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Background: Maternal obesity is increasing worldwide but the consequences for maternal physiology and fetal growth are not fully understood., Objective: To study whether changes in glucose and lipid metabolism during pregnancy differ between women with normal weight and overweight/obesity, and investigate which of these metabolic factors are associated with birthweight., Design: Prospective, longitudinal study., Setting: Department of Obstetrics, Oslo University Hospital, Rikshospitalet., Population: 1031 healthy pregnant women with singleton pregnancies., Methods: Blood samples from early and late pregnancy were analyzed for fasting glucose, insulin and lipids (total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides). Associations between metabolic factors and birthweight (z-scores) were explored by linear regression models. Main Outcome Measures: Group-dependent longitudinal changes in glucose and lipids and their association with birthweight (z-scores)., Results: Compared to women with normal weight (BMI < 25), women with overweight (BMI 25-29.9) and obesity (BMI > 30) had significantly higher fasting glucose (4.54, 4.68 and 4.84 mmol/l), insulin (23, 33 and 50 pmol/l), total cholesterol (4.85, 4.99 and 5.14 mmol/l), LDL-C (2.49, 2.66 and 2.88 mmol/l) and triglycerides (1.10, 1.28 and 1.57 mmol/l), but lower HDL-C (1.86, 1.75 and 1.55 mmol/l). BMI (B 0.05, 95% CI 0.03-0.06, p<0.001), gestational weight gain (GWG) (B 0.06, 0.05-0.08, p<0.001) and an increase in fasting glucose (B 0.30, 0.16-0.43, p<0.001) were positively associated with birthweight, whereas a decrease in HDL-C (B -0.72, -0.96- -0.53, p<0.001) had a negative association with birthweight., Conclusions: Overweight/obesity was associated with an unfavorable metabolic profile in early pregnancy which was associated with increased birthweight. However, modifiable factors like gestational weight gain and an increase in fasting glucose were identified and can be targeted for interventions., Competing Interests: The authors have declared that no competing interests exist.

Introduction: Increased BMI has been identified as a risk factor for most pregnancy complications, but the underlying metabolic factors mediating the detrimental effects of BMI are largely unknown. We aimed to compare metabolic profiles in overweight/obese women (body mass index [BMI] ≥ 25 kg/m2) and normal weight/underweight women (BMI < 25 kg/m2) across gestation. We also explored how gestational weight gain (GWG) affected maternal metabolic profiles. Material and methods: Exploratory nested case–control study based on a prospective longitudinal cohort of women who were healthy prior to pregnancy and gave birth at Oslo University Hospital from 2002 to 2008. The sample consisted of 48 women who were overweight/obese and 59 normal‐weight/underweight women. Plasma samples from four time points in pregnancy (weeks 14–16, 22–24, 30–32 and 36–38) were analyzed by nuclear magnetic resonance spectroscopy and 91 metabolites were measured. Linear regression models were fitted for each of the metabolites at each time point. Results: Overweight or obese women had higher levels of lipids in very‐low‐density lipoprotein (VLDL), total triglycerides, triglycerides in VLDL, total fatty acids, monounsaturated fatty acids, saturated fatty acids, leucine, valine, and total branched‐chain amino acids in pregnancy weeks 14–16 compared to underweight and normal‐weight women. Docosahexaenoic acid and degree of unsaturation were significantly lower in overweight/obese women in pregnancy weeks 36–38. In addition, overweight or obese women had higher particle concentration of XXL‐VLDL and glycoprotein acetyls (GlycA) at weeks 14–16 and 30–32. GWG did not seem to affect the metabolic profile, regardless of BMI group when BMI was treated as a dichotomous variable, ≥25 kg/m2 (yes/no). Conclusions: Overweight or obese women had smaller pregnancy‐related metabolic alterations than normal‐weight/underweight women. There was a trend toward higher triglyceride and VLDL particle concentration in overweight/obese women. As this was a hypothesis‐generating study, the similarities with late‐onset pre‐eclampsia warrant further investigation. The unfavorable development of fatty acid composition in overweight/obese women, with possible implication for the offspring, should also be studied further in the future. [ABSTRACT FROM AUTHOR]

