The effects of different physiologic concentrations of prolactin in association with reproductive hormones on the incidence of type 2 diabetes mellitus in men: Tehran Lipid and Glucose Study.

BACKGROUND: Data is inconsistent and, for the most part, not sufficient to demonstrate the association between serum Prolactin (PRL) concentration within the physiologic range and the incidence rate of type 2 Diabetes Mellitus (DM) among men. Moreover, since both PRL and type 2 DM are associated with reproductive hormones, investigating these hormones might improve our understanding of how PRL might impose its effect on the incidence rate of type 2 DM. METHODS: For the present study, 652 eligible men aged 29-70 with a normal baseline PRL concentration were selected from the Tehran Lipid and Glucose Study (TLGS). Participants were sub-classified into three groups (tertiles) according to the serum concentration of PRL and were followed for 15.8 years. The incidence of type 2 DM and PRL, LH, FSH, testosterone, and AMH concentrations were measured. The effect of hormonal variables on the incidence of type 2 DM was estimated using the log-binomial model, adjusted for major confounding factors. The correlations between PRL and the indicators of glucose and lipid metabolism and other hormonal variables were also explored. RESULTS: In the unadjusted model, PRL was not significantly associated with the incidence rate of type 2 DM (RR = 0.98, 95% CI: 0.94 - 1.03). After adjusting for potential confounders, the inverse effect of AMH on the incidence rate of type 2 DM was the only significant association. The analyses also indicated a significant positive association between PRL and LH/FSH ratio (r = 0.1, P = 0.01). CONCLUSION: No significant association was found between serum PRL concentrations within the physiologic range and the incidence rate of type 2 diabetes mellitus among middle-aged men. Men with higher concentrations of PRL within the physiologic range tended to show higher levels of LH and LH/FSH. AMH was the only variable significantly linked to the incidence rate of type 2 DM in men.

Spatial arrangement of testicular cells disrupted by transient scrotal hyperthermia and subsequent impairment of spermatogenesis.

The spermatogenesis is temperature-dependent and heat stress have destructive effects on spermatogenesis and reduces sperm quality. Sixteen adult mice were allocated to two groups: hyperthermia and control groups. Scrotal hyperthermia was induced by water bath with 43°C for 30 min. Then, the spermatozoon was isolated through the tail region of epididymis for sperm parameters analysis. The testicular tissues were taken for stereological studies, hormonal assay, TUNEL assay and molecular studies. We found a marked decrease in sperm parameters and serum testosterone level in mice induced by scrotal hyperthermia as well as stereological analysis indicated a significant reduction in testicular cells and changes in the spatial arrangement of testicular cells in the scrotal hyperthermia groups compared to the control groups. Moreover, the TUNEL assay results showed that apoptotic cells were enhanced significantly in the group of scrotal hyperthermia compared to the control groups. Furthermore, scrotal hyperthermia caused a reduction in the expression of retinoic acid 8 (STRA8), c-kit and proliferating cell nuclear antigen (PCNA) genes in the scrotal hyperthermia groups compared to the control. According to results, induction of transient scrotal hyperthermia leads to a fluctuation in the spatial arrangement of testicular cells, which finally influences the normal function of spermatogenesis.

Polycystic Ovary Syndrome, Subclinical Hypothyroidism, the Cut-Off Value of Thyroid Stimulating Hormone; Is There a Link? Findings of a Population-Based Study.

Despite solid evidence regarding the association of over-hypothyroidism with polycystic ovary syndrome (PCOS), the relationship between PCOS and subclinical hypothyroidism (SCH) is still a topic of debate. In the present population-based study, we aimed to assess if there is a difference between PCOS and the control group regarding the upper reference limit of thyroid stimulating hormone (TSH). We also aimed to identify the prevalence of SCH in women with PCOS compared to controls. This study was conducted on data collected in the Iranian PCOS prevalence study and the Khuzestan PCOS prevalence study. Participants that met our eligibility criteria were categorized into two groups: PCOS (n = 207) and control (n = 644). Quantile and logistic regression models were used to explore the effect of PCOS status on TSH cut-off values and SCH, respectively. The 95 percentiles of TSH were not significantly different in the PCOS group compared to control ones (6.12 and 6.56 microU/mL, respectively). There was no statistically significant association between PCOS status and SCH (OR adjusted: 1.40; 95%CI: 0.79, 2.50; p = 0.2). The prevalence of SCH and the upper reference limit of TSH were not significantly different in PCOS and controls. Investigation of SCH in women with PCOS might be questionable.

Impact of Polycystic Ovary Syndrome on Silent Coronary Artery Disease and Cardiovascular Events; A Long-term Population-based Cohort Study.

BACKGROUND: The existing data regarding the impact of Polycystic Ovary Syndrome (PCOS) on the risk of developing cardiovascular disease (CVD) are conflicting. AIM: To explore the effect of PCOS status on the occurrence of silent coronary artery disease (CAD)/CVD. METHODS: A total of 1591 women without CVD at baseline, aged 18-45 years, including 356 PCOS patients (defined by the Rotterdam criteria) and 1235 eumenorrheic non-hirsute women without polycystic ovarian morphology (controls), were selected from the Tehran Lipid and Glucose Study (TLGS). The median follow-up was 15.4 years, and most participants were in their late reproductive years at the end of the study. Silent CAD and CVD outcomes in PCOS and control groups were compared according to the multivariable-adjusted hazard ratios (HRs) and cumulative hazard functions. RESULTS: There was no difference in CVD risk factors between the PCOS and control groups. After controlling for confounders, PCOS status did not increase the risk of silent CAD (HR: 0.96, 95% CI 0.86-1.08). Regardless of PCOS status, women with a history of silent CAD showed 2.25 times higher CVD events than those without this history (95% CI 1.63-3.10). PCOS status reduced the CVD incidence by 42%, independently of silent CAD or traditional risk factors (HR: 0.58, 95% CI 0.35-0.98). CONCLUSIONS: Whereas silent CAD, regardless of PCOS, accelerated CVD, PCOS preserved it, most likely due to a combination of protective factors, including the endocrine pattern in the late reproductive period, environmental/social elements, and recruiting additional counseling and lifestyle modifications.