To investigate the effects of Zingiber Officinale on male reproductive functions and study the mechanisms underlying these effects, aqueous extract of Zingiber Officinale were administered orally to two groups of male rats at 500mg/kg b.w. and 1000mg/kg b.w. A third group served as control and received the treatment vehicle, distilled water. Treatment lasted for 14 and 28 days before sacrifice. Organ weight, epididymal sperm counts, motility, viability and morphology, seminal fructose, testicular malonhydialdehyde, and serum testosterone were determined. The treatment caused a significant increase (P<0.05) in the weight of the testis and epididymis. There were dose and duration dependent increases in sperm count and motility (P<0.05). There was also a significant increase (P<0.05) in serum testosterone level. Malonhydialdehyde levels were significantly reduced (P<0.05). Our results indicated that extract of Zingiber Officinale possesses pro-fertility properties in male rats which might be a product of both its potent antioxidant properties and androgenic activities.
These findings demonstrate that magnesium may mediate effective metabolic control by stimulating the antioxidant defense, and increased levels of INSR and GLUT4 in diabetic rats.
To investigate the mechanism by which maternal obesity disrupts reproductive function in offspring, we examined Kiss1 expression in the hypothalamic arcuate (ARC) and anteroventral periventricular (AVPV) nuclei, and posterodorsal medial amygdala (MePD) of pre-pubertal and young adult offspring. Sprague-Dawley rats were fed either a standard or energy-dense diet for six weeks prior to mating and throughout pregnancy and lactation. Male and female offspring were weaned onto normal diet on postnatal day (pnd) 21. Brains were collected on pnd 30 or 100 for qRT-PCR to determine Kiss1 mRNA levels. Maternal obesity increased Kiss1 mRNA expression in the MePD of pre-pubertal male and female offspring, whereas Kiss1 expression was not affected in the ARC or AVPV at this age. Maternal obesity reduced Kiss1 expression in all three brain regions of 3 month old female offspring, but only in MePD of males. The role of MePD kisspeptin on puberty, estrous cyclicity and preovulatory LH surges was assessed directly in a separate group of post-weanling and young adult female rats exposed to a normal diet throughout their life course. Bilateral intra-MePD cannulae connected to osmotic mini-pumps for delivery of kisspeptin receptor antagonist (Peptide 234 for 14 days) were chronically implanted on pnd 21 or 100. Antagonism of MePD kisspeptin delayed puberty onset, disrupted estrous cyclicity and reduced the incidence of LH surges. These data show that the MePD plays a key role in pubertal timing and ovulation and that maternal obesity may act via amygdala kisspeptin signaling to influence reproductive function in the offspring.
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