Oestrogen regulates several hypothalamic and pituitary hormones, which in turn control ovarian functions. Oestrogen and its metabolites, such as catecholoestrogens, also have direct effects within the ovary. This review examines the roles of oestrogen in regulating ovarian folliculogenesis, ovulation and corpus luteum formation. Oestrogen promotes follicular development, which culminates in ovulation, by potentiating follicular development, granulosa cell expression of gonadotrophin receptors, steroidogenesis, and gap junction formation by granulosa cells, and by inhibiting granulosa cell apoptosis. In addition, oestrogen may be needed for corpus luteum formation and maintenance. Studies on mutant mice that either lack one or both of the known oestrogen receptors or are unable to synthesize oestrogen support some but not all of these prior inferences of the roles of oestrogen within the ovary. Although these transgenic mice have proved useful in determining some of the intraovarian actions of oestrogen, they present confounding problems, including hormonal imbalances, that hinder interpretation. Transgenic mice with conditional or tissue-directed mutations in their oestrogen receptors are needed to dissect the ovarian actions of oestrogen further. In addition, microarray technologies, combined with specific hormone treatment regimens are likely to provide an attractive, alternative approach to using mutant mice in clarifying the direct actions of oestrogen in the ovaries of other species.
Coronary arteries and arterioles in the left and right ventricles from normal and hyperthyroid rats were examined histochemically to determine and to compare their metabolic activities. The test animals were made hyperthyroid by administration of desiccated thyroid for 8–10 weeks. Using histochemical techniques, selected enzymes and components of key metabolic pathways were examined. These pathways included an evaluation of aerobic (oxidative phosphorylation, Kreb’s cycle and respiratory chain) and anaerobic metabolic capacity, hexose-monophosphate shunt activity, amounts of deoxyribonucleic and ribonucleic acids present and activity of β-oxidation of fatty acids. Our results indicate that normal coronary arteriolar metabolism is predominantly aerobic. The findings also suggest a reduction in aerobic metabolism with an accompanying increase in anaerobic potential in the hyperthyroid coronary arterioles. Thus, during thyrotoxicosis, the coronary arterioles may partially shift from aerobic to anaerobic metabolism. Moreover, in both the normal and thyrotoxic rat heart, the coronary microvasculature appears quite stable with little cell proliferation. In contrast, both the control and hyperthyroid rat coronary arteries appear to utilize primarily anaerobic pathways, while the control and hyperthyroid myocardium seem highly dependent upon aerobic metabolism. The tremendous reduction in glucose-6-phosphate dehydrogenase activity in hyperthyroid, when compared to normal coronary arteries and some larger arterioles, implies a reduced capacity for nucleic acid and protein synthesis in the test animals.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.