内科学
内分泌学
瘦素
支持细胞
生物
间质细胞
芳香化酶
生殖细胞
促黄体激素
小鼠苗条素受体
激素
睾酮(贴片)
精子发生
肥胖
医学
基因
癌症
乳腺癌
生物化学
作者
Fabiane Ferreira Martins,Márcia Barbosa Águila,Carlos Alberto Mandarim‐de‐Lacerda
标识
DOI:10.1016/j.acthis.2017.05.003
摘要
The obesity and its comorbidities, including resistance to leptin, impacts the reproductive function. Testes express leptin receptors in the germ cells and Leydig cells. Then, leptin-deficient animals are obese and infertile. We aimed to evaluate the structure and steroidogenic pathway of the testis of deficient leptin mice. Three months old male C57BL/6 mice (wild-type, WT) and deficient leptin (ob/ob) mice had their testes dissected and prepared for analyses. Compared to the WT group, the ob/ob group showed a greater body mass with smaller testes, and alterations in the germinative epithelium: fewer spermatogonia, spermatocytes, and spermatids. The Sertoli cells and the germ cells showed condensed nuclei and nuclear fragmentation indicating cell death, in agreement with a low expression of the proliferating cell nuclear antigen and a high expression of Caspase3. In the ob/ob group, the sperm was absent in the seminiferous tubules, and the steroidogenic pathway was compromised (low 3Beta hydroxysteroid dehydrogenase and steroidogenic acute regulatory protein). Further, all hormone receptors involved in the testicular function were down expressed (androgen, estrogen, follicle-stimulating, luteinizing, aromatase, and nicotinamide adenine dinucleotide phosphate). In conclusion, the findings indicate significant morphological, hormonal and enzymatic changes in the testis of the ob/ob mice. The shifts in the enzymatic steroidogenic pathway and the enzymes related to spermatic activity support the insights about the failures in the fertility of these animals. The study provides new evidence and contributes to the understanding of how the lack of leptin and obesity might negatively modulate the testicular function leading to infertility.
科研通智能强力驱动
Strongly Powered by AbleSci AI