This study examined the effects of PI3K and AMPK signalling pathway inhibitors on leptin‐induced adverse effects on rat spermatozoa. Sprague‐Dawley rats, aged 14–16 weeks, were randomised into control, leptin‐, leptin + dorsomorphin (AMPK inhibitor)‐, and leptin+LY294002 (PI3K inhibitor)‐treated groups with six rats per group. Leptin was given once daily for 14 days via the intraperitoneal (i.p.) route at a dose of 60 ug kg−1 body weight. Rats in the leptin and inhibitor‐treated groups received concurrently either dorsomorphin (5 mg kg−1 day−1) or LY294002 (1.2 mg kg−1 day−1) i.p. for 14 days. Controls received 0.1 ml of normal saline. Upon completion, sperm count, sperm morphology, seminiferous tubular epithelial height (STEH), seminiferous tubular diameter (STD), 8‐hydroxy‐2‐deoxyguanosine (8‐OHdG) and phospho‐Akt/total Akt ratio were estimated. Data were analysed using ANOVA. Sperm count, STEH and STD were significantly lower, while the percentage of spermatozoa with abnormal morphology and the level of 8‐OHdG were significantly higher in rats treated with leptin and leptin + dorsomorphin when compared to those in controls and LY294002‐treated rats. Testicular phospho‐Akt/total Akt ratio was significantly higher in leptin and leptin + LY294002‐treated rats. In conclusion, LY294002 prevents leptin‐induced changes in rat sperm parameters, suggesting the potential role of the PI3K signalling pathway in the adverse effects of leptin on sperm parameters.

Infertility is somewhat more prevalent in men who are obese. They are also reported to have low sperm concentration, higher fraction of spermatozoa that look morphologically abnormal, higher DNA fragmentation index and evidence of oxidative stress.The precise cause for this remains uncertain. Leptin levels in serum and percentage

Introduction: Leptin is an adipokine that has strong correlation with the body mass index (BMI). Gestational diabetes mellitus (GDM) is a common medical complication associated with pregnancy. Leptin may lose its correlation with the body mass index (BMI) during diabetes due to hormonal rearrangement. Diet control is the first line management in GDM. Leptin reported to increase in pregnancy and further increases in diabetic patients during GDM screening. There is paucity in the reports concerning Leptin levels in GDM patients on diet control. The present study was aimed to evaluate the changes in maternal leptin in pregnancy complicated by GDM on diet control compared to the normal pregnancy in the 3rd trimesters by comparing the means and to find the correlation of Leptin with the body mass index in both groups. Methods: The study included 2 groups: normal pregnancy (n = 40) and pregnancy with GDM under diet control (n = 60) both groups are at 38-40 weeks of gestation. Leptin concentration in serum was measured in both groups and statistically tested using student t test. The BMI were measured and correlated with the Leptin level in test groups. Results: the results indicated that Leptin will nearly triple in the third trimester (38±30 ng/ml) of pregnancy compared to the standard normal non-pregnant. Leptin level was significantly lower in diabetic women on diet control (28±16 ng/ ml) when compared with the non-diabetics (38±30 ng/ml). The hormone has no correlation with the age of the patients but have a positive correlation with the body mass index before and during pregnancy in both groups. Conclusion: Leptin is increasing in pregnancy as part of the physiological changes. Dieting can decrease Leptin level in diabetics’ pregnant women. Diet can restore the hormonal dysregulation of Leptin. Assessment of Leptin level might be used as an indicator for good diet control during pregnancy.