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Objective: To estimate the association between maternal body mass index (BMI) and risk of spontaneous preterm delivery (sPTD) and elective preterm delivery (ePTD) in singleton and multiple pregnancies., Design: Retrospective cohort study., Setting: Electronic records of all deliveries from 2009 through 2013 in a tertiary university hospital were abstracted for demographic and obstetrical information., Participants: A total of 38 528 deliveries were included. Participants with missing data were excluded from the study. BMI was calculated from the measurement of height and weight at the first prenatal visit and categorised. Sonographic confirmation of gestational age was standard., Outcome Measures: Primary outcomes, sPTD and ePTD in singleton and multiple pregnancies, were evaluated by multinomial logistic regression analyses, stratified by parity, controlling for confounding variables., Results: Overall rate of PTD was 5.9%, from which 2.7% were sPTD and 3.2% ePTD. The rate of PTD was 50.4% in multiple pregnancies and 5.0% in singleton pregnancies. The risk of sPTD was increased in obese nulliparas (adjusted OR (aOR) 2.8, 95% CI 1.7 to 4.4) and underweight multiparas (aOR 2.2, 95% CI 1.3 to 3.8). The risk of ePTD was increased in underweight nulliparas (aOR 1.8; 95% CI 1.04 to 3.4) and severely obese multiparas (aOR 1.4, 95% CI 1.02 to 3.8).Severe obesity increased the risk of both sPTD (aOR 1.4; 95% CI 1.01 to 2.1) and ePTD (aOR 1.4; 95% CI 1.1 to 1.8) in singleton pregnancies. Obesity did not influence the rate of either sPTD or ePTD in multiple pregnancies., Conclusion: Maternal obesity is an independent risk factor for PTD in singleton pregnancies but not in multiple pregnancies. Obesity and nulliparity increase the risk of sPTD, whereas obesity and multiparity increase the risk of ePTD., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Introduction: Maternal obesity has been identified as an important clinical priority in contemporary obstetrics. This study aimed to determine the incidence of maternal obesity in early pregnancy and track recent trends in body mass index (BMI) categories over 5 years 2009-2013., Material and Methods: This prospective observational study included all women who delivered an infant weighing ≥500 g during the 5 years 2009-2013 in a large university teaching hospital in Ireland. Body mass index was calculated using early pregnancy weight and height measured at first antenatal visits. Sociodemographic and clinical data were gathered prospectively. Trends in maternal obesity were tracked over 5 years and epidemiological associations with obesity were examined using logistic regression, adjusted for confounding variables., Results: Of 42 362 women, 99.0% (n = 41 927) were eligible for analysis with a mean BMI of 25.5 kg/m(2) , mean age of 30.7 years and 40.7% (n = 17054) primigravidas. The absolute number of cases of severe obesity (BMI ≥40.0 kg/m(2) ) increased by 48.5% from 2009 to 2013 (p < 0.001). After multivariate logistic regression analyses, obesity incidence increased with increasing parity, advancing age and socioeconomic disadvantage. The maternal obesity rate among women born in the 13 European Union Accession countries was 8.6%, nearly half that of those born in existing European Union countries (p < 0.001)., Conclusion: It is concerning that while the overall obesity rate remained stable, the number of cases of severe obesity increased over 5 years. We recommend renewed public health efforts addressing obesity rates before pregnancy and reinforcing attempts to optimize a woman's weight after delivery., (© 2015 Nordic Federation of Societies of Obstetrics and Gynecology.)

