Maternal high-fat diet during pregnancy and lactation affects factors that regulate cell proliferation and apoptosis in the testis of adult progeny
Helen Viotti A , Daniel Cavestany A , Graeme B. Martin B * , Mark H. Vickers C , Deborah M. Sloboda D E F G and Graciela Pedrana AA
B
C
D
E
F
G
Abstract
A maternal high-fat diet is thought to pose a risk to spermatogenesis in the progeny.
We tested whether a maternal high-fat diet would affect Sertoli cell expression of transcription factors (insulin-like growth factor I (IGF-I); glial-cell line-derived neurotrophic factor (GDNF); Ets variant 5 (ETV5)) and cell proliferation and apoptotic proteins, in the testis of adult offspring.
Pregnant rats were fed ad libitum with a standard diet (Control) or a high-fat diet (HFat) throughout pregnancy and lactation. After weaning, male pups were fed the standard diet until postnatal day 160. Males were monitored daily from postnatal day 34 to determine onset of puberty. On postnatal day 160, their testes were processed for morphometry and immunohistochemistry.
The HFat diet increased seminiferous-tubule diameter (P < 0.03), the numbers of Sertoli cells (P < 0.0001) and Ki-67-positive spermatogonia (P < 0.0006), and the areas immunostained for ETV5 (P < 0.0001), caspase-3 (P < 0.001) and Bcl-2 (P < 0.0001). By contrast, the HFat diet reduced the areas immunostained for IGF-I (P < 0.01) and GDNF (P < 0.0001).
A maternal high-fat diet alters the balance between spermatogonia proliferation and spermatid apoptosis.
A maternal high-fat diet seems to ‘program’ adult male fertility.
Keywords: apoptosis, cell proliferation, developmental programming, high-fat diet, rat, reproduction, Sertoli cell, spermatogenesis, testis.
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