Abstract
Obesity was shown to cause reproductive dysfunctions such as reduced conception, infertility and early pregnancy loss. However, the possible effects of obesity on oocyte quality are still not fully understood. In this study we investigated the effects of both diet and gene mutation induced obesity on impairments in mouse oocyte polarization, oxidative stress, and epigenetic modifications. Our results showed that high-fat diet induced obesity (HFD) and gene mutation induced obesity (ob/ob) could both impair oocyte meiotic maturation, disrupt spindle morphology, and reduce oocyte polarity. Oocytes from obese mice underwent oxidative stress, as shown by high DHE and ROS levels. Abnormal mitochondrial distributions and structures were observed in oocytes from obese groups of mice and early apoptosis signals were detected, which suggesting that oxidative stress had impaired mitochondrial function and resulted in oocyte apoptosis. Our results also showed that 5 mC levels and H3K9 and H3K27 methylation levels were altered in oocytes from obese mice, which indicated that DNA methylation and histone methylation had been affected. Our results showed that both HFD and ob/ob induced obesity affected oocyte maturation and that oxidative stress-induced early apoptosis and altered epigenetic modifications may be the reasons for reduced oocyte quality in obese mice.
Highlights
Obesity was shown to cause reproductive dysfunctions such as reduced conception, infertility and early pregnancy loss
Our results showed that the germinal vesicle (GV) oocyte number we collected from the ovaries of high-fat diet induced obesity (HFD) mice (12.00 ± 1.00, n = 12) and from ob/ob mice (9.67 ± 2.33, n = 12) were significantly reduced as compared to those from the ovaries of control mice (25.5 ± 1.57, n = 12) (Fig. 1C,D)
We found that oocytes from HFD and ob/ob mice with obesity were suffering from oxidative stress, had alterations in mitochondria distributions, and experienced early apoptosis
Summary
Obesity was shown to cause reproductive dysfunctions such as reduced conception, infertility and early pregnancy loss. In this study we investigated the effects of both diet and gene mutation induced obesity on impairments in mouse oocyte polarization, oxidative stress, and epigenetic modifications. Our results showed that high-fat diet induced obesity (HFD) and gene mutation induced obesity (ob/ ob) could both impair oocyte meiotic maturation, disrupt spindle morphology, and reduce oocyte polarity. Our results showed that both HFD and ob/ ob induced obesity affected oocyte maturation and that oxidative stress-induced early apoptosis and altered epigenetic modifications may be the reasons for reduced oocyte quality in obese mice. Gene mutation obesity (ob/ob) and high-fat diet induced obesity (HFD) have been shown to be associated with reproductive problems, such as infertility, embryo implantation failure, abortion, fetal congenital abnormalities, adult offspring adiposity, and metabolic dysfunction[1,2,3,4]. It was shown that cells that were suffering from oxidative stress resulted in their apoptosis, which may have resulted from impaired mitochondrial function and the activation of apoptotic factors in mouse kidneys[19]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 call
