Growth and Growth Hormone. III. Growth Hormone Release in Children with Primary Hypothyroidism and Thyrotoxicosis<sup>1</sup>

Katz, Harvey P.; Youlton, R; Kaplan, Selna L.; Grumbach, Melvin M.

doi:10.1210/jcem-29-3-346

Cited by 88 publications

(30 citation statements)

References 16 publications

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“…Spontaneous nocturnal secretion of GH is low in hypothyroidism and hyperthyroidism (27,28). The rate and the amount of GH released are reduced in adolescents with untreated thyrotoxicosis compared with normal controls.…”

Section: Hypothyroidism and Thyrotoxicosismentioning

confidence: 98%

The multiple effects of thyroid disorders on bone and mineral metabolism

Cardoso

Maciel

Paula

2014

Arq Bras Endocrinol Metab

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Differently from most hormones, which commonly are specialized molecules able to influence other cells, tissues and systems, thyroid hormones (TH) are pleiotropic peptides, whose primordial function is difficult to identify. The complex action of TH on human economy can be easily witnessed by examining the diverse consequences of TH excess and deficiency during development and after maturity. In particular, different manifestations in bone modeling and remodeling reflect the circumstantial consequences of thyroid disturbances, which are age dependent. While hyperthyroidism during childhood enhances bone mineralization and accelerates epiphyseal maturation, in adults it induces bone loss by predominant activation of osteoclast activity. Furthermore, the syndrome of TH resistance is a multifaceted condition in which different sites exhibit signs of hormone excess or deficiency depending on the configuration of the TH receptor isoform. The investigation of the impact of TH resistance on the skeleton still remains to be elucidated. We present here a thorough review of the action of TH on bone and of the impact of thyroid disorders, including hyper-and hypothyroidism and the syndrome of TH resistance, on the skeleton. Arq Bras Endocrinol Metab. 2014;58(5):452-63 Keywords Thyroid hormones; osteoporosis; thyrotoxicosis; hypothyroidism; thyroid hormone resistance ReSumoDiferentemente da maioria dos hormônios, que usualmente são moléculas especializadas capazes de influenciar outras células, tecidos e sistemas, os hormônios da tireoide (HT) são peptídeos pleiotrópicos, cuja função primordial é difícil de identificar. A ação complexa dos HT na fisiologia humana pode ser facilmente reconhecida ao observar as diversas consequências do excesso e da deficiência de HT durante e após o pleno desenvolvimento. Em particular as diferentes manifestações na modelação e remodelação óssea refletem que as consequências esqueléticas das disfunções tireoidianas dependem das circunstâncias e variam com a idade. Enquanto o hipertireoidismo durante a infância aumenta a mineralização óssea e acelera a maturação epifisária, em adultos induz a perda óssea pela ativação predominante da ação osteoclástica. Além disso, a síndrome de resistência ao HT é uma condição multifacetada na qual diferentes tecidos apresentam sinais de excesso ou deficiência hormonal, dependendo da predominância da expressão das diversas isoformas do receptor de HT. O impacto da resistência ao HT sobre o esqueleto ainda é motivo de investigação. Apresentamos aqui uma revisão abrangente sobre as ações ósseas dos HT e o impacto no esqueleto dos distúrbios da tireoide, incluindo hipo e hipertireoidismo e síndrome de resistência ao HT. Arq Bras Endocrinol Metab.

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Section: Hypothyroidism and Thyrotoxicosismentioning

confidence: 98%

The multiple effects of thyroid disorders on bone and mineral metabolism

Cardoso

Maciel

Paula

2014

Arq Bras Endocrinol Metab

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“…In part, thyroid hormone may exert these effects by stimulating the formation of growth hormone (GH).1 Thus, the levels of radioimmunoassayable pituitary and circulating GH are extremely low in hypothyroid animals (2), and studies ofhypothyroid children indicate that plasma GH response to insulin administration is blunted. The serum GH value, however, does not appear to be as uniformly depressed in hypothyroid patients as in hypothyroid rats (3). Recently, Hervas et al (4) have shown by use of a sensitive radioimmunoassay that the circulating levels of pituitary GH IAbbreviations used in this paper: GH, growth hormone; a-GPD, a-glycerophosphate dehydrogenase; k, plasma concentration yielding half-nuclear occupancy; M, binding capacity; ME, malic enzyme; q, fractional nuclear occupancy; R, responsivity or rate of induction; T3, triiodothyronine.…”

Section: Introductionmentioning

confidence: 73%

“…These doses were selected because they are known to saturate the nuclear sites for the period of the experiment. At designated intervals (3,6,12,16,20, and 24 h) after the injection, rats were killed and pituitary GH content was measured. As shown in Fig.…”

Section: Determination Of Basic Parametersmentioning

confidence: 99%

Relationship between the Accumulation of Pituitary Growth Hormone and Nuclear Occupancy by Triiodothyronine in the Rat

