Disparity between Post-thaw Survival and Functional Integrity of Vitrified-thawed Oocytes from Obese Mice

Obesity in women is known to be associated with compromised ovarian function. The oocytes are characterized by elevated cytoplasmic oxidative stress and poor cytoplasmic organization under such conditions, which might affect their tolerance to exogenous stresses such as the freeze-thaw process. This study investigates the cryosusceptibility of oocytes derived from mice with high-fat diet (HFD)-induced obesity.

Three-weeks-old female mice were divided into a control group (fed a normal chow diet) and an obese group (fed with HFD for 12 weeks). Oocytes from both groups were subjected to vitrification and thawing. Post-thaw survival, reactive oxygen species (ROS) levels, mitochondrial and endoplasmic reticulum (ER) distribution, ER stress, and the maturation potential of GV stage oocytes were evaluated.

Despite increased lipid accumulation and higher ROS levels observed in the oocytes of obese mice, the post-thaw survival rate of GV oocytes was comparable between the groups. However, obesity induced alterations in mitochondrial and ER distribution. Additionally, MII oocytes derived from vitrified-thawed germinal vesicle (GV) stage oocytes of obese mice showed a significantly higher percentage of spindle defects. A notable increase in ER stress markers GRP78 and ATF4 was detected in frozen-thawed GV oocytes compared to the control group.

These findings suggest that maternal obesity does not significantly affect the cryosurvival of oocytes, but it does compromise oocyte quality after vitrification, underscoring the need for optimized cryopreservation strategies in obese patients undergoing ART.