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연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제60권 제7호
발행연도
2019.1
수록면
667 - 678 (12page)

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Purpose: The aim of this study was to investigate how type I diabetes mellitus (T1D) affects the folliculogenesis and oocyte development,fertilization, and embryo development. Materials and Methods: A comparative animal study was conducted using two different mouse models of T1D, a genetic AKITAmodel and a streptozotocin-induced diabetes model. Ovarian function was assessed by gross observation, immunoblot, immunohistochemistry,oocyte counting, and ELISA for serum hormones (insulin, anti-Mullerian hormone, estradiol, testosterone,and progesterone). Maturation and developmental competence of metaphase II oocytes from control and T1D animals was evaluatedby immunofluorescent and immunohistochemical detection of biomarkers and in vitro fertilization. Results: Animals from both T1D models showed increased blood glucose levels, while only streptozotocin (STZ)-injected miceshowed reduced body weight. Folliculogenesis, oogenesis, and preimplantation embryogenesis were impaired in both T1D mousemodels. Interestingly, exogenous streptozotocin injection to induce T1D led to marked decreases in ovary size, expression of luteinizinghormone/chorionic gonadotropin receptor in the ovaries, the number of corpora lutea per ovary, oocyte maturation, andserum progesterone levels. Both T1D models exhibited significantly reduced pre-implantation embryo quality compared withcontrols. There was no significant difference in embryo quality between STZ-injected and AKITA diabetic mice. Conclusion: These results suggest that T1D affects folliculogenesis, oogenesis, and embryo development in mice. However, thephysiological mechanisms underlying the observed reproductive effects of diabetes need to be further investigated.

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