Advances in the Study of Endometrial Receptivity and Glucose Metabolism Mechanisms in Insulin Resistance.

INTRODUCTION

Insulin resistance (IR) is one of the important pathologic bases of polycystic ovary syndrome (PCOS) and an important factor contributing to infertility. In patients with PCOS, IR acts not only on insulin-sensitive tissues, such as skeletal muscle, adipose tissue, and liver, but also on the ovaries and endometrium. Localised endometrial IR is closely associated with impaired endometrial receptivity, and proper glucose metabolism is a key factor for embryo implantation.

METHODS

This paper describes the signalling pathways of endometrial glucose metabolism and the transcription factors regulated by endometrial glucose metabolism signalling pathways.

RESULTS

The purpose of this paper is to explore the mechanism of endometrial glucose uptake in local IR and find key intersections in this mechanism. For example, Foxo1, as the intersection of the Insulin Receptor Substrate-Phosphatidylinositol3-kinase-Protein Kinase B-Glucose Transporters (IRS-PI3K-Akt-GLUTs) pathway and the Cyclic Adenosine Monophosphate- Protein Kinase A- Calcium ion (cAMP-PKA-Ca2+) pathway, and as an important biomarker for evaluating endometrial receptivity. It is of great significance for studying the improvement of endometrial receptivity.

CONCLUSIONS

This article summarises the therapeutic approaches targeting insulin resistance and the enhancement of endometrial receptivity based on the above pathways, so as to provide references and suggestions for future therapeutic strategies.