Schwartz¹,

Oppenheimer²

1978

J. Clin. Invest.

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A B S T R A C T Studies were undertaken in hypothyroid rats in an effort to define the kinetics of growth hormone (GH) accumulation in response to i.v. pulse injections of triiodothyronine (T3) and to calculate the relationship between nuclear occupancy by T3 and the instantaneous rate of accumulation of pituitary GH. Results were contrasted to the findings in previous studies of the induction of hepatic mitochondrial a-glycerophosphate dehydrogenase (a-GPD) and malic enzyme (ME) by T3. The dose of T3 required to achieve halfmaximal accumulation of GH in 24 h was 0.6 ,ug/100 g body wt, a value 15-fold less than the half-maximal dose for a-GPD and ME induction at a comparable time after injection. Although significant increases in pituitary GH were evident as early as 3 h after injection of maximally effective doses of T3, the rate of increase became linear only 12 h after injection. After achievement of peak values, the pituitary content of GH decayed with a similar terminal tl2 of3.9 days and 4.1 days in two groups of animals injected with a single dose of 1.0 and 50 ,ug TJ100 g body wt, respectively. In vivo isotopic displacement studies carried out at the equilibrium time point indicated that the pituitary nuclear binding capacity was 5.5 ng T3/g tissue and that the plasma concentration at which one-half of the nuclear sites are occupied is 1.0 ng/ml. Nuclear occupancy as a function of time was calculated from the estimated plasma T3 concentration after injection of the dose and the half-occupancy plasma concentration. These data were then analyzed by application of the mathematical model previously developed to ascertain the relation- 1020 ship between nuclear occupancy and the rate of hepatic enzyme induction. Results indicated that the pituitary nuclear occupancy-response relationship was generally linear, in marked contrast to the highly amplified relationship between nuclear occupancy and the response of ME and a-GPD to T3 in the liver. In supplementary experiments, euthyroid rats received daily injections of 200 ,ug of T3 for 7 days to keep nuclear sites nearly saturated for the duration of the experiment. No significant increase in the pituitary GH content above euthyroid base-line levels was noted. This also contrasts with the marked increase above euthyroid levels in a-GPD and ME observed in previous studies. Our findings suggest the existence of major differences between the specific mechanisms which lead to the induction of pituitary GH and the hepatic enzymes by T3.

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“…However, various reports including data in humans indicated that THs may also exert inhibitory effects on GH. Children with thyrotoxicosis have normal GH responses to provocative stimuli (Katz et al 1969) but diminished 24-h GH secretion (Finkelstein et al 1974). In hyperthyroid patients, sleep-related GH release is decreased (Sazaki et al 1985).…”

Section: Introductionmentioning

confidence: 99%

Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

Rousseau¹,

Belle²,

Sbaihi³

et al. 2002

Journal of Endocrinology

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The regulation of growth hormone (GH) by thyroid hormones (THs) has been shown to present species variation. We investigated the regulation of GH in the eel, a representative of an ancient group of teleosts. In vivo administration of triiodothyronine (T 3 ) or thyroxine (T 4 ) significantly reduced pituitary and serum GH levels, as measured by homologous RIA. In order to investigate the ability of THs to regulate GH production directly at the pituitary level, we used a long-term, serum-free primary culture of eel pituitary cells. Both T 3 and T 4 inhibited GH release in a concentration-dependent manner, producing up to 50% inhibition at 10 nM, with an ED 50 of <0·2 nM, within the range of their physiological circulating levels. Other hormones also acting via the nuclear receptor superfamily, such as sex steroids (testosterone, estradiol and progesterone) and corticosteroid (cortisol), had no effect on GH release in vitro, underlining the specificity of the regulatory effect of THs on GH. Measurement of both GH release and cellular content for calculation of GH production in vitro indicated that THs not only inhibited GH release but also GH synthesis. Dot-blot assay of GH messenger RNA (mRNA) using an homologous eel cDNA probe showed a decrease in GH mRNA levels in cells cultured in the presence of T 3 , as compared with control cells. This demonstrated that the inhibition of T 3 on GH synthesis was mediated by a decrease in GH mRNA steady state levels. In conclusion, we demonstrate inhibitory regulation of eel GH synthesis and release by THs, exerted directly at the pituitary level. These data contrast with the rat, where THs are known to have a stimulatory effect and suggest that the pattern observed here in an early vertebrate and also found in birds, reptiles and some mammals including humans, may represent an ancestral and more generalized vertebrate pattern of TH regulation of pituitary GH.

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Growth and Growth Hormone. III. Growth Hormone Release in Children with Primary Hypothyroidism and Thyrotoxicosis¹

Cited by 88 publications

References 16 publications

The multiple effects of thyroid disorders on bone and mineral metabolism

The multiple effects of thyroid disorders on bone and mineral metabolism

Relationship between the Accumulation of Pituitary Growth Hormone and Nuclear Occupancy by Triiodothyronine in the Rat

Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

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Growth and Growth Hormone. III. Growth Hormone Release in Children with Primary Hypothyroidism and Thyrotoxicosis1

Cited by 88 publications

References 16 publications

The multiple effects of thyroid disorders on bone and mineral metabolism

The multiple effects of thyroid disorders on bone and mineral metabolism

Relationship between the Accumulation of Pituitary Growth Hormone and Nuclear Occupancy by Triiodothyronine in the Rat

Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

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Growth and Growth Hormone. III. Growth Hormone Release in Children with Primary Hypothyroidism and Thyrotoxicosis¹