4302 healthy nulliparous women from the Calcium for Preeclampsia Prevention trial who were delivered at >/=20 weeks' gestation. We selected as the study group normotensive women who developed proteinuria within 7 days of a rise in diastolic blood pressure of >/=15 mm Hg with respect to baseline on 2 occasions 4 to 168 hours apart. Baseline blood pressure was the mean of measurements at 2 clinic visits before 22 weeks' gestation. Other normotensive women used for comparison were those who did not develop gestational hypertension or a rise in diastolic blood pressure of >/=15 mm Hg in association with proteinuria. RESULTS: Except for greater weight (P <.001), body mass index (P <.001), and systolic blood pressure (P =.05) the baseline characteristics of the 82 women with a rise in diastolic blood pressure of >/=15 mm Hg in association with proteinuria did not differ significantly from those of the other normotensive women. Although they had a greater rate of weight gain (P <.005), larger babies (P =.06), and a 2-fold increase in abdominal delivery (P <.001), there was little other evidence of adverse pregnancy outcomes among these women. CONCLUSION: During normotensive pregnancy a rise in diastolic blood pressure of >/=15 mm Hg in association with proteinuria appears to be benign and is not a useful clinical construct.

Birth Weight↗

Decreased insulin receptor tyrosine kinase activity and plasma cell membrane glycoprotein-1 overexpression in skeletal muscle from obese women with gestational diabetes mellitus (GDM): evidence for increased serine/threonine phosphorylation in pregnancy and GDM.

The cellular mechanisms for the insulin resistance of pregnancy and gestational diabetes mellitus (GDM) are unknown. The membrane protein plasma cell membrane glycoprotein-1 (PC-1) has been identified as an inhibitor of insulin receptor tyrosine kinase (IRTK) activity. We investigated insulin receptor function and PC-1 levels in muscle from three groups of obese subjects: women with GDM, pregnant women with normal glucose tolerance, and nonpregnant control subjects. Subjects (n = 6 for each group) were similar in age and degree of obesity (body fat >30%). IRTK activity, insulin receptor tyrosine phosphorylation, and protein levels of membrane glycoprotein PC-1 were determined in rectus abdominus muscle biopsies obtained at the time of either elective cesarean section or gynecological surgery. No significant differences were evident in basal insulin receptor tyrosine phosphorylation or IRTK activity in the three groups. After maximal insulin (10(-7) mol/l) stimulation, IRTK activity measured with the artificial substrate poly(Glu,Tyr) increased in all subjects but was lower in women with GDM by 25% (P < 0.05) and 39% (P < 0.001) compared with pregnant and nonpregnant control subjects, respectively. Similarly, insulin receptor tyrosine phosphorylation was significantly decreased in subjects with GDM (P < 0.05) compared with pregnant and nonpregnant control subjects. Treatment of the insulin receptors with alkaline phosphatase to dephosphorylate serine/threonine residues increased insulin-stimulated IRTK activity significantly in pregnant control and GDM subjects (P < 0.05), but these rates were still lower compared with nonpregnant control subjects (P < 0.05). PC-1 content in muscle from GDM subjects was increased by 63% compared with pregnant control subjects (P < 0.05) and by 206% compared with nonpregnant control subjects (P < 0.001). PC-1 content was negatively correlated with insulin receptor phosphorylation (r = -0.55, P < 0.05) and IRTK activity (r = -0.66, P < 0.05). These results indicate that pregnant control and GDM subjects had increased PC-1 content and suggest excessive phosphorylation of serine/threonine residues in muscle insulin receptors and that both may contribute to decreased IRTK activity. These changes worsen in women with GDM when controlling for obesity. These postreceptor defects in insulin signaling may contribute to the pathogenesis of GDM and the increased risk for type 2 diabetes later in life.

Alkaline Phosphatase↗

Longitudinal changes in glucose metabolism during pregnancy in obese women with normal glucose tolerance and gestational diabetes mellitus.

OBJECTIVE: This study prospectively evaluated the longitudinal changes in insulin sensitivity, insulin response, and endogenous (primarily hepatic) glucose production and suppression during insulin infusion in women with normal glucose tolerance (control) and gestational diabetes mellitus before and during a planned pregnancy. STUDY DESIGN: Eight control subjects and 7 subjects in whom gestational diabetes mellitus developed were evaluated with an oral glucose tolerance test, an intravenous glucose tolerance test, and hyperinsulinemic-euglycemic clamp with infusion of [6,6 (2)H2 ]glucose before conception and at 12 to 14 and 34 to 36 weeks' gestation. Insulin response was estimated as the area under the curve during the intravenous glucose tolerance test. Basal endogenous glucose production was estimated from isotope tracer dilution during steady state with [6,6 (2)H2 ]glucose and suppression during insulin infusion. Insulin sensitivity to glucose was defined as the glucose infusion rate required to maintain euglycemia during steady-state insulin infusion. Body composition was estimated with hydrodensitometry. Data were analyzed with 2-way analysis of variance with repeated measures for 2 groups. RESULTS: There were increases in first-phase (P =.006) and second-phase (P =. 0001) insulin responses in both groups with advancing gestation, but the increase in second-phase response was significantly greater (P =. 02) in the gestational diabetes mellitus group than in the control group. Basal glucose production increased significantly (P =.0001) with advancing gestation, and there was resistance to suppression during insulin infusion in both groups (P =.0001). There was less suppression of endogenous glucose production however, in the gestational diabetes mellitus group than in the control group (P =. 01). Insulin sensitivity decreased with advancing gestation in both groups (P =.0001), and there was lower insulin sensitivity in the gestational diabetes mellitus group than in the control group (P =. 04). Significant decreases in insulin sensitivity with time (P =. 0001) and between groups (P =.03) remained when the data were adjusted for differences in insulin concentration or residual hepatic glucose production. CONCLUSION: Obese women in whom gestational diabetes mellitus develops have a significant increase in insulin response but decreases in insulin sensitivity and suppression of hepatic glucose production during insulin infusion with advancing gestation with respect to a matched control group. These metabolic abnormalities in glucose metabolism are the hallmarks of type 2 diabetes, for which these women are at increased risk in later life.

