Treatment with Laevo ( l )-carnitine reverses the mitochondrial function of human embryos
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EMBRYO BIOLOGY
Treatment with Laevo (L)-carnitine reverses the mitochondrial function of human embryos Naoharu Morimoto 1,2,3 & Shu Hashimoto 2 & Masaya Yamanaka 1 & Manabu Satoh 1 & Yoshiharu Nakaoka 1 & Atsushi Fukui 3 & Yoshiharu Morimoto 4 & Hiroaki Shibahara 3 Received: 30 June 2020 / Accepted: 7 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose Laevo (l)-carnitine plays important roles in reducing the cytotoxic effects of free fatty acids by forming acyl-carnitine and promoting beta-oxidation, leading to alleviation of cell damage. Recently, the mitochondrial functions in morula has been shown to decrease with the maternal age. Here, we assessed the effect of l-carnitine on mitochondrial function in human embryos and embryo development. Methods To examine the effect of L-carnitine on mitochondrial function in morulae, 38 vitrified–thawed embryos at the 6–11cell stage on day 3 after ICSI were donated from 19 couples. Each couple donated two embryos. Two siblings from each couple were divided randomly into two groups and were cultured in medium with or without 1 mM L-carnitine. The oxygen consumption rates (OCRs) were measured at morula stage. The development of 1029 zygotes cultured in medium with or without Lcarnitine was prospectively analyzed. Results Addition of L-carnitine to the culture medium significantly increased the OCRs of morulae and improved the morphologically-good blastocyst formation rate per zygote compared with sibling embryos. Twenty healthy babies were born from embryos cultured in L-carnitine-supplemented medium after single embryo transfers. Conclusion(s) L-carnitine is a promising culture medium supplement that might be able to counteract the decreased mitochondrial function in human morula stage embryos. Keywords Mitochondrial function . Laevo (L)-carnitine . Oxygen consumption rate
Introduction The fertility of women decreases with their age [1]. One of the reasons for the poor development of embryos obtained from older women is an increase of chromosomal aberrations [2] caused by premature bivalent separation into univalents during meiosis [3]. In addition, mitochondrial function at morula stage of human embryos has been shown to decrease with the
* Shu Hashimoto [email protected] 1
IVF Namba Clinic, Osaka 550-0015, Japan
2
Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan
3
Department of Obstetrics and Gynecology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan
4
HORAC Grand Front Osaka Clinic, Osaka 530-0011, Japan
maternal age without changing the copy number of mitochondrial DNA (mtDNA) and a decrease of mitochondrial function leads to slow-paced development and lower developmental rate from morulae to blastocysts [4]. In mammalian cells, adenosine triphosphate (ATP) is mainly generated by the mitochondrial electron transport system. It has also been shown that the mitochondrial function of mammalian embryos before implantation increases as their development advances toward the
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