Effects Of Diabetes Mellitus On Sexual Function, Histomorphology And α-smooth Muscle Actin Expression in Cavernous Body Of Penis in Rats

3 Discussion

This experiment preliminarily explored the biological basis of ED concurrent with DM. First, after DM model induction, the diabetes group showed slower body weight gain compared to the control group, and random blood glucose levels were significantly higher than those in the control group, consistent with the characteristics of diabetes. Studies on rat erections, both domestically and internationally, often use the APO test, which is widely recognized. Therefore, this experiment used the APO stimulation test for further study after successful modeling. The results showed that sexual function in the diabetes group was lower than in the control group, consistent with the high incidence of ED among DM patients.

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Pathological observations revealed that testicular interstitial tissue in the diabetes group exhibited edema, irregular cell morphology, loose intercellular spaces, disordered arrangement, disrupted intracellular structures, and signs of dedifferentiation, losing structural features.

These findings are consistent with pathological results from other animal studies on DMED [5].

The data also showed that sex hormone levels in the DM group were significantly lower than in the control group, indicating that low levels of testosterone (T), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) may be associated with DMED. It is well known that T is an essential sex hormone synthesized primarily by testicular interstitial cells. For men, T plays a critical role in regulating penile integrity and erectile function [6]. Recent studies [7] have also reported that hyperglycemia reduces testosterone secretion, which is closely related to structural and functional changes in the testes, as further confirmed in this study. Additionally, hyperglycemia can lead to excessive reactive oxygen species (ROS) release from testicular interstitial cells, further reducing testosterone levels, decreasing nitric oxide production, and exacerbating ED [8]. Wang Lingxiao et al. [9] also proposed that reduced T levels are an independent risk factor for DMED, consistent with this study.

Moreover, LH and FSH are important gonadotropins secreted by the pituitary gland, promoting male gonadal and adrenal androgen secretion. Under physiological conditions, LH binds specifically to receptors in testicular interstitial cells, promoting T synthesis and secretion. If LH levels decrease, the ability of testicular interstitial cells to secrete T declines, leading to insufficient T secretion and resulting in ED. Yaday et al. [10] found that rats exhibiting sexual dysfunction had decreased serum gonadotropins (LH and FSH) and T levels, consistent with the findings of this study.

Previous research [11] has shown that structural changes in the penile cavernous body are the pathological basis of ED, and tissue fibrosis reduces the elasticity and compliance of the penis. In this study, histopathological observations revealed that hyperglycemia further altered the structure of penile cavernous tissue: the proportion of collagen fibers increased, while the proportion of smooth muscle cells decreased, significantly exacerbating fibrosis. Fibrosis of the penile cavernous tissue reduced the compliance of penile tissue, decreased the dilation space of the cavernous sinuses, impaired blood flow perfusion of the cavernous body, and inhibited the closure of subtunical veins, preventing sufficient penile erection and causing ED. This is consistent with conclusions from previous studies. cavernous smooth muscle cells (CCSMCs) can be divided into undifferentiated and differentiated types based on structural and functional differences. These types can transform into each other under specific conditions. α-SMA is primarily distributed in CCSMCs in the penile cavernous body [12] and serves as a molecular marker of contractile CCSMCs. Reduced synthesis and secretion of α-SMA can be used to evaluate the dedifferentiation process of CCSMCs [13]. Studies [12–14] have suggested that this transformation can occur in various diseases, such as DM and hypertension, and when this transformation reaches a certain degree, it leads to ED. Recent research [15] also found that in DM rats exposed to long-term hyperglycemic conditions, the ratio of proliferation to apoptosis of CCSMCs in penile tissue decreased. Combined with the results of this study, it is speculated that hyperglycemia induces and accelerates the dedifferentiation of CCSMCs in penile tissue, which may be an important microscopic mechanism underlying the high incidence of ED in DM.