Objective: To review induction of labor analyzed by body mass index (BMI) category in primigravidas and multigravidas., Design: Prospective observational study., Population: Women enrolled after sonographic confirmation of singleton pregnancy in the first trimester., Setting: Large university teaching hospital., Methods: Maternal height and weight were measured accurately before BMI calculation. Clinical details were recorded after review of individual obstetric records., Main Outcome Measures: Emergency cesarean section and obstetric interventions., Results: Of 2000 women enrolled, 50.4% (n = 1008) were primigravidas and 17.3% (n = 346) were obese. The induction rate was 25.6% and the overall cesarean section rate 22.0%. Primigravidas were more likely to have labor induced than multigravidas (38.1% vs. 23.4%, p < 0.001). Compared with women with a normal BMI, obese primigravidas but not obese multigravidas were more likely to have labor induced. In primigravidas who had labor induced, the cesarean section rate was 20.6% (91/442) compared with 8.3% (17/206) in multigravidas who had labor induced (p < 0.001). In obese primigravidas, induction of labor was also more likely to be associated with other interventions such as epidural analgesia, fetal blood sampling and emergency cesarean section. In contrast, induction of labor in obese multigravidas was not only less common but also not associated with an increase in other interventions compared with multigravidas with a normal BMI., Conclusions: Due to the short-term and long-term implications of an unsuccessful induction in an obese primigravida, we recommend that induction of labor should only be undertaken for strict obstetric indications after careful consideration by an experienced clinician., (© 2013 Nordic Federation of Societies of Obstetrics and Gynecology.)

Obesity is a chronic inflammatory state characterized by infiltration of adipose tissue by immune cell populations, including T lymphocytes. Natural killer T (NKT) cells, a specialized lymphocyte subset recognizing lipid antigens, can be pro- or anti-inflammatory. Their role in adipose inflammation continues to be inconclusive and contradictory. In obesity, the infiltration of tissues by invariant NKT (iNKT) cells is decreased. We therefore hypothesized that an excess iNKT cell complement might improve metabolic abnormalities in obesity. Vα14 transgenic (Vα14tg) mice, with increased iNKT cell numbers, on a LDL receptor-deficient (Ldlr(-/-)) background and control Ldlr(-/-) mice were placed on an obesogenic diet for 16 weeks. Vα14tg.Ldlr(-/-) mice gained 25% more weight and had increased adiposity than littermate controls. Transgenic mice also developed greater dyslipidemia, hyperinsulinemia, insulin resistance, and hepatic triglyceride accumulation. Increased macrophage Mac2 immunostaining and proinflammatory macrophage gene expression suggested worsened adipose inflammation. Concurrently, these mice had increased atherosclerotic lesion area and aortic inflammation. Thus, increasing the complement of iNKT cells surprisingly exacerbated the metabolic, inflammatory, and atherosclerotic features of obesity. These findings suggest that the reduction of iNKT cells normally observed in obesity may represent a physiological attempt to compensate for this inflammatory condition.

Adipose tissue inflammation and specifically, pro-inflammatory macrophages are believed to contribute to insulin resistance (IR) in obesity in humans and animal models. Recent studies have invoked T cells in the recruitment of pro-inflammatory macrophages and the development of IR. To test the role of the T cell response in adipose tissue of mice fed an obesogenic diet, we used two agents (CTLA-4 Ig and anti-CD40L antibody) that block co-stimulation, which is essential for full T cell activation. C57BL/6 mice were fed an obesogenic diet for 16 weeks, and concomitantly either treated with CTLA-4 Ig, anti-CD40L antibody or an IgG control (300 µg/week). The treatments altered the immune cell composition of adipose tissue in obese mice. Treated mice demonstrated a marked reduction in pro-inflammatory adipose tissue macrophages and activated CD8+ T cells. Mice treated with anti-CD40L exhibited reduced weight gain, which was accompanied by a trend toward improved IR. CTLA-4 Ig treatment, however, was not associated with improved IR. These data suggest that the presence of pro-inflammatory T cells and macrophages can be altered with co-stimulatory inhibitors, but may not be a significant contributor to the whole body IR phenotype.

Objective: The purpose of this nested cohort study was to compare the rate of pre-pregnancy supplementation in obese women with that of women with a normal BMI., Methods: Pregnant women were enrolled at their convenience in a large university hospital. Weight and height were measured in the first trimester and BMI categorised., Results: Of the 288 women, 35.1% were in the normal, 29.5% in the overweight and 35.4% in the obese BMI categories. Only 45.1% (n = 46) of the obese women took pre-pregnancy folic acid compared with 60.4% (n = 61) of women with a normal BMI (p < 0.03). The lower incidence of folic acid supplementation in obese women was associated with an unplanned pregnancy in 36.3% of women compared with 22.8% in the normal BMI category (p < 0.04)., Conclusions: Obese women should take folate supplements whether they are planning to conceive or not.

