Determination of Glucose Uptake and Glycolysis via IGF1R and Insulin Receptor Pathways in Mink Uterine Epithelial Cells

Additional Funding Sources

The project described was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under Grant No. P20GM103408.

Presentation Date

7-2020

Abstract

Glycogen metabolism is a crucial factor in implantation success, and many reproductive hormones are known to play a role in carbohydrate metabolism in the uterus, but the pathways they take are unknown. In our research, GMMe cells were treated with Insulin (15 µg/ml), Prolactin (100 µg/ml), and Insulin + Prolactin for 24 hours. PCR and qPCR were performed after the DNA was isolated from the cells using the Thermofisher Fast SYBR protocol to test the activation or inhibition of INSR. We show for the first time that prolactin may inhibit the expression of INSR in GMMe cells. In future research, we hope to determine the effects of prolactin, estrogen, and progesterone on the expression of INSR, IGF1R, IRA, and IRB. We hypothesize that prolactin directly inhibits the expression of INSR.

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Determination of Glucose Uptake and Glycolysis via IGF1R and Insulin Receptor Pathways in Mink Uterine Epithelial Cells

Glycogen metabolism is a crucial factor in implantation success, and many reproductive hormones are known to play a role in carbohydrate metabolism in the uterus, but the pathways they take are unknown. In our research, GMMe cells were treated with Insulin (15 µg/ml), Prolactin (100 µg/ml), and Insulin + Prolactin for 24 hours. PCR and qPCR were performed after the DNA was isolated from the cells using the Thermofisher Fast SYBR protocol to test the activation or inhibition of INSR. We show for the first time that prolactin may inhibit the expression of INSR in GMMe cells. In future research, we hope to determine the effects of prolactin, estrogen, and progesterone on the expression of INSR, IGF1R, IRA, and IRB. We hypothesize that prolactin directly inhibits the expression of INSR.