Abstract
Reproductive dysfunction associated with obesity is increasing among women of childbearing age. Emerging evidence indicates that maternal obesity impairs embryo development and offspring health, and these defects are linked to oxidative stress in the ovary and in oocytes. Phycocyanin (PC) is a biliprotein from Spirulina platensis that possesses antioxidant, anti-inflammatory, and radical-scavenging properties. Our previous studies have shown that PC can reduce reactive oxygen species (ROS) accumulation in oocytes in D-gal-induced aging mice. Here, at the Institute of Cancer Research (ICR) mice fed a high-fat diet (HFD) to model obesity were used to test the effect of PC on reversing the fertility decline caused by obesity. We observed a significant increase in litter size and offspring survival rates after PC administration to obese mice. Further, we found that PC not only ameliorated the level of ovarian antioxidant enzymes, but also reduced the occurrence of follicular atresia in obese female mice. In addition, the abnormal morphology of the spindle-chromosome complex (SCC), and the abnormal mitochondrial distribution pattern in oocytes both recovered. The obesity-related accumulation of ROS, increased number of early apoptotic cells, and the abnormal expression of H3K9me3 in oocytes were all partially reversed after PC administration. In summary, this is the first demonstration that PC can improve fertility by partially increasing ovarian and oocyte quality in obese female mice and provides a new strategy for clinically treating obesity-related infertility in females.
Highlights
The proportion of obese people has increased significantly as the general quality of life has improved (Darbre, 2017), and maternal obesity has been reported to cause a variety of diseases (Rogero and Calder, 2018)
We used mice that had been fed a high-fat diet as a model system for obesity, and observed that obesity-induced adverse effects on ovary antioxidant enzymes, follicular development, oocyte maturation, and meiotic spindle morphology were responsible for the reduced litter sizes and decreased survival rates
These results showed that intragastric administration of PC reduced ovarian antioxidant enzymes, the number of atretic follicles, oocyte meiotic errors, reactive oxygen species (ROS) levels, and early apoptosis in obese mice
Summary
The proportion of obese people has increased significantly as the general quality of life has improved (Darbre, 2017), and maternal obesity has been reported to cause a variety of diseases (Rogero and Calder, 2018). Obesity can reduce ovarian and oocyte quality, increase the level of oxidative stress in them (Igosheva et al, 2010; Luzzo et al, 2012; Grindler and Moley, 2013), and damage female fertility (Jungheim and Moley, 2010; Silvestris et al, 2018). Maternal obesity has been associated with spindle defects and chromosome misalignment during meiotic oocyte maturation (Jungheim et al, 2010; Luzzo et al, 2012), and Phycocyanin Improve Obese Mice Fertility obesity-related maternal metabolic syndrome induced structural, spatial, and metabolic alterations in oocyte mitochondria (Reynolds et al, 2015; Saben et al, 2016). Reactive oxygen species, (ROS), a by-product of oxidative phosphorylation, are simultaneously produced in mitochondria (Balaban et al, 2005), and their levels were dramatically elevated in obese female oocytes (Zhang et al, 2015). Obesity is harmful to female reproductive capability (Catalano and Ehrenberg, 2006)
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