Early intervention with breast milk mesenchymal stem cells attenuates the development of diabetic-induced testicular dysfunction via hypothalamic Kisspeptin/Kiss1r-GnRH/GnIH system in male rats.
The current study thus aimed to examine the efficacy of adiponectin in improving testicular dysfunction in high-fat diet/streptozotocin-induced T2D mice.
The present study was aimed to demonstrate the recuperative effect of nesfatin-1 on testicular dysfunction in the high-fat diet (HFD)/streptozotocin (STZ)-induced type-2 diabetes mellitus (T2DM) mice.
Proinsulin C-peptide as an alternative or combined treatment with insulin for management of testicular dysfunction and fertility impairments in streptozotocin-induced type 1 diabetic male rats.
ERβ receptor activation during the post-ischemic period may be beneficial in protection against torsion-related oxidant testicular injury and infertility.
Therefore, we hypothesize that hyperglycemia-mediated TLR4 activation in testicular cells, especially Leydig cells might be a crucial event triggering oxidative stress and inflammation, which in turn, drives testicular dysfunction.
The accumulation of the VLCFA and the associated oxidative stress can present with a spectrum of significant neurologic disease, adrenal insufficiency, and testicular dysfunction in males with ABCD1 gene mutations.
These findings suggest that the CXorf6 mutations cause hypospadias primarily because of testicular dysfunction and resultant compromised testosterone production around that period, and provide useful information for the molecular network involved in fetal testosterone production.
However, the descriptions of testicular dysfunction and behavioral deficits leading to complete infertility in male mice lacking estrogen receptor alpha (ERalpha) have indicated the importance of estrogen action in fertility of the male rodent.