Ovarian steroidogenesis pdf

Mechanisms regulating the normal progression of ovarian follicular growth versus onset of atresia in fishes are poorly understood. To gain a better understanding of these processes, we exposed immature female coho salmon (Oncorhynchus kisutch) to prolonged fasting to induce follicular atresia and monitored body growth, development of the ovarian follicles, changes in reproductive hormones, and transcripts for ovarian genes. Prolonged fasting reduced body and ovary weight and increased the appearance of atretic follicles relative to normally fed controls. Endocrine analyses showed that fasting reduced plasma insulin-like growth factor 1 (IGF1), estradiol-17β (E2), and pituitary, but not plasma, levels of follicle-stimulating hormone (FSH). Transcripts for ovarian fsh receptor (fshr) and steroidogenesis-related genes, such as steroidogenic acute regulatory protein (star), 3β-hydroxysteroid dehydrogenase (hsd3b), and P450 aromatase (cyp19a1a) were significantly lower in fasted fish. Ovarian expression of apoptosis-related genes, such as Fas-associated death domain (fadd), caspase 8 (casp8), caspase 3 (casp3), and caspase 9 (casp9) were significantly elevated in fasted fish compared to fed fish, indicating that apoptosis is involved in the process of atresia in this species. Interestingly, some genes such as fadd, casp8, casp3, and hsd3b, were differentially expressed prior to increases in the number of atretic follicles and reductions in hormone levels induced by fasting, and may therefore have potential as early indicators of atresia. Together these results suggest that prolonged nutritional stress may disrupt the reproductive system and induce follicular atresia in part via reductions in ovarian IGF and FSH signaling, and downstream effects on steroidogenesis-related genes and E2 production.

Statistical analysis . Demographic characteristics of the study participants (mean and percentage) are reported separately for each outcome measure because the number of participants varied by outcome. These characteristics are also reported for participants with any ovarian reserve outcome measured. The distribution of day-3 FSH, AFC, and OV are described using the mean ± SD, median and interquartile range (IQR), and range. We computed the within-person geometric mean (GM) of all urinary paraben concentrations (MP, PP, and BP) measured prior to outcomes as a summary exposure measure for each participant. We summarized the distribution of exposures using the median, IQR, and range of urinary paraben concentrations. We assigned urinary concentrations below the LOD with a value equal to the LOD divided by the square root of two ( Hornung and Reed 1990 ). We corrected urinary paraben concentrations for SG using a modification of a previously described formula ( Duty et al. 2005 ):

The majority of patients who are going to ovulate will do so after the first course of therapy. If ovulation does not occur after three courses of therapy, further treatment with Clomid is not recommended and the patient should be reevaluated. If three ovulatory responses occur, but pregnancy has not been achieved, further treatment is not recommended. If menses does not occur after an ovulatory response, the patient should be reevaluated. Long-term cyclic therapy is not recommended beyond a total of about six cycles (see PRECAUTIONS ).

Overview of mathematical H295R steroidogenesis model. The computational model is based on an in vitro steroidogenesis experimental design with two compartments: culture medium and H295R cells ( Figure 1 ). The model consists of steroid transport and metabolic pathways. The transport pathways include cellular uptake of CHOL (steroid precursor) and MET and the import and secretion of 14 adrenal steroids (PREG, HPREG, DHEA, PROG, HPROG, DIONE, T, DCORTICO, CORTICO, ALDO, DCORT, CORT, E 1 , and E 2 ). The metabolic pathway includes conversion of CHOL into the 14 adrenal steroids and inhibition of steroidogenic enzymes by MET. Development of various aspects of the model is described in detail below.

Ovarian steroidogenesis pdf

ovarian steroidogenesis pdf

Overview of mathematical H295R steroidogenesis model. The computational model is based on an in vitro steroidogenesis experimental design with two compartments: culture medium and H295R cells ( Figure 1 ). The model consists of steroid transport and metabolic pathways. The transport pathways include cellular uptake of CHOL (steroid precursor) and MET and the import and secretion of 14 adrenal steroids (PREG, HPREG, DHEA, PROG, HPROG, DIONE, T, DCORTICO, CORTICO, ALDO, DCORT, CORT, E 1 , and E 2 ). The metabolic pathway includes conversion of CHOL into the 14 adrenal steroids and inhibition of steroidogenic enzymes by MET. Development of various aspects of the model is described in detail below.

Media:

ovarian steroidogenesis pdfovarian steroidogenesis pdfovarian steroidogenesis pdfovarian steroidogenesis pdfovarian steroidogenesis pdf

http://buy-steroids.org