Influence of Thyroidal Status on Pituitary Content of Thyrotropin β- and α-Subunit, Growth Hormone, and Prolactin Messenger Ribonucleic Acids

Cj, Mirell; Yanagisawa, Masashi; R, Lau; Ae, Pekary; Ww, Chin; Jm, Hershman

doi:10.1210/mend-1-6-408

Cited by 17 publications

(4 citation statements)

References 19 publications

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“…Thyroid hormone has long been known to be a potent inducer of GH gene expression (29,38,39). TRβ2 is expressed in the somatotroph (28), and there is evidence from studies in pituitary cell lines that TRβ2 is the major isoform mediating the stimulatory effect of thyroid hormone on GH gene expression (40).…”

Section: Discussionmentioning

confidence: 99%

Divergent roles for thyroid hormone receptor β isoforms in the endocrine axis and auditory system

Abel¹,

Boers²,

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Divergent roles for thyroid hormone receptor β isoforms in the endocrine axis and auditory system

Abel¹,

Boers²,

et al. 1999

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“…At the molecular level, this accords with the induction of increased levels of TSH mRNA in the anterior pituitary by PTU and a concomitant fall in growth hormone mRNA (120,121). The profound effect on cytoplasmic TSH levels affected both TSH a and 03 subunits in a dose-and time-dependent manner (117,120,122), but the increases were relatively greater in TSH P than in the a subunit. T3 replacement reversed these specific subunit changes (117).…”

Section: Rodent Thyroid Cancer Studiesmentioning

confidence: 53%

Recent developments in the investigation of thyroid regulation and thyroid carcinogenesis.

Hard

1998

Environ Health Perspect

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This review covers new mechanistic information spanning the past 10 years relevant to normal and abnormal thyroid growth and function that may assist in the risk assessment of chemicals inducing thyroid follicular cell neoplasia. Recent studies have shown that thyroid regulation occurs via a complex interactive network mediated through several different messenger systems. Increased thyroid-stimulating hormone (TSH) levels activate the signal transduction pathways to stimulate growth and differentiation of the follicular cell. The important role of TSH in growth as well as in function helps to explain how disruptions in the thyroid-pituitary axis may influence thyroid neoplasia in rodents. New investigations that couple mechanistic studies with information from animal cancer bioassays (e. g., sulfamethazine studies) confirm the linkage between prolonged disruption of the thyroid-pituitary axis and thyroid neoplasia. New initiation/promotion studies in rodents also support the concept that chronic stimulation of the thyroid induced by goitrogens can result in thyroid tumors. Some of these studies confirm previous suggestions regarding the importance of chemically induced thyroid peroxidase inhibition and the inhibition of 3,3',5, 5'-tetraiodothyronine (T4, thyroxine) deiodinases on disruption of the thyroid-pituitary axis leading to thyroid neoplasia. Some comparative physiologic and mechanistic data highlight certain differences between rodents and humans that could be expected to confer an increased vulnerability of rodents to chronic hypersecretion of TSH. New data from epidemiologic and molecular genetic studies in humans contribute further to an understanding of thyroid neoplasia. Acute exposure to ionizing radiation, especially in childhood, remains the only verified cause of thyroid carcinogenesis in humans. Iodine deficiency studies as a whole remain inconclusive, even though several new studies in humans examine the role of dietary iodine deficiency in thyroid cancer. Specific alterations in gene expression have been identified in human thyroid neoplasia, linked to tumor phenotype, and thus oncogene activation and tumor-suppressor gene inactivation may also be factors in the development and progression of thyroid cancer in humans. An analysis by the U.S. EPA Risk Assessment Forum, prepared as a draft report in 1988 and completed in 1997, focused on the use of a threshold for risk assessment of thyroid follicular tumors. New studies, involving several chemicals, provide further support that there will be no antithyroid activity until critical intracellular concentrations are reached. Thus, for chemically induced thyroid neoplasia linked to disruptions in the thyroid-pituitary axis, a practical threshold for thyroid cancer would be expected. More information on thyroid autoregulation, the role of oncogene mutations and growth factors, and studies directly linking persistently high TSH levels with the sequential cellular development of thyroid follicular cell neoplasia would provide further confirmation.

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“…THs (T 4 and T 3 ) exert a negative feedback effect on the release of pituitary TSH and on the activity of hypothalamic TRH neurons 18, 19, 124 . Although it is clear that TH regulates the expression of TSH 153–155 and TRH 18, 123, 124, 156 in a negative feedback manner, it is also clear that the functional characteristics of negative feedback must include more than simply the regulation of the gene encoding the secreted protein/peptide. In addition, fasting suppresses the activity of TRH neurons by a neural mechanism that may involve leptin 157, 158 .…”

Section: Thyroid Hormone Insufficiency—to What Extent Can Compensatormentioning

confidence: 99%

Collision of Basic and Applied Approaches to Risk Assessment of Thyroid Toxicants

THOMAS ZOELLER

2006

Annals of the New York Academy of Sciences

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Thyroid hormone (TH) is essential for normal brain development; therefore, any environmental chemical that interferes sufficiently with thyroid function, TH metabolism, or TH action may exert adverse effects on brain development. Important known differences in aspects of thyroid endocrinology between the fetus, infant, and adult allow us to identify age-dependent vulnerabilities to thyroid toxicants with some confidence. These differences include the size of the hormone pool stored in the thyroid gland at different ages as well as the age-dependent sensitivity to mild TH insufficiency. Several recent studies that describe risk assessments of the environmental contaminant, ammonium perchlorate, provide good examples of conclusions based on the selective consideration of these known aspects of the thyroid system. Specifically, authors who consider age-dependent differences in thyroid endocrinology suggest that safe levels of perchlorate should be set at relatively low levels (low parts per billion). In contrast, authors who do not consider these known age-dependent differences in thyroid endocrinology recommend safe levels of perchlorate at high (hundreds) parts per billion to parts per million. Emerging evidence indicates that a variety of high production volume chemicals can directly interact with the TH receptor. As testing paradigms are designed by regulatory agencies, these age-dependent differences in thyroid endocrinology must be considered.

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Influence of Thyroidal Status on Pituitary Content of Thyrotropin β- and α-Subunit, Growth Hormone, and Prolactin Messenger Ribonucleic Acids

Cited by 17 publications

References 19 publications

Divergent roles for thyroid hormone receptor β isoforms in the endocrine axis and auditory system

Divergent roles for thyroid hormone receptor β isoforms in the endocrine axis and auditory system

Recent developments in the investigation of thyroid regulation and thyroid carcinogenesis.

Collision of Basic and Applied Approaches to Risk Assessment of Thyroid Toxicants

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