Diabetes mellitus has emerged as a widespread global health concern, contributing significantly to morbidity and mortality rates. The metabolic disturbances associated with diabetes can adversely impact the male reproductive system, leading to reduced fertility. This review offers an in-depth evaluation of recent global research exploring the impact of diabetes on male reproductive health. Relevant experimental and clinical studies were identified, with a focus on diabetes-related effects on reproductive organs, hormones, and sexual function. The review highlights that insulin deficiency and resistance in diabetic conditions disrupt the hypothalamic-pituitary-gonadal axis, reducing levels of key reproductive hormones such as gonadotropin releasing hormone, luteinizing hormone, follicle stimulating hormone, and testosterone. These hormonal disruptions lead to structural and functional damage in reproductive organs including the testes, Sertoli cells, epididymis, sperm, and accessory glands. Moreover, diabetes contributes to erectile and ejaculatory dysfunctions. Various pathophysiological mechanisms such as oxidative stress, hormonal imbalances, germ cell apoptosis, autophagy, mitochondrial dysfunction, and endoplasmic reticulum stress are identified as underlying contributors to diabetes-induced male infertility. The findings of this review provide valuable insights into the complex mechanisms by which diabetes affects the male reproductive function. By integrating current research, it highlights the critical need for further studies and the development of targeted therapies to effectively address diabetes-induced infertility.

Objective: To evaluate the impact of a group embryo culture approach for women of advanced age.

Methods: In this prospective study, two embryo culturing strategies—group and individual—were compared in women who were older (≥35 years) and younger (<35 years). Data was collected from 450 embryos over 291 intracytoplasmic sperm injection (ICSI) cycles performed on 291 patients. A grouped embryo culture group and an individual embryo culture group were generated by selecting the zygotes into two groups based on the type of culture that was used. The main outcomes compared between the groups were the pregnancy and the live birth rates.

Results: The pregnancy, and live births rates were significantly higher when group culture was carried out in an advanced-aged women group (41.5% vs. 25.0%, P=0.04; 14.3% vs. 6.6%, P=0.04; respectively). Similarly, the cleavage rate was better in the same group (98.6% vs. 91.2%, P=0.001). However, in the group of young women, there were not significant differences in these rates.

Conclusions: Group embryo culturing seems to be a promising strategy to improve embryo development and live births for patients over 35 years of age.

Objective: To explore the effects of deltamethrin exposure during prepubertal stage on male reproductive parameters in rats.

Methods: Forty male Wistar rats, aged 23 postnatal days, were randomly divided into four groups of ten rats each. The control group received tap water, while the vehicle control group was administered with 1 mL of peanut oil. Experimental groups received deltamethrin 3 mg/kg and 6 mg/kg, respectively. All treatments were administered orally. At postnatal day 91, all the rats were sacrificed to assess the histology of testes and serum testosterone levels. We also evaluated the binding of deltamethrin to 3β-hydroxysteroid dehydrogenase (HSD), a key enzyme involved in steroidogenesis, using in silico docking and molecular dynamics simulations to assess the stability and binding energy of the 3β-HSD and deltamethrin complex over 100 ns time frame.

Results: Deltamethrin-exposed rats showed significant weight loss, followed by a marked reduction in serum testosterone levels. They also demonstrated the suppression of testicular steroidogenic enzymes like 3β-HSD and 17β-HSD levels, which were accompanied by sperm morphological abnormalities when compared with the control group rats. Moreover, molecular docking studies indicated that deltamethrin interacts with 3β-HSD competitively with pregnenolone which may be the reason for impaired steroidogenesis.

Conclusions: Early life exposure to deltamethrin may induce reproductive toxicity at adult stage. Further exploration studies are warranted to record conclusive evidence for the effects of deltamethrin early exposure.

Objective: To examine the effect of an neurokinin 3 receptor (NK3R) agonist, senktide, on neuronal nitric oxide synthase (nNOS) activation in the median eminence-arcuate nucleus (ME-ARC) and preoptic area (POA) regions of the hypothalamus across proestrus, diestrus, and ovariectomized states in female rats and its correlation with luteinizing hormone (LH) secretion.

Methods: Adult female Sprague-Dawley rats were examined for proestrus and diestrus phases of the estrous cycle. Female rats were categorized into proestrus and diestrus groups, and each was further divided into four subgroups (n=4). In both the diestrus and proestrus categories, Group 1 was the control group. Groups 2, 3, and 4 received senktide (100 μg/kg^-1), NK3R antagonist SB222200 (10 mg/kg^-1), and SB222200 followed by senktide, respectively. To evaluate the effect of sex steroids on NK3R agonist-induced nNOS activation, female rats underwent bilateral ovariectomy and were divided into four groups (n=3). Group 1 served as the control. Group 2 received a subcutaneous injection of 17 β-estradiol 3-benzoate (E2, 3 μg/rat). Group 3 received E2 and progesterone (30 μg/rat). Group 4 was administered senktide (100 μg/kg). Female rats from each group were sacrificed, blood was collected for LH ELISA, and hypothalamic tissues were collected for Western blotting.

Results: Senktide increased nNOS phosphorylation in the ME-ARC during both the proestrus and diestrus phases. In the POA, senktide increased nNOS phosphorylation only during the diestrus phase. In ovariectomized rats, senktide activated nNOS independent of sex steroid levels. Senktide also increased serum LH concentration in diestrus and ovariectomized female rats.

Conclusions: Senktide, an NK3R agonist, activates nNOS in the POA and ME-ARC regions of the hypothalamus in a phase dependent manner. The activation of nNOS by senktide suggests a potential mechanism by which neurokinin B triggers nNOS activation in the ARC and POA regions and regulates GnRH/LH secretion.