Neighborhood walkability and risk of gestational diabetes.

OBJECTIVE: Higher neighborhood walkability has been associated with a lower risk of type 2 diabetes mellitus (T2DM) by promoting greater physical activity (thereby reducing weight and lowering insulin resistance). However, it is not known if walkability may similarly reduce maternal risk of gestational diabetes mellitus (GDM), which arises in the setting of the severe physiologic insulin resistance of pregnancy. Indeed, the insulin resistance of pregnancy is primarily driven by placental hormones and not maternal weight gain. Thus, we sought to evaluate the impact of neighborhood walkability on maternal risk of GDM and the pathophysiologic determinants thereof (insulin sensitivity and pancreatic beta-cell function). METHODS: In this study, 1318 women reported their pregravid physical activity (Baecke questionnaire) while undergoing an oral glucose tolerance test (OGTT) at mean 29.3 weeks' gestation. The OGTT identified 290 women with GDM and enabled assessment of insulin sensitivity and beta-cell function. Based on their residential Walk Score, the women were stratified into the following four established categories of neighborhood walkability: car dependent (n=328), somewhat walkable (n=315), very walkable (n=406), and walker's paradise (n=269). RESULTS: There was a progressive increase in pregravid total physical activity (p=0.002), non-sport leisure-time activity (p=0.009) and sport activity (p=0.01) across the walkability groups (from car dependent to somewhat walkable to very walkable to walker's paradise), coupled with a concomitant decline in pre-pregnancy body mass index (p=0.007). However, in pregnancy, the groups did not differ in gestational weight gain (p=0.80). Moreover, the walkability groups also did not differ in mean adjusted insulin sensitivity, beta-cell function, or glycemia on the antepartum OGTT. On logistic regression analysis, Walk Score did not predict GDM (OR=1.001, 95% CI 0.995 to 1.007). CONCLUSION: Neighborhood walkability is not a significant determinant of maternal risk of GDM. Thus, in contrast to T2DM, the effect of neighborhood design on incidence of GDM will be comparatively modest.

Fetal sex and maternal risk of gestational diabetes mellitus: the impact of having a boy.

OBJECTIVE: Retrospective analyses of perinatal databases have raised the intriguing possibility of an increased risk of gestational diabetes mellitus (GDM) in women carrying a male fetus, but it has been unclear if this was a spurious association. We thus sought to evaluate the relationship between fetal sex and maternal glucose metabolism in a well-characterized cohort of women reflecting the full spectrum of gestational glucose tolerance from normal to mildly abnormal to GDM. RESEARCH DESIGN AND METHODS: A total of 1,074 pregnant women underwent metabolic characterization, including oral glucose tolerance test (OGTT), at mean 29.5 weeks' gestation. The prevalence of GDM, its pathophysiologic determinants (ß-cell function and insulin sensitivity/resistance), and its clinical risk factors were compared between women carrying a female fetus (n = 534) and those carrying a male fetus (n = 540). RESULTS: Women carrying a male fetus had lower mean adjusted ß-cell function (insulinogenic index divided by HOMA of insulin resistance: 9.4 vs. 10.5, P = 0.007) and higher mean adjusted blood glucose at 30 min (P = 0.025), 1 h (P = 0.004), and 2 h (P = 0.02) during the OGTT, as compared with those carrying a female fetus. Furthermore, women carrying a male fetus had higher odds of developing GDM (odds ratio 1.39 [95% CI 1.01-1.90]). Indeed, male fetus further increased the relative risk of GDM conferred by the classic risk factors of maternal age >35 years and nonwhite ethnicity by 47 and 51%, respectively. CONCLUSIONS: Male fetus is associated with poorer ß-cell function, higher postprandial glycemia, and an increased risk of GDM in the mother. Thus, fetal sex potentially may influence maternal glucose metabolism in pregnancy.

Postpartum microalbuminuria after gestational diabetes: the impact of current glucose tolerance status.

CONTEXT: It has been reported that women with a history of gestational diabetes mellitus (GDM) have an increased risk of microalbuminuria compared with that of their peers. Because previous GDM predicts an increased risk of prediabetes, which itself is associated with microalbuminuria, we hypothesized that current glucose intolerance may confound any association between GDM and microalbuminuria. OBJECTIVE: The purpose of this study was to evaluate the relative impact of gestational and current dysglycemia on postpartum microalbuminuria in a cohort of women reflecting the full spectrum of gestational glucose tolerance from normal to mildly abnormal to GDM. DESIGN/SETTING/PARTICIPANTS: In this prospective observational cohort study, 320 women underwent a glucose challenge test (GCT) and an oral glucose tolerance test (OGTT) in pregnancy, which identified 100 women with GDM, 58 with gestational impaired glucose tolerance, 90 with an abnormal GCT but a normal OGTT, and 72 with a normal GCT and OGTT. At 3 years postpartum, they underwent measurement of urine microalbumin and a repeat OGTT that identified 63 women with glucose intolerance (prediabetes/diabetes). RESULTS: The postpartum urine microalbumin to creatinine ratio did not differ among the 4 gestational glucose tolerance groups (P = .23). Furthermore, on logistic regression analysis, GDM did not independently predict an elevated urine microalbumin to creatinine ratio of ≥1.5 g/mol of creatinine (odds ratio, 0.43; 95% confidence interval, 0.17-1.11), after adjustment for age, ethnicity, family history of diabetes, body mass index, blood pressure, estimated glomerular filtration rate, and current glucose intolerance. In contrast, current glucose intolerance independently predicted a urine microalbumin to creatinine ratio of ≥1.5 (odds ratio, 3.4; 95% confidence interval, 1.4-8.2, P = .005). CONCLUSION: Current glucose intolerance, rather than previous GDM, may be associated with an increased risk of microalbuminuria in the early postpartum years.

