A breakthrough study has revealed that a common compound found in most living cells, spermidine, can reverse declining fertility in older mice and even increase the number of offspring they produce. These findings, published in Nature Aging, hold promising implications for the development of treatments for human fertility issues.
As individuals age, the chances of natural conception or assisted reproduction, such as in vitro fertilization (IVF), diminish. This is largely due to the deterioration and decreasing number of reproductive cells in the ovaries, called oocytes.
Spermidine, initially isolated from sperm but known to have functions in various cell types, has previously demonstrated the ability to extend lifespan in yeast, flies, worms, and human immune cells. Increased dietary intake of spermidine has also been linked to a reduction in age-related issues in laboratory animals, such as cardiovascular disease in mice and cognitive decline in fruit flies. However, its impact on aging oocytes had not been thoroughly explored.
The study, led by Bo Xiong, a reproductive biologist at Nanjing Agricultural University in China, compared ovarian tissue samples from young and middle-aged mice. They discovered that older mice had significantly less spermidine in their ovaries, along with lower-quality oocytes and more degenerated follicles, structures responsible for holding and releasing oocytes during ovulation.
To investigate the potential link between spermidine and these observations, the researchers administered spermidine to older mice and observed remarkable results. The oocytes in spermidine-treated mice developed more rapidly, had fewer defects, and showed signs of delayed aging compared to untreated aging mice. Additionally, the supplement increased the number of follicles, a measure often used to estimate the quality and quantity of oocytes in humans.
The research also indicated that spermidine enhanced the success rate of blastocyst formation, the early stage of embryo development. Aging mice who received spermidine and conceived naturally produced roughly twice as many offspring per litter compared to control aging mice.
To understand the mechanism behind spermidine’s effects, the researchers examined the cellular processes. They found that oocytes from untreated mice were less efficient in clearing damaged mitochondria (cellular energy producers) compared to younger oocytes. Spermidine seemed to rejuvenate the oocytes by enhancing their ability to remove damaged components and improving the function of healthy mitochondria. These findings suggest that spermidine’s mechanism of action may be consistent across species.
While spermidine holds promise as a fertility enhancer, researchers emphasize the importance of conducting further studies to ensure its safety, potential side effects, and its impact on various bodily processes. Clinical trials will be essential to determine the precise dosage and its effects on fertility in humans. Researchers also noted that excessive amounts of spermidine can lead to poorer quality oocytes in mice, emphasizing the need for precise clinical trials before applying spermidine to boost fertility in humans.
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Reference: https://www.nature.com/articles/d41586-023-03244-7
