Metformin Differentially Regulates Insulin Signaling and Glucose Metabolism in GMMe Mink Uterine Epithelial Cells
Faculty Mentor Information
Dr. Ayokunle Hodonu, Northwest Nazarene University
Presentation Date
7-16-2026
Abstract
Metformin is widely prescribed for the treatment of type 2 diabetes because it improves insulin sensitivity and glucose metabolism. It is also commonly used to manage reproductive disorders such as polycystic ovary syndrome (PCOS), suggesting that it may influence uterine function. Our study investigated how metformin regulates glucose metabolism in insulin-treated mink uterine epithelial cells (GMMe). We designed gene-specific primers using NCBI to support conventional PCR (cPCR) and quantitative PCR (qPCR) analyses of genes involved in insulin signaling and glucose metabolism. GMMe cells were treated with insulin alone or insulin + metformin (5, 10, or 50 mM). Preliminary qPCR results showed a significant increase in insulin receptor (INSR) mRNA expression following metformin treatment, with the greatest response observed at 10 mM, while IGF1R expression was not significantly altered. Additional analyses of glucose transporters, glycolytic enzymes, and glycogen metabolism are ongoing. These findings suggest that metformin differentially regulates various aspects of insulin signaling and may enhance uterine glucose metabolism through increased insulin receptor expression, AKt regulation, glucose transport expression and increase in glycogen pathway enzymes. This work contributes to our understanding of uterine energy metabolism and the potential role of metformin in implantation and early pregnancy.
Metformin Differentially Regulates Insulin Signaling and Glucose Metabolism in GMMe Mink Uterine Epithelial Cells
Metformin is widely prescribed for the treatment of type 2 diabetes because it improves insulin sensitivity and glucose metabolism. It is also commonly used to manage reproductive disorders such as polycystic ovary syndrome (PCOS), suggesting that it may influence uterine function. Our study investigated how metformin regulates glucose metabolism in insulin-treated mink uterine epithelial cells (GMMe). We designed gene-specific primers using NCBI to support conventional PCR (cPCR) and quantitative PCR (qPCR) analyses of genes involved in insulin signaling and glucose metabolism. GMMe cells were treated with insulin alone or insulin + metformin (5, 10, or 50 mM). Preliminary qPCR results showed a significant increase in insulin receptor (INSR) mRNA expression following metformin treatment, with the greatest response observed at 10 mM, while IGF1R expression was not significantly altered. Additional analyses of glucose transporters, glycolytic enzymes, and glycogen metabolism are ongoing. These findings suggest that metformin differentially regulates various aspects of insulin signaling and may enhance uterine glucose metabolism through increased insulin receptor expression, AKt regulation, glucose transport expression and increase in glycogen pathway enzymes. This work contributes to our understanding of uterine energy metabolism and the potential role of metformin in implantation and early pregnancy.