Additional Funding Sources
The project described was supported by the Center of Excellence in Biomedical Research through the Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under Grant Nos. P20GM109095 and P20GM103408 and the National Science Foundation S-STEM Gateway Scholarships in Biological Sciences under Grant Award No. DUE-1644233.
Abstract
The epithelial cells of mammalian endometrial tissue have shown to express insulin receptor (INSR) and insulin-like growth factor-1 (IGF1R) which is used in the production of glycogen. Glycogen is needed in the uterus to meet the energy requirements of the blastocyst prior to implantation. Our results show that treating immortalized mink uterine cells (GMMe) with insulin caused an increase in the gene expression of INSR, IGF1R, and glycogenic enzymes. When treated for 48 hours with insulin and S961 or insulin and Picro Podophyllotoxin (PPP), which serves as an INSR blocker or IGF1R blocker respectively, there was decreased expression of the receptors when compared to the control treatment. There was also a decrease in glycogenic enzyme expression levels when compared to the control treatment. Finally, when treated with insulin and both blockers, there was once again a decrease in gene expression when compared to control-treated cells.
In a prior experiment, GMMe cells were treated with insulin at different concentrations, the results showed that gene expression of receptors increased with increasing insulin concentration.
These two experiments have supported that insulin may play a role in the regulation of uterine glycogenic receptors and enzymes.
Blocking Insulin and Insulin-Like Growth Factor Receptors and Its Effect on the Insulin Metabolic Pathway
The epithelial cells of mammalian endometrial tissue have shown to express insulin receptor (INSR) and insulin-like growth factor-1 (IGF1R) which is used in the production of glycogen. Glycogen is needed in the uterus to meet the energy requirements of the blastocyst prior to implantation. Our results show that treating immortalized mink uterine cells (GMMe) with insulin caused an increase in the gene expression of INSR, IGF1R, and glycogenic enzymes. When treated for 48 hours with insulin and S961 or insulin and Picro Podophyllotoxin (PPP), which serves as an INSR blocker or IGF1R blocker respectively, there was decreased expression of the receptors when compared to the control treatment. There was also a decrease in glycogenic enzyme expression levels when compared to the control treatment. Finally, when treated with insulin and both blockers, there was once again a decrease in gene expression when compared to control-treated cells.
In a prior experiment, GMMe cells were treated with insulin at different concentrations, the results showed that gene expression of receptors increased with increasing insulin concentration.
These two experiments have supported that insulin may play a role in the regulation of uterine glycogenic receptors and enzymes.