Gestational diabetes mellitus was related to ambient air pollutant nitric oxide during early gestation

2017 ◽  
Vol 158 ◽  
pp. 318-323 ◽  
Author(s):  
Shih-Chun Pan ◽  
Ching-Chun Huang ◽  
Shio-Jean Lin ◽  
Bing-Yu Chen ◽  
Chang-Chuan Chan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Ambient Air ◽  
Air Pollutant ◽  
Early Gestation

scholarly journals Fetoplacental Vascular Endothelial Dysfunction as an Early Phenomenon in the Programming of Human Adult Diseases in Subjects Born from Gestational Diabetes Mellitus or Obesity in Pregnancy

2011 ◽  
Vol 2011 ◽  
pp. 1-18 ◽  
Author(s):  
Andrea Leiva ◽  
Fabián Pardo ◽  
Marco A. Ramírez ◽  
Marcelo Farías ◽  
Paola Casanello ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Convincing Evidence ◽  
Amino Acid Transporters ◽  
Pathological State ◽  
Metabolic Marker ◽  
Obesity In Pregnancy ◽  
In Pregnancy

Gestational diabetes mellitus (GDM) and obesity in pregnancy (OP) are pathological conditions associated with placenta vascular dysfunction coursing with metabolic changes at the fetoplacental microvascular and macrovascular endothelium. These alterations are seen as abnormal expression and activity of the cationic amino acid transporters and endothelial nitric oxide synthase isoform, that is, the “endothelial L-arginine/nitric oxide signalling pathway.” Several studies suggest that the endogenous nucleoside adenosine along with insulin, and potentially arginases, are factors involved in GDM-, but much less information regards their role in OP-associated placental vascular alterations. There is convincing evidence that GDM and OP prone placental endothelium to an “altered metabolic state” leading to fetal programming evidenced at birth, a phenomenon associated with future development of chronic diseases. In this paper it is suggested that this pathological state could be considered as a metabolic marker that could predict occurrence of diseases in adulthood, such as cardiovascular disease, obesity, diabetes mellitus (including gestational diabetes), and metabolic syndrome.

Gestational diabetes mellitus and exposure to ambient air pollution and road traffic noise: A cohort study

2017 ◽  
Vol 108 ◽  
pp. 253-260 ◽  
Author(s):  
Marie Pedersen ◽  
Sjurdur F. Olsen ◽  
Thorhallur I. Halldorsson ◽  
Cuilin Zhang ◽  
Dorrit Hjortebjerg ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Air Pollution ◽  
Cohort Study ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Road Traffic ◽  
Traffic Noise ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Road Traffic Noise

scholarly journals Outdoor Air Pollution and Gestational Diabetes Mellitus: A Systematic Review and Meta-Analysis

2019 ◽  
Author(s):  
Mohamed H. ELSHAHIDI
Keyword(s):  
Diabetes Mellitus ◽  
Air Pollution ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Meta Analysis ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Cochrane Library ◽  
Ambient Air Pollutants ◽  
Race Ethnicity

Background: During the past 20 years, the prevalence of gestational diabetes mellitus (GDM) has increased by ∼10%-100% in several race/ethnicity groups. There is an association between ambient air pollution (AAP) and GDM. This study aimed to summarize the evidence about the association between AAP and GDM. Methods: PubMed, Embase, Scopus, Web of Science and Cochrane Library were searched from inception till Oct 2017. Studies about the association between ambient air pollutants levels and GDM were included. Pooled effect estimates and their 95% confidence interval (CI) were calculated using R. Results: Eight studies met the inclusion criteria. The odds of developing GDM upon exposure to CO (per 1 ppm), NO (per 1 ppb), NO2 (per 10 µg/m3), NOx (per 1 ppb), O3 (per 10 ppb), SO2 (per 10 ppb), PM10 (per 10 µg/m3) and PM2.5 (per 10 µg/m3) were 1.47 (95% CI 0.88-2.06), 1.04 (95% CI 1.03-1.06), 1 (95% CI 0.93-1.08), 1.02 (95% CI 1-1.04), 1.05 (95% CI 0.94-1.16), 1.39 (95% CI 1.04-1.73), 0.97 (95% CI 0.94-0.99) and 1.12 (95% CI 0.93-1.31), respectively. Conclusion: The current literature showed evidence for an association between AAP and GDM. However, further well-designed studies are needed.

