Leptin and its actions on reproduction in males / 亚洲男科学杂志(英文版)

Leptin, an adipocyte-derived hormone, serves numerous physiological functions in the body, particularly during puberty and reproduction. The exact mechanism by which leptin activates the gonadotropin-releasing hormone (GnRH) neurons to trigger puberty and reproduction remains unclear. Given the widespread distribution of leptin receptors in the body, both central and peripheral mechanisms involving the hypothalamic-pituitary-gonadal axis have been hypothesized. Leptin is necessary for normal reproductive function, but when present in excess, it can have detrimental effects on the male reproductive system. Human and animal studies point to leptin as a link between infertility and obesity, a suggestion that is corroborated by findings of low sperm count, increased sperm abnormalities, oxidative stress, and increased leptin levels in obese men. In addition, daily leptin administration to normal-weight rats has been shown to result in similar abnormalities in sperm parameters. The major pathways causing these abnormalities remain unidentified; however, these adverse effects have been attributed to leptin-induced increased oxidative stress because they are prevented by concurrently administering melatonin. Studies on leptin and its impact on sperm function are highly relevant in understanding and managing male infertility, particularly in overweight and obese men.

Effect of melatonin supplementation on pregnancy outcome in Wistar-Kyoto and Sprague-Dawley rats / 生理学报

Although melatonin supplementation is known to influence numerous physiological functions, little is however known of its effects on pregnancy outcome. This study investigated the effects of melatonin supplementation on pregnancy outcome in Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats aged 12-13 weeks. Upon confirmation of proestrus, each female rat was housed overnight with a male of the same strain. On the next morning, following confirmation of mating (vaginal smear), WKY female rats were isolated into individual metabolic cages and given 0, 25, 50 or 100 mg/kg per day of melatonin in drinking water from day 1 of pregnancy to day 21 postpartum. SD females were given 0 or 100 mg/kg per day of melatonin. Maternal weight, duration of pregnancy, litter size, birth weight and body weight of pups up to day 42, and pup mortality were recorded. Data were analyzed using ANOVA for repeated measures. Compared to controls, maternal weight gain during pregnancy was significantly lower in melatonin-supplemented dams (P < 0.01). Litter size was significantly smaller in melatonin-supplemented dams (P < 0.01). Mean birth weight of pups was significantly lower only in pups of dams given 100 mg/kg per day of melatonin (P < 0.001). Mean body weight of pups of dams given melatonin was significantly lower than controls (P < 0.01). Pup mortalities were 9.5% and 21.6% in WKY dams given 25 and 100 mg/kg per day of melatonin respectively, and all pup deaths occurred after day 21 of weaning. The results suggest that melatonin supplementation during antenatal and postpartum period appears to adversely affect litter size, pup growth and mortality in WKY and SD rats. The precise mechanism causing the death is not clear.

Changes in bone turnover markers and bone mass with reducing levels of jumping exercise regimens in female rats

To date, little is known about the effects of a reduced level of jumping exercise regimens on bone turnover markers and mass. This study investigates the effects of different jumping exercise regimens with varying exercise loads on serum bone turnover markers and bone mass in female rats. A total of 144 female rats aged 12 weeks, were divided into 12 groups as follows: no exercise for 8 [8S] or 32 weeks [32S], or 8 weeks of standard training program [8STP] consisting of 200 jumps per week [200J/w], given at 40 jumps per day [40J/d] for 5 days per week [5d/w] [8STP24E], followed by 24 weeks of exercise at loads of either 10J/d or 20J/d or 40J/d, for either 5d/w, or 3d/w, or 1d/w. Serum osteocalcin, alkaline phosphatase, C-terminal telopeptide of type 1 collagen [1CTP] concentrations, and tibial fat free dry weight were measured. Tibial mass was significantly higher in 8STP than 8S. No changes were evident in serum markers of bone turnover parameters after 8STP. Significant increases in tibial mass were observed in rats that continued to exercise at workloads of 30J/w and above after 8STP. Serum alkaline phosphatase concentrations increase whereas serum 1CTP concentrations decrease in rats given workloads of 40 J/W and above it appears an exercise load of 30 J/W. i.e. 10 j/d for 3 D/W, was the minimum level of continuous exercise load that was required to maintain the 8STP-induced bone gains in addition significant increase in bone mass in young rats following 8STP might not always be reflected changes in serum levels of osteocalcin alkaline phosphatase and ICTP

Pre-Eclampsia: Is It All In The Placenta?

Hypertensive disorders of pregnancy complicate almost 7 – 10 % of all pregnancies. The dyad of hypertension and proteinuria after 20 weeks of gestation is referred to as pre-eclampsia. It is a major cause of maternal morbidity and mortality and is also associated with increased perinatal problems. Despite intensive research over the years the exact cause of pre-eclampsia remains unknown. Nevertheless, information gleaned from published studies point to the placenta as the probable pathogenetic focus of pre-eclampsia, as the disease usually resolves within 24 – 48 hours after delivery of the placenta. Although the precise involvement of the placenta in pre-eclampsia remains unclear there are indications that the trophoblastic invasion of the uterine spiral arteries is abnormal in women who develop pre-eclampsia. This impaired invasion leads to decreased placental perfusion and ultimately to placental hypoxia. The distressed or ischaemic placenta then secretes a factor(s) into the maternal circulation, which cause/s widespread endothelial cell dysfunction characterized by vasospasm, activation of coagulation system and organ ischaemia. The cause of the defective cytotrophoblastic invasion of the spiral arteries and the link between placental ischaemia and generalized maternal endothelial dysfunction remain unknown. Although the placenta appears to have a major role in the pathogenesis of pre-eclampsia, evidence also suggests that factors like maternal genetic predisposition, dietary, environmental and behaviour, which surface during the stress of pregnancy might also be involved in the development of pre-eclampsia. It is known that not all women with poor cytotrophoblast invasion develop pre-eclampsia and not all women with preeclampsia show poor cytotrophoblast invasion. Over the years, a number of potential risk factors associated with the development of pre-eclampsia are being recognized and it might be appropriate now to develop some preventative strategies based upon the available information.