scholarly journals Experimental Gestational Diabetes Mellitus Induces Blunted Vasoconstriction and Functional Changes in the Rat Aorta

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Cecilia Tufiño ◽  
Cleva Villanueva-López ◽  
Maximiliano Ibarra-Barajas ◽  
Ismael Bracho-Valdés ◽  
Rosa Amalia Bobadilla-Lugo

Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT1R, AT2R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response(P<0.05versus SD) in intact (e+) but not in endothelium-free (e−) vessels. Losartan reduced GDM but not SD e− vasoconstriction(P<0.01versus SD). AT1R, AT2R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels(P<0.05versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT2vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations.

2018 ◽  
Vol 26 (10) ◽  
pp. 1382-1388 ◽  
Author(s):  
Chao Li ◽  
Yubin Zhou ◽  
Binglong Qiao ◽  
Lin Xu ◽  
Yan Li ◽  
...  

Aims: This study was conducted to investigate the relationship between a genetic polymorphism and the expression of melatonin receptor 1B (MTNR1B) in the placenta of Han Chinese women with gestational diabetes mellitus (GDM). Methods: In this study, 215 patients with GDM and 243 healthy controls were genotyped using direct sequencing for the MTNR1B single-nucleotide polymorphism rs10830963. The expression of MTNR1B in placenta was detected by immunohistochemistry and Western blotting. The association of rs10830963 with the expression of MTNR1B, plasma glucose, and insulin levels as well as blood lipid levels was investigated. Results: The genotype and allele frequencies of rs10830963 were significantly different between women with GDM and controls ( P < .05). Fasting blood glucose, fasting insulin, and homeostasis model assessment for insulin resistance in women with GDM with the GG and GC genotypes were significantly higher than those with the CC genotype ( P < .05). The expression level of MTNR1B in placenta was significantly higher in the GDM group than in the control group ( P < .05). The expression of MTNR1B was significantly higher in all participants with the GG and GC genotypes (1.31 [0.74]) than in pregnant women with the CC genotype (0.92 [0.52], P < .05). Conclusions: The genetic polymorphism rs10830963 in MTNR1B and its protein expression levels in placenta are associated with an increased risk of developing GDM. Furthermore, rs10830963 may tag a molecular mechanism leading to insulin resistance in Han Chinese women with GDM.


Neonatology ◽  
2021 ◽  
Vol 118 (1) ◽  
pp. 64-72
Author(s):  
Aisling Smith ◽  
Orla Franklin ◽  
Naomi McCallion ◽  
Fionnouala Breatnach ◽  
Afif EL-Khuffash

Background and Aims: Infants born to mothers with gestational diabetes mellitus (GDM) have impaired myocardial performance and are at risk of pulmonary hypertension. We aimed to assess myocardial deformation and left ventricular (LV) rotational mechanics in this population. Methods: We studied 40 infants of mothers with GDM and 40 control infants. Three echocardiograms were carried out over the first 3 days after birth. Results: GDM infants had a lower gestation at birth and a thicker septal wall, a higher LV eccentricity index (indicating septal bowing), and a lower PAATi (indicating higher pulmonary vascular resistance) (all p < 0.05). GDM infants had lower LV strain, systolic and early diastolic strain rates, lower right ventricular (RV) strain, and early diastolic strain rates over the study period (all p < 0.05). By day 3, GDM infants had higher twist, torsion, and higher LV twist and untwist rates (all p < 0.05). GDM status was an independent predictor of LV and RV function and pulmonary vascular resistance (p < 0.01). Conclusion: Infants of mothers with GDM demonstrate important changes in myocardial function in addition to pulmonary vascular resistance that do not resolve by hospital discharge. The observed LV twist increase in GDM infants may be a compensatory mechanism for the lower longitudinal function in this cohort.


1970 ◽  
Vol 8 (1) ◽  
pp. 34-38 ◽  
Author(s):  
Fahima Akhter ◽  
Mst Laila Anjuman Banu ◽  
Roxana Ferdausi

Context: Preterm birth is the major cause of perinatal mortality and morbidity. For the last few decades, it has become an important issue in public health policies of developing countries. Gestational diabetes mellitus (GDM) is one of the high-risk factors for the preterm birth and altered fetal development. This pregnancy induced disorder leads to an increased level of all metabolic substances to the fetal circulation due to development of maternal insulin resistance. It imposes a heavy burden on the mother who is pregnant and these patients have a tendency toward metabolic instability. As there is an intimate relationship between the fetus and placenta, the present study aimed to observe the effect of this pregnancy induced disorder to the preterm placenta. Study design: The study was observational, analytical and cross sectional. Place and period of study: The study was carried out in the Department of Anatomy, BSMMU, Dhaka during the study period of January 2005 to December 2005. Materials and Methods: A total of forty-four samples were collected from women during 28 weeks to 36 completed weeks of gestation. Among them, twenty-two samples belonged to mothers having GDM and twenty-two belonged to normal pregnancy (control group). The placentas were examined to measure their diameter, thickness, cotyledons number, weight, and volume. Result: In this study, the GDM group showed significantly higher values for the variables of diameter, weight and volume. On the other hand, the thickness of the placenta showed lower values and cotyledons number showed higher values in GDM group but the result did not reach a significant level. Conclusion: The findings in this study supported that the gross morphological structure of the placentas in GDM mother did not present any specific, constant or uniform pattern of abnormality. Therefore, it is difficult to establish a clear cut correlation between the placental changes and diabetic state in the mother during pregnancy. However, increased placental weight, volume and diameter found in gestational diabetic mother have supported that these changes may be a long term compensatory mechanism, aiming to secure a sufficient nutrient supply to support the growth of large-for-gestational age (LGA) fetus. But the hormonal and metabolic abnormalities present in the diabetic mother and the fetus are important variables to be considered when studying the placenta. Key words: Preterm Placenta; GDM; Gross morphology. DOI: 10.3329/bja.v8i1.6107 Bangladesh Journal of Anatomy January 2010, Vol. 8 No. 1 pp. 34-38


2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Ya Xiao ◽  
Weihao Chen ◽  
Ruixue Chen ◽  
Anling Luo ◽  
Dayi Chen ◽  
...  

Objective. Gestational diabetes mellitus (GDM) is a pathological condition, affecting an increasing number of pregnant women worldwide. Safe and effective treatment for GDM is very important for the public health. In this study, we utilized a high-fat diet-induced GDM model to evaluate the effects of LBP on GDM and examined the changes of exosomal microRNA expression profiling to decipher the potential underlying mechanism of LBP. Methods. Female C57BL/6J mice were fed a control diet, HFD, or 150 mg/kg LBP-supplemented HFD for 6 weeks before conception and throughout gestation. Oral glucose tolerance test and plasma lipid levels were determined, and liver histopathology was assessed. Sequencing was used to define the microRNA expression profiling of plasma exosomes in the three groups of mice, and protein expression levels of the candidate target genes were analyzed. Results. LBP significantly relieved glucose intolerance, abnormal plasma lipid levels, and pathomorphological changes of liver histopathology in HFD-induced GDM mice. Moreover, we found that this effect of LBP was mediated by downregulation of the increase of 6 miRNAs (miR-93-3p, miR-188-5p, miR-466k, miR-1188-5p, miR-7001-3p, and miR-7115-5p) and reversing the increase of the protein expression of CPT1A, which is the target gene of miR-188-5p. Conclusions. Our findings provide novel insights into the biological activities of LBP in the treatment of GDM.


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