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      Hypertensive Disorders of Pregnancy in Women with Gestational Diabetes Mellitus on Overweight Status of Their Children

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          Abstract

          Hypertensive disorders of pregnancy (HDP) as a group of medical complications in pregnancy are believed to be associated with an increased risk of poor fetal growth, but the influence on offspring’s body composition is not clear. The aim of the present study was to evaluate the association between maternal hypertensive disorders of pregnancy and overweight status in the offspring of mothers with gestational diabetes mellitus (GDM).

          A cross-sectional study among 1263 GDM mother-child pairs was performed in Tianjin, China. General linear models and logistic regression models were used to assess the associations of maternal hypertension in pregnancy with anthropometry and overweight status in the offspring from birth to 1–5 years old.

          Offspring of GDM mothers who were diagnosed with hypertensive disorders during pregnancy had higher mean values of Z scores for birth weight for gestational age and birth weight for length, and higher mean values of Z scores for weight for age, weight for length/height, and body mass index for age at 1–5 years old than those of GDM mothers with normal blood pressure during pregnancy. Maternal hypertensive disorders of pregnancy were associated with increased risks of large for gestational age (OR 1.74, 95%CI 1.08–2.79) and macrosomia (OR 2.02, 95%CI 1.23–3.31) at birth and childhood overweight/obesity at 1–5 years old age (OR 1.88, 95%CI 1.16–3.04).

          For offspring of mothers with GDM, maternal hypertension during pregnancy was a risk factor for macrosomia at birth and childhood overweight and obesity, and controlling the maternal hypertension may be more important for preventing large for gestational age babies and childhood obesity.

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          Most cited references33

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          Combined associations of prepregnancy body mass index and gestational weight gain with the outcome of pregnancy.

          Although both maternal prepregnancy body mass index (BMI) and gestational weight gain (GWG) may affect birth weight, their separate and joint associations with complications of pregnancy and delivery and with postpartum weight retention are unclear. We aimed to investigate the combined associations of prepregnancy BMI and GWG with pregnancy outcomes and to evaluate the trade-offs between mother and infant for different weight gains. Data for 60892 term pregnancies in the Danish National Birth Cohort were linked to birth and hospital discharge registers. Self-reported total GWG was categorized as low ( or=20 kg). Adjusted associations of prepregnancy BMI and GWG with outcomes of interest were estimated by logistic regression analyses. High and very high GWG added to the associations of high prepregnancy BMI with cesarean delivery and were strongly associated with high postpartum weight retention. Moreover, greater weight gains and high maternal BMI decreased the risk of growth restriction and increased the risk of the infant's being born large-for-gestational-age or with a low Apgar score. Generally, low GWG was advantageous for the mother, but it increased the risk of having a small baby, particularly for underweight women. Heavier women may benefit from avoiding high and very high GWG, which brings only a slight increase in the risk of growth restriction for the infant. High weight gain in underweight women does not appear to have deleterious consequences for them or their infants, but they may want to avoid low GWG to prevent having a small baby.
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            Oxidative stress and inflammation interactions in human obesity.

            Obesity is often characterized by increased oxidative stress and exacerbated inflammatory outcomes accompanying infiltration of immune cells in adipocytes. The oxidative stress machinery and inflammatory signaling are not only interrelated, but their impairment can lead to an inhibition of insulin responses as well as a higher risk of cardiovascular diseases and associated features. Mitochondria, in addition to energy transformation, play a role in apoptosis, cellular proliferation, as well as in the cellular redox state control. Under certain circumstances, protons are able to re-enter the mitochondrial matrix via different uncoupling proteins, disturbing free radical production by mitochondria. Disorders of the mitochondrial electron transport chain, over-generation of reactive oxygen species, and lipoperoxides or alterations in antioxidant defenses have been reported in situations of obesity and type-2 diabetes. On the other hand, obesity has been linked to a low grade pro-inflammatory state, in which impairments in the oxidative stress and antioxidant mechanism could be involved. The current scientific evidence highlights the need of investigating the interplay between oxidative stress and inflammation with obesity/diabetes onset as well as the interactions of such factors either as a cause or consequence of obesity. The signaling mediated by the activation of inflammatory markers or nuclear factor kappa β and other transcription factors as central regulators of inflammation are key issues to understanding oxidative stress responses in obesity. This review aims at summarizing the main mechanisms and interplay factors between oxidative stress and inflammation in human obesity according to the last 10 years of research in the field.
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              The predisposition to obesity and diabetes in offspring of diabetic mothers.

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                Author and article information

                Journal
                8811625
                5250
                J Hum Hypertens
                J Hum Hypertens
                Journal of human hypertension
                0950-9240
                1476-5527
                24 January 2017
                16 March 2017
                19 September 2017
                : 10.1038/jhh.2017.17
                Affiliations
                [1 ]Tianjin Women’s and Children’s Health Center, 96 Guizhou Road, Heping Districts, Tianjin, China
                [2 ]Chronic Disease Epidemiology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, USA
                [3 ]Department of Environmental Health Sciences | Columbia University Mailman School of Public Health, New York, NY, USA
                [4 ]Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
                Author notes
                Address for correspondence: Gang Hu, PhD, Chronic Disease Epidemiology Laboratory, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, USA Tel: 225-763-3053, Fax: 225-763-3009, gang.hu@ 123456pbrc.edu
                Article
                NIHMS844663
                10.1038/jhh.2017.17
                5600626
                28300070
                783634f8-abb3-40d8-a343-c5ccfe61cdc6

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                Cardiovascular Medicine
                Cardiovascular Medicine

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