Cardiometabolic implications of postpartum weight changes in the first year after delivery.

OBJECTIVE: The cumulative effect of postpartum weight retention from each pregnancy in a woman's life may contribute to her ultimate risk of diabetes and vascular disease. However, there is little direct evidence supporting this hypothesis. In this context, we sought to evaluate the cardiometabolic implications of patterns of postpartum weight change and the time course thereof in the first year after pregnancy. RESEARCH DESIGN AND METHODS: Three hundred five women underwent cardiometabolic characterization at recruitment in pregnancy and at 3 and 12 months postpartum. Based on their respective weight changes between prepregnancy and 3 months postpartum (loss or gain) and between 3 and 12 months postpartum (loss or gain), participants were stratified into four groups: loss/loss, gain/loss, loss/gain, and gain/gain. RESULTS: Most women (81.0%) had higher weight at 3 months postpartum compared with prepregnancy. Between 3 and 12 months, most women (74.4%) lost weight. At 3 months, there were modest differences between the four groups in mean adjusted LDL cholesterol (P = 0.01) and apolipoprotein-B (apoB; P = 0.02) but no significant differences in adjusted blood pressure, fasting and 2-h glucose, HDL, triglycerides, homeostasis model assessment of insulin resistance (HOMA-IR), adiponectin, and C-reactive protein. By 12 months postpartum, however, clear gradients emerged, with mean adjusted diastolic blood pressure (P = 0.02), HOMA-IR (P = 0.0003), LDL (P = 0.001), and apoB (P < 0.0001) all progressively increasing from the loss/loss group to gain/loss to loss/gain to gain/gain. Similarly, at 12 months, mean adjusted adiponectin showed a stepwise decrease from loss/loss to gain/loss to loss/gain to gain/gain (P = 0.003). CONCLUSIONS: An adverse cardiometabolic profile emerges as early as 1 year postpartum in women who do not lose weight between 3 and 12 months after delivery.

Vitamin D status and cardiometabolic assessment in infancy.

BACKGROUND: Infants are at risk of vitamin D insufficiency, owing to their limited exposure to direct sunlight and the low levels of vitamin D in breast milk. Although vitamin D insufficiency has been associated with cardiometabolic risk factors in children, these associations have not been studied in infants, despite their unique risks. Therefore, we sought to determine whether vitamin D status was associated with cardiometabolic measures in infants. METHODS: Ninety-nine full-term infants were evaluated at the age of 1 y with measurement of 25-hydroxy vitamin D (25-OH-D) and an array of traditional (fasting glucose, insulin, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol, triglycerides) and emerging (C-reactive protein, adiponectin, leptin) cardiometabolic risk factors. On the basis of 25-OH-D levels, infants were classified as vitamin D sufficient (n = 59), vitamin D insufficient (n = 29), or vitamin D deficient (n = 11). RESULTS: Duration of exclusive breastfeeding and prevalence of nonwhite ethnicity were highest in the vitamin D-deficient group (P = 0.05 and 0.03, respectively). Current use of vitamin D supplementation was highest in the sufficient group (P = 0.02). Of note, however, there were no significant differences among the three groups in any of the cardiometabolic risk factors, on both unadjusted and covariate-adjusted analyses. CONCLUSION: Vitamin D insufficiency/deficiency is not associated with an adverse cardiometabolic risk factor profile in 1-y-old infants.

Postpartum metabolic function in women delivering a macrosomic infant in the absence of gestational diabetes mellitus.

OBJECTIVE: Gestational diabetes mellitus (GDM) is associated with fetal macrosomia and maternal postpartum dysglycemia, insulin resistance, and ß-cell dysfunction. Indeed, in practice, a prior pregnancy that resulted in a large-for-gestational-age (LGA) delivery is often considered presumptive evidence of GDM, whether or not it was diagnosed at the time. If this clinical assumption is correct, however, we would expect these women to exhibit postpartum metabolic dysfunction. Thus, to test this hypothesis, we assessed metabolic function during and after pregnancy in a cohort of women stratified according to the presence/absence of GDM and LGA delivery, respectively. RESEARCH DESIGN AND METHODS: A total of 562 women underwent metabolic characterization, including oral glucose tolerance test (OGTT), in late pregnancy and at 3 months' postpartum. The women were stratified into three groups: those with neither GDM nor LGA delivery (nonGDM, n = 364), those without GDM but with LGA delivery (nonGDM-LGA, n = 46), and those with GDM (n = 152). RESULTS: On logistic regression, GDM predicted postpartum glucose intolerance (OR 4.1 [95% CI 2.5-6.8]; P < 0.0001), whereas nonGDM-LGA did not (P = 0.65). At 3 months' postpartum, the mean adjusted levels of fasting glucose and area under the glucose curve on the OGTT were significantly higher in the GDM women compared with either nonGDM or nonGDM-LGA (all P < 0.05), with no differences between the latter two groups. In a similar manner, mean adjusted insulin sensitivity (Matsuda index) and ß-cell function (Insulin Secretion-Sensitivity Index-2) were lower in GDM women compared with either nonGDM or nonGDM-LGA (all P < 0.05), again with no differences between the latter two groups. CONCLUSIONS: Women with nonGDM-LGA do not exhibit postpartum metabolic dysfunction, arguing against the assumption of undiagnosed GDM in these patients.