Growth Hormone, Somatomedin and Cartilage Sulfation in Failure of Catch-up Growth After Propylthiouracil-Induced Hypothyroidism in the Rat

Mosier, H. David; Dearden, Lyle C.; Jansons, Regina A; Hill, R. R.

doi:10.1210/endo-100-6-1644

Cited by 42 publications

(14 citation statements)

References 2 publications

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“…Meisami (1984). The reduction in levels of T4 and T3 accompanied by increased plasma TSH level in the PTU-treated rats is in agreement with several studies on this subject (Dussault and Walker, 1978;Mosier, Dearden, Janson, & Hill, 1977) including ours (Tamasy et al, 1984). In the latter study we showed completely diminished T4 and greatly increased TSH levels in the postnatal PTU-treated rats as early as day 10 after birth.…”

Section: Discussionsupporting

confidence: 93%

“…A puzzling result, however, is the persistence of low levels of T3 in the hypothyroid rats that exhibited all the signs and symptoms of cretinoid condition, including retardation in somatic growth, delays in development of face, hair, eye opening, ear opening and ear growth, reflexes, and motor development. Presumably this residual T3, which has been found by other investigators as well (Mosier et al, 1977;Takeuchi, Suzuki, & Tsuchiya, 1978), is either an artifact or, if real, is devoid of biological activity. When PTU is withdrawn in the adult rats, T4 levels return to normal within a week (Mosier et al, 1977).…”

Section: Discussionmentioning

confidence: 68%

“…Presumably this residual T3, which has been found by other investigators as well (Mosier et al, 1977;Takeuchi, Suzuki, & Tsuchiya, 1978), is either an artifact or, if real, is devoid of biological activity. When PTU is withdrawn in the adult rats, T4 levels return to normal within a week (Mosier et al, 1977). The fact that in our rehabilitating animals T4 level was still below normal three weeks after withdrawal of PTU, while TSH level was normalized, may be due to the younger age of our animals and changes in the peripheral factors controlling T4 levels.…”

Section: Discussionmentioning

confidence: 68%

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Exploratory behavior, learning ability, and thyroid hormonal responses to stress in female rats rehabilitating from postnatal hypothyroidism

Tamásy

Meisami

et al. 1986

Developmental Psychobiology

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Newborn female Long-Evans rats were divided into groups of normal, hypothyroid [0.1% propylthiouracil (PTU) a reversible antithyroid goitrogen in the litter's drinking water], and hypothyroid rehabilitated (PTU water from birth to day 25, normal water thereafter). The rats were tested for several adaptive behavioral tasks between 40 and 90 days of age. At day 50, serum concentration of TSH and thyroid hormones revealed no detectable amounts of T4 and a 10-fold increase in TSH in the hypothyroid rats. At the same age in the rehabilitated animals, TSH levels were still below normal, a deficit fully normalized by day 90. Normal 50-day-old rats responded to pain stress (electric footshocks) by a significant depression of serum T4 and elevation of T3 levels within 10 min of treatment, whereas the rehabilitated animals exhibited an opposite pattern of response, i.e., an increase in the circulating T4 and a decrease in T3. At 50 days of age, both hypothyroid and rehabilitated rats showed decreased exploratory activity and no habituation in the hole-board test, whereas the locomotor activity of the rehabilitated females was significantly higher than that of the normals. No differences were found in the scores of passive avoidance learning (one trial step-through) among the three groups. Similarly, the rate of acquisition of the active one-way conditioned avoidance response (CAR) of the hypothyroid and rehabilitated rats did not differ significantly from that of the controls. However, the hypothyroid rats required significantly more unconditioned stimuli (footshocks) to acquire CAR and showed longer response latency and less intertrial responses. Although the hypothyroid rats showed no extinction of CAR, the rehabilitated rats were capable of extinction to an extent indistinguishable from normal rats. But compared with the normal animals, the rehabilitated rats showed significantly higher intertrial activity during both the acquisition and extinction phases of CAR.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 68%

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Exploratory behavior, learning ability, and thyroid hormonal responses to stress in female rats rehabilitating from postnatal hypothyroidism

Tamásy

Meisami

et al. 1986

Developmental Psychobiology

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“…They found only a slight increase of SM in thyroxine fed rats, but a mar¬ kedly increased growth rate and proliferation of chondrocytes in the proximal epiphyseal cartilage. Similarly, Mosier et al (1977) did not find any significant fall of SM in propylthiouracil (PTU) treated rats and claimed that PTU induced hypo-' thyroidism resulted in a disturbance of the intrinsic cartilage function. On the other hand no rise in sulphation activity was seen in the cartilage after addition of physiological doses of thyroxine and/or triiodothyronine to incubation media without sera (Holder & Wallis 1977;Gaspard et al 1978;Froeschetal.…”