Adult↗

Pregnancy and lactation in relation to range of acceptable carbohydrate and fat intake.

The additional energy requirements of pregnancy are needed for increases in maternal (breast, uterus and adipose) and feto-placental tissue accrued during pregnancy as well as the additional running cost of pregnancy for example increased cardiac output. Based on prospective longitudinal studies, the additional energy requirements of pregnancy range from > 500 MJ in Swedish women to net savings of approximately 50 MJ in women in The Gambia with their usual nutritional intake. In addition to the wide variation in estimated energy expenditure among various ethnic populations, there is as much as a 10-20 fold range in the total energy cost of pregnancy and lactation within relatively homogenous populations. The estimates of energy intake in these studies, however, are generally less than the estimates of total energy expenditure. The discrepancy between energy intake and energy expenditure during pregnancy is most probably due to several factors including decreased maternal activity, unreliable reporting of energy intake and possibly increased metabolic efficiency of basal metabolic rate, thermic effect of foods and physical activity. Based on recent studies, variations in maternal pregravid glucose insulin sensitivity may account for part of the observed variability associated with maternal metabolic adaptations during pregnancy. Decreases in insulin sensitivity have a significant inverse correlation with accretion of adipose tissue in early pregnancy. Likewise, there is a significant inverse correlation between decreases in basal oxygen consumption with increases in endogenous glucose production. The mechanism for these changes remain speculative. Additionally, although serum leptin concentrations increase 66% in early pregnancy and are correlated with maternal fat mass and basal energy expenditure, the increases in serum leptin occur prior to any significant increases in body fat or basal metabolic rate suggesting that pregnancy represents another leptin resistant state. Based on these data, specific recommendations for acceptable carbohydrate and fat intake during pregnancy and lactation are not possible for every woman at this time. Additional prospective studies, evaluating long-term maternal and neonatal outcome are needed before more meaningful nutritional recommendations can be proposed.

Adipose Tissue↗

The relationship between abnormal glucose tolerance and hypertensive disorders of pregnancy in healthy nulliparous women. Calcium for Preeclampsia Prevention (CPEP) Study Group.

OBJECTIVE: The study's aim was to determine whether healthy nulliparous women with abnormal glucose tolerance during pregnancy are at increased risk for development of pregnancy-associated hypertension or preeclampsia. STUDY DESIGN: A series of 4589 healthy nulliparous women from 5 university centers were evaluated prospectively to determine whether calcium supplementation would prevent preeclampsia. Pregnancy-associated hypertension was a diastolic blood pressure > or = 90 mm Hg on 2 occasions 4 hours to 1 week apart. Pregnancy-associated proteinuria was proteinuria > or = 1+ by dipstick testing on 2 occasions 4 hours to 1 week apart, proteinuria > or = 300 mg/24 h, a protein to creatinine ratio of > or = 0.35, or a single dipstick measurement of > or = 2+. Preeclampsia was defined as pregnancy-associated hypertension and pregnancy-associated proteinuria documented within 7 days of each other. Normal glucose tolerance was a plasma glucose level < 140 mg/dL 1 hour after a 50-g oral glucose challenge. Abnormal glucose tolerance was a plasma glucose level > or = 140 mg/dL 1 hour after a 50-g oral glucose challenge followed by a 3-hour 100-g oral glucose tolerance test yielding < 2 abnormal values. Gestational diabetes mellitus was a plasma glucose level > or = 200 mg/dL 1 hour after a 50-g oral glucose challenge in the absence of an oral glucose tolerance test or > or = 2 abnormal plasma glucose values in a 3-hour 100-g oral glucose tolerance test (> or = 105 mg/dL fasting, > or = 190 mg/dL at 1 hour, > or = 165 mg/dL at 2 hours, or > or = 145 mg/dL at 3 hours). For purposes of this study women with preeclampsia were excluded from the category of pregnancy-associated hypertension. RESULTS: Calcium supplementation did not prevent pregnancy-associated hypertension or preeclampsia. Of 3689 women with complete glucose testing data, 227 (6%) had abnormal glucose tolerance and 81 (2%) had gestational diabetes mellitus. Compared with women with normal glucose tolerance, women with abnormal glucose tolerance were significantly older, had greater body mass index, and were more likely to be white non-Hispanic, to smoke, and to have private medical insurance. Among women with gestational diabetes mellitus, after adjustment for clinical center the relative risks of preeclampsia and of all hypertensive disorders were increased (relative risk 1.67, 95% confidence interval 0.92-3.05, and relative risk 1.54, 95% confidence interval 1.28-2.11, respectively). Risk ratios were not substantially reduced after further adjustment for race and body mass index (odds ratios 1.41 and 1.48, respectively). Even within the normal range, multivariate analysis demonstrated that the level of plasma glucose 1 hour after a 50-g oral glucose challenge was an important predictor of preeclampsia. CONCLUSION: Even within the normal range, the level of plasma glucose 1 hour after a 50-g oral glucose challenge was positively correlated with the likelihood of preeclampsia. Women with gestational diabetes mellitus were at increased risk for hypertensive disorders during pregnancy after adjustment for clinical center, race, and body mass index, although the increase was not statistically significant. These findings suggest that insulin resistance may play a role in the pathogenesis of the hypertensive disorders of pregnancy.

Adult↗