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When idiopathic male infertility is rooted in maternal malnutrition during the perinatal period in mice
Author(s) -
Yuki Muranishi,
Laurent Parry,
Mélanie Vachette-dit-Martin,
Fabrice Saez,
Cécile CoudyGandilhon,
Pierre Sauvanet,
David H. Volle,
Jérémy Tournayre,
Serge P. Bottari,
Francesca Carpentiero,
Guillaume Martinez,
Jana Muroňová,
Jessica Escoffier,
Alain Bruhat,
AnneCatherine Maurin,
Julien Avérous,
Christophe Arnoult,
Pierre Fafournoux,
Céline Jousse
Publication year - 2021
Publication title -
biology of reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.366
H-Index - 180
eISSN - 1529-7268
pISSN - 0006-3363
DOI - 10.1093/biolre/ioab222
Subject(s) - biology , offspring , sperm , fertility , capacitation , infertility , spermatogenesis , andrology , physiology , human fertilization , male infertility , ovulation , estrous cycle , sperm motility , lactation , pregnancy , endocrinology , population , demography , genetics , medicine , sociology
Infertility represents a growing burden worldwide, with one in seven couples presenting difficulties conceiving. Among these, 10-15% of the men have idiopathic infertility that does not correlate with any defect in the classical sperm parameters measured. In the present study, we used a mouse model to investigate the effects of maternal undernutrition on fertility in male progeny. Our results indicate that mothers fed on a low-protein diet during gestation and lactation produce male offspring with normal sperm morphology, concentration, and motility but exhibiting an overall decrease of fertility when they reach adulthood. Particularly, in contrast to control, sperm from these offspring show a remarkable lower capacity to fertilize oocytes when copulation occurs early in the estrus cycle relative to ovulation, due to an altered sperm capacitation. Our data demonstrate for the first time that maternal nutritional stress can have long-term consequences on the reproductive health of male progeny by affecting sperm physiology, especially capacitation, with no observable impact on spermatogenesis and classical quantitative and qualitative sperm parameters. Moreover, our experimental model could be of major interest to study, explain, and ultimately treat certain categories of infertilities.

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