De León-Ramírez Yeimy Mar, Lara-García Miguel, Pacheco Pablo, Lara-García Omar, Martínez-Gómez Margarita, Cuevas-Romero Estela, Rodríguez-Antolín Jorge, Nicolás-Toledo Leticia
Doctorado en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, México.
Instituto de Neuroetología, Universidad Veracruzana, Veracruz, México.
Ann Anat. 2021 May;235:151678. doi: 10.1016/j.aanat.2021.151678. Epub 2021 Jan 28.
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.
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.
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.
Our results indicate strong damage of testis by sugar consumption during early life that may lead to the onset of infertility in adulthood.
在儿童期和青少年期,过量进食会刺激脂肪组织扩张,导致人类和小鼠体重超重。高糖饮食与肥胖和代谢综合征有关。不孕症通常与这些病症相关。我们旨在评估高糖饮食在断奶后期对精子数量诱导的可能的睾丸组织形态学变化。
将21日龄断奶的雄性Wistar大鼠随机分为两组:对照组(正常喂食和饮水)和糖组(正常喂食,但在30天内用含30%稀释蔗糖的溶液饮水)。在51日龄青春期时,处死动物并采集血样以测量睾酮和瘦素。收集睾丸,切除性腺脂肪组织和附睾精液样本。睾丸样本用于苏木精-伊红染色进行形态学描述,以及定量三酰甘油含量和乳酸脱氢酶(LDH)表达。精液样本用于评估活力、存活率和精子数量。
糖组睾丸重量增加,但生精小管横截面积减小。此外,发现支持细胞和精原细胞排列紊乱,整个生精小管内LDH表达增加,精子数量和精子活力降低。这些改变伴随着血清睾酮和瘦素水平升高。
我们的结果表明,生命早期摄入糖对睾丸有严重损害,可能导致成年期不孕症的发生。