scholarly journals Climate factors and gestational diabetes mellitus risk – a systematic review

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Emma V. Preston ◽  
Claudia Eberle ◽  
Florence M. Brown ◽  
Tamarra James-Todd
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Systematic Review ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Ambient Temperature ◽  
Ambient Air ◽  
Climate Factors ◽  
Glucose Levels ◽  
Glycemic Outcomes

Abstract Background Current and projected increases in global temperatures and extreme climate events have led to heightened interest in the impact of climate factors (i.e. ambient temperature, season/seasonality, and humidity) on human health. There is growing evidence that climate factors may impact metabolic function, including insulin sensitivity. Gestational diabetes mellitus (GDM) is a common pregnancy complication, with an estimated global prevalence of up to 14%. While lifestyle and genetic risk factors for GDM are well established, environmental factors may also contribute to GDM risk. Previous reviews have summarized the growing evidence of environmental risk factors for GDM including endocrine disrupting chemicals and ambient air pollution. However, studies of the effects of climate factors on GDM risk have not been systematically evaluated. Therefore, we conducted a systematic review to summarize and evaluate the current literature on the associations of climate factors with GDM risk. Methods We conducted systematic searches in PubMed and EMBASE databases for original research articles on associations of climate factors (i.e. ambient temperature, season/seasonality, and humidity) with GDM and/or related glycemic outcomes for all publication dates through September 20th, 2020. Results Our search identified 16 articles on the associations of ambient temperature and/or season with GDM and maternal glycemic outcomes during pregnancy, which were included in this review. Despite inconsistencies in exposure and outcome assessment, we found consistent evidence of a seasonal effect on GDM risk, with higher prevalence of GDM and higher pregnancy glucose levels in summer months. We found suggestive evidence of an association between higher ambient temperature and elevated glucose levels from GDM screening tests. Conclusion Climate factors may be associated with GDM risk. However, further research is needed to evaluate these associations and to elucidate the specific mechanisms involved.

Alterations in relaxation to lactate and H2O2in human placental vessels from gestational diabetic pregnancies

2000 ◽  
Vol 278 (3) ◽  
pp. H706-H713 ◽  
Author(s):  
Reinaldo Figueroa ◽  
Edilberto Martinez ◽  
Raisa P. Fayngersh ◽  
Nergesh Tejani ◽  
Kamal M. Mohazzab-H. ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Arachidonic Acid ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Contractile Response ◽  
Full Term ◽  
Nitrite Production ◽  
Prostaglandin F ◽  
Arteries And Veins

We determined whether alterations in the mechanism of relaxation to H2O2potentially contribute to the enhanced prostaglandin-mediated contractile response to H2O2and posthypoxic reoxygenation seen in human placental vessels of pregnancies with gestational diabetes mellitus (GDM). Isolated placental arteries and veins from GDM and uncomplicated full-term pregnancies were precontracted with prostaglandin F2α([Formula: see text] 35–38 Torr) and then exposed to lactate (1–10 mM), arachidonic acid (0.01–10 μM), nitroglycerin (1 nM–1 μM), forskolin (0.01–10 μM), or H2O2(1 μM–1 mM + 10 μM indomethacin). The rates of tissue H2O2metabolism by catalase and nitrite production were measured. The relaxation to lactate was reduced in GDM placental arteries and veins by 54–85 and 66–80%, and the relaxation to H2O2was inhibited by 80–94% in GDM placental veins compared with vessels from uncomplicated full-term pregnancies. H2O2caused only minimal relaxation of placental arteries. Responses to other relaxing agents were not altered in the GDM placental vessels. Diabetic vessels showed rates of nitrite production that were increased by 113–195% and rates of H2O2metabolism by catalase that were decreased by 44–61%. The loss of relaxation to H2O2and lactate (mediated via H2O2), perhaps as a result of the inhibition of catalase by nitric oxide, may explain the previously reported enhancement of prostaglandin-mediated contractile responses to H2O2and posthypoxic reoxygenation seen in GDM placental vessels.

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