Paul Morley
University of Western Ontario
8 Papers
68 Citations
Paul Morley is an academic researcher from University of Western Ontario. The author has contributed to research in topics: Androstenedione & Luteinizing hormone. The author has an hindex of 6, co-authored 8 publications.
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Papers
Insulin enhances luteinizing hormone-stimulated steroidogenesis by porcine theca cells.
TL;DR: It has been shown recently that insulin enhances differentiation of rat, pig, and human granulosa cells, and if insulin also plays a role in the regulation of theca cell steroidogenesis, then insulin action is exerted, at least in part, at a site(s) proximal to cyclic adenosine 3'5'-monophosphate (cAMP) generation.
Fibronectin stimulates growth but not follicle‐stimulating hormone‐dependent differentiation of rat granulosa cells in vitro
TL;DR: It is demonstrated that the principal direct effect of fibronectin‐mediated adhesion on rat granulosa cells is to enhance cell maintenance and growth, while having no generalized action on FSH‐dependent differentiation.
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Ovarian nerve extracts influence androgen production by cultured ovarian thecal cells.
TL;DR: The nervous system has the potential for modulation of follicular steroid biosynthesis via direct innervation of the ovaries, in addition to the well-established indirect mechanism of neural control exerted via the hypothalamic-pituitary system.
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Site at which ovarian nerve extracts inhibit thecal androgen production.
TL;DR: The results indicate that a factor(s) in the SON may play an important role in the regulation of follicular development, since thecal androgens are substrates for granulosa cell estrogen biosynthesis and are also involved in follicular atresia.
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Catecholestrogens inhibit basal and luteinizing hormone-stimulated androgen production by porcine thecal cells.
TL;DR: It is shown that E2 and catecholestrogen actions are exerted at a site(s) distal to cyclic adenosine 3'5' monophosphate (cyclic AMP) generation, because neither agent affected the basal or LH-stimulated accumulation of extracellular cyclicAMP, while causing a significant inhibition of androstenedione production.
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