Abstract
In mouse ovarian follicles, granulosa cells but not oocytes take up glucose to provide the oocyte with nourishments for energy metabolism. Diabetes-induced hyperglycemia or glucose absorption inefficiency consistently causes granulosa cell apoptosis and further exerts a series of negative impacts on oocytes including reduced meiosis resumption rate, low oocyte quality and preimplantation embryo degeneration. Here we compared the transcriptome of mouse oocytes from genetically derived NOD diabetic mice or chemically induced STZ diabetic mice with that of corresponding normal mice. Differentially expressed genes were extracted from the two diabetic models. Gene set enrichment analysis showed that genes associated with metabolic and developmental processes were differentially expressed in oocytes from both models of diabetes. In addition, NOD diabetes also affected the expression of genes associated with ovulation, cell cycle progression, and preimplantation embryo development. Notably, Dnmt1 expression was significantly down-regulated, but Mbd3 expression was up-regulated in diabetic mouse oocytes. Our data not only revealed the mechanisms by which diabetes affects oocyte quality and preimplantation embryo development, but also linked epigenetic hereditary factors with metabolic disorders in germ cells.
Highlights
It has been estimated that diabetes affects 6.4% of adults (285 million) worldwide by 2010, and this number is expected to increase to 7.7% by 2030 [1]
By the selection standards described in the methods, we found that the mRNA levels of 1199 genes were up-regulated and 658 genes were down-regulated in NOD diabetic oocytes, whereas mRNA levels of 1016 genes were up-regulated and 325 genes were down-regulated in STZ diabetic oocytes
Diabetes Affects Oocyte Maturation and Oocyte Quality Communication between oocytes and cumulus cells is critical for oocyte meiosis resumption and ovulation [23,24,25,26]
Summary
It has been estimated that diabetes affects 6.4% of adults (285 million) worldwide by 2010, and this number is expected to increase to 7.7% by 2030 [1]. Diabetes of STZ mice is the result of damage of pancreatic betacells induced by streptozotocin administration [4], while diabetes of NOD mice is the result of attacks on the islets by cells of the immune system [5,6]. Both STZ and NOD diabetic mice are insulin-dependent diabetes mellitus, known as type 1 diabetes, which induces mouse hyperglycemia and causes a series of metabolism-related disorders [2]. Diabetes induced oocyte mitochondrial dysfunction, which impairs the oocyte’s energy metabolism and activates the apoptosis pathway [3,12]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
