Prenatal Hyperandrogenization Induces Metabolic and Endocrine Alterations Which Depend on the Levels of Testosterone Exposure

Prenatal hyperandrogenism is able to induce polycystic ovary syndrome (PCOS) in rats. The aim of the present study was to establish if the levels of prenatal testosterone may determine the extent of metabolic and endocrine alterations during the adult life. Pregnant Sprague Dawley rats were prenatally injected with either 2 or 5 mg free testosterone (groups T2 and T5 respectively) from day 16 to day 19 day of gestation. Female offspring from T2 and T5 displayed different phenotype of PCOS during adult life. Offspring from T2 showed hyperandrogenism, ovarian cysts and ovulatory cycles whereas those from T5 displayed hyperandrogenism, ovarian cysts and anovulatory cycles. Both group showed increased circulating glucose levels after the intraperitoneal glucose tolerance test (IPGTT; an evaluation of insulin resistance). IPGTT was higher in T5 rats and directly correlated with body weight at prepubertal age. However, the decrease in the body weight at prepubertal age was compensated during adult life. Although both groups showed enhanced ovarian steroidogenesis, it appears that the molecular mechanisms involved were different. The higher dose of testosterone enhanced the expression of both the protein that regulates cholesterol availability (the steroidogenic acute regulatory protein (StAR)) and the protein expression of the transcriptional factor: peroxisome proliferator-activated receptor gamma (PPAR gamma). Prenatal hyperandrogenization induced an anti-oxidant response that prevented a possible pro-oxidant status. The higher dose of testosterone induced a pro-inflammatory state in ovarian tissue mediated by increased levels of prostaglandin E (PG) and the protein expression of cyclooxygenase 2 (COX2, the limiting enzyme of PGs synthesis). In summary, our data show that the levels of testosterone prenatally injected modulate the uterine environment and that this, in turn, would be responsible for the endocrine and metabolic abnormalities and the phenotype of PCOS during the adult life

Factors affecting the reproductive performance of Awassi sheep flocks in north-east of Jordan : an epidemiological study

A prospective cohort study was conducted using 32 randomly selected Awassi sheep flocks to identify factors hypothesized to be associated with the occurrence of pregnancy, twinning and fetal loss between August 2005 and May 2006 in the region of Al-Safawi (northeast of Jordan). Vitamins A and E and selenium concentrations were determined on 448 blood samples. Using the forward selection procedure of the logistic regression module, models with statistically significant risk factors (P < 0.05) were constructed for three outcomes; pregnancy, twinning and fetal loss. Serum vitamin A concentration levels were associated with pregnancy (OR = 2.26, 2.48), twinning (OR = 6.49, 17.74) and fetal loss (OR = 0.13, 0.19). Primiparous ewes were 48% less likely to become pregnant than fourth or higher parity ewes. The likelihood of twinning increased significantly in ewes up to the third parity. Ewes that were fed 700-900 g barley, 250-300 g wheat-bran per head per day and grazed on vegetables residues were 4.15 times more likely to have twins than ewes that were fed 600 g barley and 200 g wheat-bran per head per day. Fetal loss in first and second parity ewes was about 3 times more likely than that in third or higher-parity ewes. Ewes pregnant with twins were about 14 times more likely to have fetal loss than ewes carrying single fetus. Pregnant ewes of the stationary flocks were 37% less likely to have fetal loss than ewes of the semi-nomadic flocks. These results demonstrate that stationary Awassi sheep flocks had higher pregnancy and twinning rates and less pregnancy loss. Supplementation of vitamin A, providing sufficient quantity of dry feed and increasing ram: ewe ratio for primiparous ewes of semi-nomadic flocks is essential to improve Awassi sheep reproductive performance.S. Q. Lafi, A. Q. Talafha, N. Giadinis, E. Kalaitzakis, K. Pourliotis, N. Panousi