Category
Basic
Description
The increase in western-style dietary patterns has led to an increase in obesity prevalence and its associated comorbidities. Specifically, researchers have found that obesity due to western-style diet (WSD) is negatively correlated with reproductive health in men. This study investigated the effects of inutero exposure to a WSD on testis development, specifically of 12- week-old mice (young adult C57Bl/6J). We hypothesized that in-utero exposure to a WSD would negatively impact testis development and function in male offspring. Using histological hematoxylin and eosin staining and immunohistochemistry method, we examined spermatogenesis in seminiferous tubules, anti-Mullerian hormone (AMH) production by Sertoli cells, and cytochrome P450 17A1 (CYP17A1) enzyme expression in Leydig cells. Our research revealed that, when compared to male offspring in a control diet group, mice that were subject to in-utero exposure to a WSD had a decrease in the total number of seminiferous tubules (control: 115.5 ± 46.0; WSD: 53.5 ± 17.7; p = 0.0162) and an increase in the percentage of seminiferous tubules lacking spermatozoa in the luminal region (control: 11.2 ± 3.7%; WSD: 32.5 ± 16.7%; p = 0.0032). AMH was homogeneously distributed in the Sertoli cell layer of normal seminiferous tubules but was primarily located in the luminal region of seminiferous tubules without sperm. CYP17A1 enzyme expression in Leydig cells was typical in both control and WSD groups. In conclusion, our research highlights the negative implications of in-utero exposure to a WSD on seminiferous tubule formation, sperm production, and Sertoli cell function in the mouse testis. This research sets the stage for future studies by translating to human testicular function and highlighting remaining gaps in hormonal and cellular mechanisms, as well as future studies aimed at prevention, intervention, and public health guidelines to alter the declining trajectory of testicular function in male offspring due to maternal WSD consumption.
Effect of In-Utero Exposure to a Western-Style Diet on Testis Development
Basic
The increase in western-style dietary patterns has led to an increase in obesity prevalence and its associated comorbidities. Specifically, researchers have found that obesity due to western-style diet (WSD) is negatively correlated with reproductive health in men. This study investigated the effects of inutero exposure to a WSD on testis development, specifically of 12- week-old mice (young adult C57Bl/6J). We hypothesized that in-utero exposure to a WSD would negatively impact testis development and function in male offspring. Using histological hematoxylin and eosin staining and immunohistochemistry method, we examined spermatogenesis in seminiferous tubules, anti-Mullerian hormone (AMH) production by Sertoli cells, and cytochrome P450 17A1 (CYP17A1) enzyme expression in Leydig cells. Our research revealed that, when compared to male offspring in a control diet group, mice that were subject to in-utero exposure to a WSD had a decrease in the total number of seminiferous tubules (control: 115.5 ± 46.0; WSD: 53.5 ± 17.7; p = 0.0162) and an increase in the percentage of seminiferous tubules lacking spermatozoa in the luminal region (control: 11.2 ± 3.7%; WSD: 32.5 ± 16.7%; p = 0.0032). AMH was homogeneously distributed in the Sertoli cell layer of normal seminiferous tubules but was primarily located in the luminal region of seminiferous tubules without sperm. CYP17A1 enzyme expression in Leydig cells was typical in both control and WSD groups. In conclusion, our research highlights the negative implications of in-utero exposure to a WSD on seminiferous tubule formation, sperm production, and Sertoli cell function in the mouse testis. This research sets the stage for future studies by translating to human testicular function and highlighting remaining gaps in hormonal and cellular mechanisms, as well as future studies aimed at prevention, intervention, and public health guidelines to alter the declining trajectory of testicular function in male offspring due to maternal WSD consumption.