Background and Hypothesis Gut microbiota alterations have been reported in severe mental illness (SMI) but fewer studies have probed for signs of gut barrier disruption and inflammation. We hypothesized that gut leakage of microbial products due to intestinal inflammation could contribute to systemic inflammasome activation in SMI. Study Design We measured plasma levels of the chemokine CCL25 and soluble mucosal vascular addressin cell adhesion molecule-1 (sMAdCAM-1) as markers of T cell homing, adhesion and inflammation in the gut, lipopolysaccharide binding protein (LBP) and intestinal fatty acid binding protein (I-FABP) as markers of bacterial translocation and gut barrier dysfunction, in a large SMI cohort (n = 567) including schizophrenia (SCZ, n = 389) and affective disorder (AFF, n = 178), relative to healthy controls (HC, n = 418). We assessed associations with plasma IL-18 and IL-18BPa and leukocyte mRNA expression of NLRP3 and NLRC4 as markers of inflammasome activation. Study Results Our main findings were: (1) higher levels of sMAdCAM-1 (P =.002), I-FABP (P = 7.6E−11), CCL25 (P = 9.6E−05) and LBP (P = 2.6E−04) in SMI compared to HC in age, sex, BMI, CRP and freezer storage time adjusted analysis; (2) the highest levels of sMAdCAM-1 and CCL25 (both P = 2.6E−04) were observed in SCZ and I-FABP (P = 2.5E−10) and LBP (3) in AFF; and (3), I-FABP correlated with IL-18BPa levels and LBP correlated with NLRC4. Conclusions Our findings support that intestinal barrier inflammation and dysfunction in SMI could contribute to systemic inflammation through inflammasome activation. [ABSTRACT FROM AUTHOR]

Background: There is still no worldwide agreement on the best diagnostic thresholds to define gestational diabetes (GDM) or the optimal approach for identifying women with GDM. Should all pregnant women perform an oral glucose tolerance test (OGTT) or can easily available maternal characteristics, such as age, BMI and ethnicity, indicate which women to test? The aim of this study was to assess the prevalence of GDM by three diagnostic criteria and the predictive accuracy of commonly used risk factors.Methods: We merged data from four Norwegian cohorts (2002-2013), encompassing 2981 women with complete results from a universally offered OGTT. Prevalences were estimated based on the following diagnostic criteria: 1999WHO (fasting plasma glucose (FPG) ≥7.0 or 2-h glucose ≥7.8 mmol/L), 2013WHO (FPG ≥5.1 or 2-h glucose ≥8.5 mmol/L), and 2017Norwegian (FPG ≥5.3 or 2-h glucose ≥9 mmol/L). Multiple logistic regression models examined associations between GDM and maternal factors. We applied the 2013WHO and 2017Norwegian criteria to evaluate the performance of different thresholds of age and BMI.Results: The prevalence of GDM was 10.7, 16.9 and 10.3%, applying the 1999WHO, 2013WHO, and the 2017Norwegian criteria, respectively, but was higher for women with non-European background when compared to European women (14.5 vs 10.2%, 37.7 vs 13.8% and 27.0 vs 7.8%). While advancing age and elevated BMI increased the risk of GDM, no risk factors, isolated or in combination, could identify more than 80% of women with GDM by the latter two diagnostic criteria, unless at least 70-80% of women were offered an OGTT. Using the 2017Norwegian criteria, the combination "age≥25 years or BMI≥25 kg/m2" achieved the highest sensitivity (96.5%) with an OGTT required for 93% of European women. The predictive accuracy of risk factors for identifying GDM was even lower for non-European women.Conclusions: The prevalence of GDM was similar using the 1999WHO and 2017Norwegian criteria, but substantially higher with the 2013WHO criteria, in particular for ethnic non-European women. Using clinical risk factors such as age and BMI is a poor pre-diagnostic screening method, as this approach failed to identify a substantial proportion of women with GDM unless at least 70-80% were tested. [ABSTRACT FROM AUTHOR]

Endothelial inflammation may be involved in the pathogenesis of schizophrenia, and cellular adhesion molecules (CAMs) on endothelial cells may facilitate leukocyte binding and transendothelial migration of cells and inflammatory factors. The aim of the present study was to assess levels of soluble cellular adhesion molecules, including intercellular adhesion molecule (ICAM)-1, vascular adhesion molecule (VCAM)-1, mucosal addressin cell adhesion molecule (MADCAM), junctional adhesion molecule (JAM-A) and neural cadherin (N-CAD) in patients with schizophrenia compared to healthy controls. The study population consists of 138 patients with schizophrenia-spectrum disorder, of whom 54 were drug-naïve, compared to 317 general population controls. The potential confounders age, gender, smoking and body mass index (BMI) were adjusted for in linear regression models. The total patient group showed significantly higher levels of ICAM-1 (p < 0.001) and VCAM-1 (p < 0.001) compared to controls. Previously medicated patients showed higher ICAM-1 levels compared to drug-naïve patients (p = 0.042) and controls (p < 0.001), and elevated VCAM-1 levels compared to controls (p < 0.001). Drug-naive patients had elevated levels of VCAM-1 (p = 0.031) compared to controls. In our study, patients with schizophrenia – including the drug-naïve – have higher levels of soluble CAMs compared to healthy controls. These findings suggest activation of the endothelial system as in inflammation. [ABSTRACT FROM AUTHOR]