Altered Umbilical Cord Blood Nutrient Levels, Placental Cell Turnover and Transporter Expression in Human Term Pregnancies Conceived by Intracytoplasmic Sperm Injection (ICSI)

Bloise, Enrrico; Braga, Jair R S; Andrade, Cherley Borba Vieira de; Império, Güínever E.; Martinelli, Lilian M.; Antunes, Roberto de Azevedo; Silva, Karina R.; Nunes, Cristiana Buzelin; Cobellis, Luigi; Bloise, Flávia Fonseca; Matthews, Stephen G.; Connor, Kristin L.; Ortiga-Carvalho, Tânia M.

doi:10.3390/nu13082587

Cited by 9 publications

(10 citation statements)

References 61 publications

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“…Nonetheless, there were no differences in placental and fetal birth weight in their study cohort, composed of ART and normal pregnancies [ 138 ]. In contrast, Bloise et al found no between-group differences in the GLUT1 expression in pregnancies conceived by intracytoplasmic sperm injection and normal control pregnancies [ 139 ]. The expression of GLUTs can also be affected by the various preparation and embryo transfer techniques applied in ART procedures (summarized in Table 3 ) [ 140 ].…”

Section: Correlation With Fetal Growth and Other Gestational Outcomesmentioning

confidence: 99%

Fetomaternal Expression of Glucose Transporters (GLUTs)—Biochemical, Cellular and Clinical Aspects

et al. 2022

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Several types of specialized glucose transporters (GLUTs) provide constant glucose transport from the maternal circulation to the developing fetus through the placental barrier from the early stages of pregnancy. GLUT1 is a prominent protein isoform that regulates placental glucose transfer via glucose-facilitated diffusion. The GLUT1 membrane protein density and permeability of the syncytial basal membrane (BM) are the main factors limiting the rate of glucose diffusion in the fetomaternal compartment in physiological conditions. Besides GLUT1, the GLUT3 and GLUT4 isoforms are widely expressed across the human placenta. Numerous medical conditions and molecules, such as hormones, adipokines, and xenobiotics, alter the GLUT’s mRNA and protein expression. Diabetes upregulates the BM GLUT’s density and promotes fetomaternal glucose transport, leading to excessive fetal growth. However, most studies have found no between-group differences in GLUTs’ placental expression in macrosomic and normal control pregnancies. The fetomaternal GLUTs expression may also be influenced by several other conditions, such as chronic hypoxia, preeclampsia, and intrahepatic cholestasis of pregnancy.

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Section: Correlation With Fetal Growth and Other Gestational Outcomesmentioning

confidence: 99%

Fetomaternal Expression of Glucose Transporters (GLUTs)—Biochemical, Cellular and Clinical Aspects

et al. 2022

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“…Placental morphometry analysis was undertaken using methodology previously described in the literature with specific adaptations, outlined below [23]. Image acquisition and analysis were performed on H&Estained sections using an Aperio AT2 microscope (Leica Biosystems, IL, EUA), coupled with a computer using the software ImageScope x64.…”

Section: Placental Morphometrymentioning

confidence: 99%

“…Relative volume estimates of placental histological components (syncytiotrophoblast, syncytial knots, cytotrophoblasts, connective tissue, and fetal vascular endothelium) were quantified by superimposing placental histological photomicrographs with a grid of equidistant points (measuring 25 μm distance between two points). Previous studies using morphometric analysis in human placentae recorded 190-1000 points (grid intercepts) to evaluate the volumetric proportion of each placental histological component [23][24][25]. In this study, we first assessed placentae by recording 1500 points overlapping with each of the histological components for the first 39 placentae.…”

Section: Placental Morphometrymentioning

confidence: 99%

“…The total average area of evaluated histological sections per placenta was 393,173.22 μm 2 , and there were no differences in median area (μm ). The volumetric proportion (VP) of each histological component was calculated as VP = NP ×100/600 for placentae for which 600 points were recorded, and as VP = NP ×100/1500 for placentae for which 1500 points were recorded, where NP = number of equivalent points on each histological component [23,26,27].…”

Section: Placental Morphometrymentioning

confidence: 99%

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Gestational age and infection are greater predictors of placental histopathology than maternal prepregnancy BMI

Duffley¹,

Grynspan

Scott³

et al. 2021

Preprint

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The placenta undergoes morphological and functional adaptions to adverse exposures during pregnancy. The effects of suboptimal maternal body mass index (BMI), preterm birth, and infection on placental histopathological phenotypes remain unclear, despite the association between these conditions and poor offspring outcomes. We hypothesized that suboptimal maternal prepregnancy BMI and preterm birth (with and without infection) would associate with altered placental maturity and morphometry, and that altered placental maturity would associate with poor birth outcomes. Clinical data and human placentae were collected from 96 pregnancies where mothers were underweight, normal weight, overweight, or obese, without other major complications. Placental histopathological characteristics were scored with an anatomical pathologist. Associations between maternal BMI, placental pathology (immaturity and hypermaturity), placental morphometry, and infant outcomes were investigated at term and preterm, with and without infection. Fetal vascular endothelium volumetric proportion was decreased, whereas syncytial knot volumetric proportion was increased, in placentae from preterm pregnancies with chorioamnionitis compared to term placentae. At term and preterm, pregnancies with overweight and obesity had a high percentage increase in proportion of immature placentae compared to normal weight. Placental maturity did not associate with infant birth outcomes. We observed placental hypermaturity and altered placental morphometry among preterm pregnancies with chorioamnionitis, suggestive of altered placental development, which may inform about pregnancies susceptible to preterm birth and infection. Our data increase our understanding of how common metabolic exposures and preterm birth, in the absence of other comorbidities or perinatal events, potentially contribute to poor pregnancy outcomes and the programming of offspring development.

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“…Following this, an article is included that reports on the possible mechanism that may increase the risk for abnormal placental development in assisted reproductive technologies, studied through tissual evaluation of human placenta and fasting blood nutrient levels from term pregnancy conceived naturally or by intracytoplasmic sperm injection. Hence, in term pregnancy, intracytoplasmic sperm injection impairs placental amino acids transporter expression, cell turnover, and altern umbilical vein levels of specific nutrients [ 3 ].…”

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confidence: 99%

Nutrition in Gynecologic Disease

Ciarmela

2022

Nutrients

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Altered Umbilical Cord Blood Nutrient Levels, Placental Cell Turnover and Transporter Expression in Human Term Pregnancies Conceived by Intracytoplasmic Sperm Injection (ICSI)

Cited by 9 publications

References 61 publications

Fetomaternal Expression of Glucose Transporters (GLUTs)—Biochemical, Cellular and Clinical Aspects

Fetomaternal Expression of Glucose Transporters (GLUTs)—Biochemical, Cellular and Clinical Aspects

Gestational age and infection are greater predictors of placental histopathology than maternal prepregnancy BMI

Nutrition in Gynecologic Disease

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