In Utero and Postnatal Exposure to High Fat, High Sucrose Diet Suppressed Testis Apoptosis and Reduced Sperm Count.

Research paper by Jiude J Mao, Kathleen A KA Pennington, Omonseigho O OO Talton, Laura C LC Schulz, Miriam M Sutovsky, Yan Y Lin, Peter P Sutovsky

Indexed on: 18 May '18Published on: 18 May '18Published in: Scientific Reports


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.