Obesity-associated increases in adipose tissue (AT) CD11c(+) cells suggest that dendritic cells (DC), which are involved in the tissue recruitment and activation of macrophages, may play a role in determining AT and liver immunophenotype in obesity. This study addressed this hypothesis. With the use of flow cytometry, electron microscopy, and loss-and-gain of function approaches, the contribution of DC to the pattern of immune cell alterations and recruitment in obesity was assessed. In AT and liver there was a substantial, high-fat diet (HFD)-induced increase in DC. In AT, these increases were associated with crown-like structures, whereas in liver the increase in DC constituted an early and reversible response to diet. Notably, mice lacking DC had reduced AT and liver macrophages, whereas DC replacement in DC-null mice increased liver and AT macrophage populations. Furthermore, delivery of bone marrow-derived DC to lean wild-type mice increased AT and liver macrophage infiltration. Finally, mice lacking DC were resistant to the weight gain and metabolic abnormalities of an HFD. Together, these data demonstrate that DC are elevated in obesity, promote macrophage infiltration of AT and liver, contribute to the determination of tissue immunophenotype, and play a role in systemic metabolic responses to an HFD.

Objective: We evaluated screening with a diagnostic oral glucose tolerance test earlier than 20 weeks gestation in women with moderate to severe obesity., Design: Prospective observational study., Setting: Large university teaching hospital., Population: We enrolled 100 women booking for antenatal care in the first trimester at their convenience., Methods: Height and weight were measured and body mass index calculated. Only women with a body mass index > 34.9 kg/m(2) were included. Women were booked for a 100 g oral glucose tolerance test before 20 weeks and, if normal, another test at 28 weeks gestation., Main Outcome Measures: Impaired glucose tolerance and gestational diabetes mellitus., Results: Of the 100 women given an appointment for an oral glucose tolerance test before 20 weeks gestation, 92 attended. Of these, 10 (10.8%) women had an abnormal result, with impaired glucose tolerance in five (5.4%) cases and gestational diabetes mellitus in five (5.4%) cases. Of those with a normal result at 20 weeks, 81 attended for a repeat test at 28 weeks gestation. A further four (4.9%) had impaired glucose tolerance and four (4.9%) had gestational diabetes mellitus. A total of 18 (20.5%) of the 88 women who complied with screening had an abnormal test., Conclusions: Women who have moderate/severe obesity have a one in five chance of having an abnormal diagnostic oral glucose tolerance test when screened for gestational diabetes mellitus. To optimize maternal glycemic control in pregnancy, we suggest that women with a body mass index > 34.9 kg/m(2) may need to be screened early in pregnancy and, if the test is normal, again at 28 weeks gestation., (© 2012 The Authors Acta Obstetricia et Gynecologica Scandinavica© 2012 Nordic Federation of Societies of Obstetrics and Gynecology.)

Objective: To compare the incidence of spontaneous miscarriage in women with moderate to severe obesity to that in women with a normal BMI after sonographic confirmation of the foetal heart rate in the first trimester., Methods: Women were enrolled in a prospective observational study at their convenience in the first trimester after an ultrasound confirmed an ongoing singleton pregnancy with foetal heart activity present. Maternal height and weight were measured digitally and BMI was calculated., Results: In the 3,000 women enrolled, the miscarriage rate overall was 3.9% (n = 117). The mean gestational age at enrolment was 11.1 weeks. In the class 2-3 (BMI > 34.9 kg/m(2)) obese primigravidas the miscarriage rate was 11.3% (n = 8) compared with 2.7% (n = 24) in the normal BMI category (p = 0.003), and 3.7% (n = 5) in the class 1 obese category (not significant). In multigravidas, there was no increased rate of miscarriage among class 2-3 obese women compared with multigravidas in the normal BMI category. The mean body composition values showed that primigravidas who miscarried had both increased fat and fat-free masses compared with those who did not, but multigravidas who miscarried had a similar fat mass and fat-free mass with those who did not., Conclusions: In women with sonographic evidence of foetal heart activity in the first trimester, the rate of spontaneous miscarriage is low. It was increased in moderate to severely obese primigravidas, but was not increased in other obese women compared to women in the normal BMI category.

