Citation
Adipokine Regulation of Human Placental GLUT-1 Transporter

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Title:
Adipokine Regulation of Human Placental GLUT-1 Transporter
Creator:
Orlando Jr, Michael James
Publication Date:
Language:
English

Notes

Abstract:
In the United States, 48% of women start their pregnancies being overweight or obese. There is a well-known association between maternal obesity and adverse pregnancy outcomes. Fetal macrosomia occurs 2 to 3 times more frequently in infants of obese women than in those from healthy-weight women, and the risk of fetal macrosomia increases with increasing maternal BMI and maternal blood glucose concentration. Adipose tissue is responsible for the production of adipokines. TNF-alpha and leptin are two adipokines that have been implicated in the pathogenesis of maternal diabetes and obesity and fetal growth abnormalities and metabolic dysfunction. Maternofetal glucose transport is primarily mediated by the GLUT proteins family, in particular GLUT-1. Despite our current understanding of human placental GLUT-1, little is known about its regulation. In this experiment, we hypothesize that the adipokines leptin and TNF-alpha increase human placental GLUT-1 protein expression. BeWo human choriocarcinoma cells were treated with leptin (10, 50, and 100 ng/mL) and TNF-alpha (0.1, 10, 50 ng/mL) for 24 hours, and cell protein was extracted in RIPA buffer. Total protein concentration was measured using BCA assay, and the total cell membrane GLUT-1 protein was quantified. There appears to be a positive dose-dependent relationship between the concentration of leptin and GLUT-1 expression and the concentration of TNF-alpha and GLUT-1 expression. The in vitro expression of GLUT-1 protein is upregulated by adipokines leptin and TNF-alpha. ( en )
General Note:
Awarded Bachelor of Science in Chemical Engineering, summa cum laude, on May 8, 2018. Major: Chemical Engineering
General Note:
College or School: College of Engineering
General Note:
Advisor: Kathryn Patrick MD. Advisor Department or School: Department of Obstetrics and Gynecology

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Source Institution:
University of Florida
Holding Location:
University of Florida
Rights Management:
Copyright Michael James Orlando Jr. Permission granted to the University of Florida to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.

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In the United States, 48% of women start their pregnancies being overweight or obese. There is a well known association between maternal obesity and adverse pregnancy outcomes Fetal macrosomia occurs 2 to 3 times m ore frequently in infants of obese women than in those from healthy weight women, and the risk of fetal macrosomia increases with increasing maternal BMI and maternal blood glucose concentration Adipose tissue is responsible for the production of adipokin es TNF alpha and leptin are two adipokines that have been implicated in the pathogenesis of maternal diabetes and obesity and fetal growth abnormalities and metabolic dysfunction Maternofetal glucose transport is primarily mediated by the GLUT proteins f amily, in particular GLUT 1 Despite our current understanding of human placental GLUT 1, little is known about its regulation. In this experiment, we hypothesize that the adipokines leptin and TNF alpha increase human placental GLUT 1 protein expression. BeWo human choriocarcinoma cells were treated with leptin (10, 50, and 100 ng/mL) and TNF alpha (0.1, 10, 50 ng/mL) for 24 hours, and cell protein was extracted in RIPA buffer. Total protein concentration was measured using BCA assay, and the total cell me mbrane GLUT 1 protein was quantified. There appears to be a positive dose dependent relationship between the concentration of leptin and GLUT 1 expression and the concentration of TNF alpha and GLUT 1 expression. The in vitro expression of GLUT 1 protein i s upregulated by adipokines leptin and TNF alpha.