Section: Discussionmentioning

confidence: 99%

Effect of thyroid function on serum somatomedin activity

Jakóbisiak¹,

Schüllerová

Schreiberová

et al. 1981

Acta Endocrinologica

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To obtain more information about a possible role of somatomedins in mediating the effects of thyroid hormones on the development and function of epiphyseal cartilage, somatomedin activity, measured on the basis of 35S incorporation in embryonic chick cartilage, was studied in thyrotoxic patients before and after treatment with carbimazole or surgery and in a group of patients with primary hypothyroidism. In 29 hyperthyroid patients mean values of somatomedin were 1.29 \ m=+-\ 0.03 sem and differed significantly (P < 0.01) from normals (1.04 \ m=+-\0.03). In 15 carbimazole treated patients and in 5 operated patients with thyrotoxicosis somatomedin levels fell from 1.29 \ m=+-\0.04 to 1.03 \m=+-\0.04 (P < 0.01) when the patients became euthyroid. Correspondingly, somatomedin levels in 12 untreated hypothyroid patients (0.82 \m=+-\0.04) were significantly less than in normals (P < 0.01) and increased from 0.77 \ m=+-\0.09 to 1.14 \m=+-\ 0.13 (P < 0.05) in 4 patients on replacement therapy. In conclusion: somatomedin levels rise when thyroid hormones are present in excess, and fall when these are deficient. This suggests that thyroid hormones are important regulators of somatomedin levels.

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“…(Pediatr Res 20: 261-264,1986) Abbreviation GH, pituitary growth hormone It is suggested that GH secretion is linked to the catch-up growth mechanism by the finding of increased G H levels in sacrificed rat plasma during recovery after transient growth arrest produced by undernutrition (8,9), glucocorticoid treatment (9), or hypothyroidism (10) and of increased pulsatile secretion of GH during recovery after fasting (1 1) and glucocorticoid treatment (12). The stunted head-irradiated rat appears to have a normal pulsatile pattern of plasma GH concentration and normal average period of bursts of GH secretion; however, there is an overall reduction in GH secretion (13).…”

mentioning

confidence: 99%

Dissociation of Catch-Up Growth Control and Neural Control of Growth Hormone Secretion in the Stunted Head-Irradiated Rat

et al. 1986

Pediatr Res

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ABSTRACT. Male Long-Evans rats were irradiated to the head only at 2 days of age; littermates of the same sex were sham-irradiated. At 40 days of age the irradiated rats were divided into two groups, one of which was fasted 48 h and the other fed a normal diet. The irradiated rats, fasted and nonfasted, were cannulated in the superior vena cava at 48 to 50 days of age. Between 54 and 58 days of age the cannulated undisturbed rats had blood samples withdrawn at 15-min intervals over an 18-h period (9 h light and 9 h dark). Body weight and tail length data showed characteristic stunting following irradiation. The superimposed fast caused transient growth retardation; on refeeding, the fasted rats showed a pattern of catch-up growth limited to the irradiated non-fasted body size. Plasma growth hormone (GH) concentration in the fastedrefed rats as compared with the nonfasted irradiated rats showed no change in the average period of the bursts of G H secretion, the numbers of values in ranges of G H concentration, or the area under the curve of the plasma G H concentration versus time. No difference in these parameters was present in light or dark, considered separately. We conclude l ) that the link between the catch-UD control and neural mechanisms controlling GH secretion is impaired as a consequence of the neonatal head-irradiation and 2) that catch-up growth acceleration is not dependent on increased G H secretion. (Pediatr Res 20: [261][262][263][264]1986) Abbreviation GH, pituitary growth hormone It is suggested that GH secretion is linked to the catch-up growth mechanism by the finding of increased G H levels in sacrificed rat plasma during recovery after transient growth arrest produced by undernutrition (8, 9), glucocorticoid treatment (9), or hypothyroidism (10) and of increased pulsatile secretion of GH during recovery after fasting (1 1) and glucocorticoid treatment (12). The stunted head-irradiated rat appears to have a normal pulsatile pattern of plasma GH concentration and normal average period of bursts of GH secretion; however, there is an overall reduction in GH secretion (13). This indicates that either the catch-up growth mechanism is not called into play by the growth stunting of head-irradiation or that the link between the catch-up growth control and the GH releasing mechanism is disturbed as a consequence of effects of irradiation on neural tissue.The present experiments were designed to determine whether GH secretion is increased in the stunted head-irradiated rat while the rat undergoes catch-up growth acceleration after a period of fasting. The design permitted a test of two hypotheses: 1) the link between the catch-up growth control and the GH releasing system is impaired by head irradiation, and 2) catch-up growth acceleration requires increased G H secretion. METHODSThe experiments were canied out on male Long-Evans rats bred from stock obtained from Simonsen Laboratories, Gilroy, CA. The animals were maintained in fresh filtered air, 35-70% relative humidity, at 21.1-23.3" C. The da...

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Growth Hormone, Somatomedin and Cartilage Sulfation in Failure of Catch-up Growth After Propylthiouracil-Induced Hypothyroidism in the Rat

Cited by 42 publications

References 2 publications

Exploratory behavior, learning ability, and thyroid hormonal responses to stress in female rats rehabilitating from postnatal hypothyroidism

Exploratory behavior, learning ability, and thyroid hormonal responses to stress in female rats rehabilitating from postnatal hypothyroidism

Effect of thyroid function on serum somatomedin activity

Dissociation of Catch-Up Growth Control and Neural Control of Growth Hormone Secretion in the Stunted Head-Irradiated Rat

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