Yeimy Mar De León-Ramírez1, Miguel Lara-García2, Pablo Pacheco3, Omar Lara-García4, Margarita Martínez-Gómez3, Estela Cuevas-Romero4, Jorge Rodríguez-Antolín4, Leticia Nicolás-Toledo5. 1. Doctorado en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, México. 2. Instituto de Neuroetología, Universidad Veracruzana, Veracruz, México. 3. Instituto de Neuroetología, Universidad Veracruzana, Veracruz, México; Departamento de Biología Celular y Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México. 4. Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México. 5. Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México. Electronic address: leticia.nicolast@uatx.mx.
Abstract
BACKGROUND: During childhood and adolescence, excessive food consumption stimulates adipose tissue expansion promoting overweight in humans, and mice. A high-sucrose diet is related to obesity and metabolic syndrome. Infertility is commonly related to these pathologies. We aim to evaluate possible histomorphological testicular changes induced by a high-sucrose diet on sperm count during the post-weaning period. METHODS: Wistar male rats aged 21 days, weaned, were randomly assigned into two groups: control (fed and hydrated normally) and sugar group (fed normally but hydrated with a solution containing 30% of diluted sucrose during 30 days). At the pubertal age of 51 days, animals were killed and blood samples were taken to measure testosterone and leptin. Testicles were collected and gonadal adipose tissue and semen samples from the epididymis were excised. Testicle samples were used for morphological description using H&E staining, as well as to quantify the triacylglycerol content and the lactate dehydrogenase (LDH) expression. Semen samples were used to assess motility, viability, and sperm count. RESULTS: The sugar group presented an increase in the testicular weight, but a reduction in the cross-sectional area of seminiferous tubules. Moreover, disorganization of Sertoli cells and spermatogonia, an increase in the LDH expression within the entire seminiferous tubule, and a reduced sperm count and spermatozoid motility were found. These alterations were accompanied by high serum levels of testosterone and leptin. CONCLUSIONS: Our results indicate strong damage of testis by sugar consumption during early life that may lead to the onset of infertility in adulthood.
BACKGROUND: During childhood and adolescence, excessive food consumption stimulates adipose tissue expansion promoting overweight in humans, and mice. A high-sucrose diet is related to obesity and metabolic syndrome. Infertility is commonly related to these pathologies. We aim to evaluate possible histomorphological testicular changes induced by a high-sucrose diet on sperm count during the post-weaning period. METHODS: Wistar male rats aged 21 days, weaned, were randomly assigned into two groups: control (fed and hydrated normally) and sugar group (fed normally but hydrated with a solution containing 30% of diluted sucrose during 30 days). At the pubertal age of 51 days, animals were killed and blood samples were taken to measure testosterone and leptin. Testicles were collected and gonadal adipose tissue and semen samples from the epididymis were excised. Testicle samples were used for morphological description using H&E staining, as well as to quantify the triacylglycerol content and the lactate dehydrogenase (LDH) expression. Semen samples were used to assess motility, viability, and sperm count. RESULTS: The sugar group presented an increase in the testicular weight, but a reduction in the cross-sectional area of seminiferous tubules. Moreover, disorganization of Sertoli cells and spermatogonia, an increase in the LDH expression within the entire seminiferous tubule, and a reduced sperm count and spermatozoid motility were found. These alterations were accompanied by high serum levels of testosterone and leptin. CONCLUSIONS: Our results indicate strong damage of testis by sugar consumption during early life that may lead to the onset of infertility in adulthood.