title: Disruption of the salmon reproductive endocrine axis through prolonged nutritional stress: changes in circulating hormone levels and transcripts for ovarian genes involved in steroidogenesis and apoptosis.
abstract: 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.
authors: School of Aquatic and Fishery Sciences, University of Washington, Seattle, WA 98195, USA.
authors: Yoji
authors: Y
authors: Yamamoto
authors: J
authors: J
authors: Adam Luckenbach
authors: Frederick W
authors: FW
authors: Goetz
authors: Graham
authors: G
authors: Young
authors: Penny
authors: P
authors: Swanson
mesh_terms: D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D017209:Apoptosis; D005260:Female; D029941:Fish Proteins / Q000235:genetics; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D005496:Follicular Atresia / Q000502:physiology; D005508:Food Deprivation; D005786:Gene Expression Regulation; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis* / Q000097:blood; D017684:Oncorhynchus kisutch / Q000033:anatomy & histology / Q000235:genetics / Q000502:physiology*; D006080:Ovarian Follicle / Q000254:growth & development / Q000502:physiology; D010053:Ovary / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D012098:Reproduction / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction; D013312:Stress, Physiological
chemical_list: D029941:Fish Proteins; D012739:Gonadal Steroid Hormones; D012333:RNA, Messenger; D005640:Follicle Stimulating Hormone