Abstract
Obesity affects male fertility and maternal diabetes affects the offspring sperm epigenome. However, the effects of in utero exposure to maternal glucose intolerance in combination with postnatal high fat, high sucrose (HFHS) diet consumption on offspring spermatogenesis is not clear. The present study was designed to test these effects. One week before and during pregnancy, dams were fed either control or HFHS diet to induce gestational glucose intolerance, and returned to standard diet during lactation. Male offspring from each maternal group were split into control and HFHS-fed groups for eight weeks prior to sacrifice at 11, 19 or 31 weeks of age, and reproductive tissues were harvested for analysis of testicular germ cell apoptosis and sperm output. Postnatal HFHS diet suppressed spermatogonia apoptosis in all age groups and maternal HFHS diet reduced testosterone levels at 11 weeks. At 31 weeks of age, the postnatal HFHS diet increased body weight, and reduced epididymis weight and sperm count. The combination of in utero and postnatal exposure impacted sperm counts most significantly. In summary, HFHS diet during pregnancy puts male offspring at greater risk of infertility, particularly when combined with postnatal high fat diet feeding.
Highlights
Paternal obesity and diabetes impact the reproductive health of offspring
Fasting insulin 2.3 ± 0.4a 2.0 ± 0.4ab 1.3 ± 0.3b 2.7 ± 0.3a intolerance during mid-late pregnancy[20]. Using this model, we ask whether maternal glucose intolerance that begins after conception, and occurs in the absence of maternal obesity, impairs fertility of male offspring
Male offspring were challenged with the same high fat, high sucrose diet that was fed to mothers during pregnancy
Summary
Paternal obesity and diabetes impact the reproductive health of offspring. For example, in rodents, male obesity alters blastocyst development, embryo metabolism[9,10], placental gene expression and methylation status[11], and reduces semen quality[12] and fertility of male offspring[13]. We have developed an animal model of gestational glucose intolerance, in which C57BL/6J dams are fed a high fat, high sucrose diet from 1 week pre-gestation through the end of pregnancy[20]. Under this acute HFHS exposure, dams fail to expand beta cell numbers during pregnancy, leading to an inadequate insulin response to glucose challenge, and glucose www.nature.com/scientificreports/. The second objective of this study was to determine whether postnatal high fat diet interacts with prenatal exposure to maternal glucose intolerance to affect male fertility. Germ cell apoptosis was measured in male offspring shortly after puberty, and at 19 and 31 weeks following exposures to maternal and postnatal high fat diets
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