Objective: This longitudinal observational study examined BMI changes between successive pregnancies.Methods: The computerized medical records of women who attended a large maternity hospital between 2009 and 2017 for their first and second singleton deliveries were analyzed. Women who had their weight first measured after 15 weeks of gestation in either pregnancy were excluded.Results: Of the 9,724 women, the incidence of obesity increased from 11.6% in the first pregnancy to 16.0% in the second. The mean interpregnancy interval was 32.5 ± 15.7 months, and median BMI change was +0.6 kg/m2 (interquartile range 2.2; P < 0.001). Overall, 10.3% (1,006/9,724) developed overweight and 5.9% (571/9,724) developed obesity by the second pregnancy. Of the nulliparas in the overweight category, 20.6% (526/2,558) entered the obesity category. The development of obesity by the second pregnancy was independently associated with a longer interpregnancy interval, formula feeding at hospital discharge, taking antidepressants or anxiolytics, and postnatal depression. Professional/managerial employment was associated with a lower odds ratio of developing obesity.Conclusions: Maternal obesity increased between the first and second pregnancy, with one-fifth of nulliparas in the overweight category developing obesity. Pregnancy-related factors were identified as predictors of developing obesity. Further research is needed to assess whether interventions targeting these related factors could optimize maternal weight management between pregnancies. [ABSTRACT FROM AUTHOR]

Obesity-associated increases in adipose tissue (AT) CD11c+ cells suggest that dendritic cells (DC), which are involved in the tissue recruitment and activation of macrophages, may play a role in determining AT and liver immunophenotype in obesity. This study addressed this hypothesis. With the use of flow cytometry, electron microscopy, and loss-and-gain of function approaches, the contribution of DC to the pattern of immune cell alterations and recruitment in obesity was assessed. In AT and liver there was a substantial, high-fat diet (HFD)-induced increase in DC. In AT, these increases were associated with crown-like structures, whereas in liver the increase in DC constituted an early and reversible response to diet. Notably, mice lacking DC had reduced AT and liver macrophages, whereas DC replacement in DC-null mice increased liver and AT macrophage populations. Furthermore, delivery of bone marrow-derived DC to lean wild-type mice increased AT and liver macrophage infiltration. Finally, mice lacking DC were resistant to the weight gain and metabolic abnormalities of an HFD. Together, these data demonstrate that DC are elevated in obesity, promote macrophage infiltration of AT and liver, contribute to the determination of tissue immunophenotype, and play a role in systemic metabolic responses to an HFD. [ABSTRACT FROM AUTHOR]

Objective. To examine the relationship between maternal glucose levels and intrauterine fetal adiposity distribution in women with a normal oral glucose tolerance test (OGTT) at 28 weeks gestation. Study Design. We recruited 231 women with a singleton pregnancy. At 28 and 37 weeks gestation, sonographic measurements of fetal body composition were performed. Multiple regression analysis was used to study the influence of different maternal variables on fetal adiposity distribution. Results. Maternal glucose levels correlated with the fetal abdominal subcutaneous tissue measurements (r = 0.2; P = 0.014) and with birth weight (r = 0.1; P = 0.04). Maternal glucose levels did not correlate with the fetal mid-thigh muscle thickness and mid-thigh subcutaneous tissue measurements. Conclusion. We found that in nondiabetic women maternal glucose levels not only influence fetal adiposity and birth weight, but also influence the distribution of fetal adiposity. This supports previous evidence that maternal glycemia is a key determinant of intrauterine fetal programming. [ABSTRACT FROM AUTHOR]