Relationship of liver and skeletal muscle IGF-1 mRNA to plasma GH profile, production of IGF-1 by liver, plasma IGF-1 concentrations, and growth rates of cattle

Growth hormone (GH), insulin-like growth factor-1 (IGF-1), and thyroid hormone (T3 and T4) concentrations in blood plasma of 18 crossbred cattle (six bulls, six steers, and six heifers) were measured over an 8-hr period. One week later at slaughter, IGF-1 production by liver slices and IGF-1 mRNA concentrations in skeletal muscle and liver were measured. Bulls had higher (P less than 0.05) mean plasma GH and GH peak amplitudes (P less than 0.01) than heifers, and values for steers were intermediate between bulls and heifers. Baseline GH concentrations and number of GH peaks were not significantly different for the three groups. Bulls had 1.6-fold (P less than 0.01) and 3.0-fold (P less than 0.01) greater liver IGF-1 mRNA concentrations than steers or heifers, respectively, whereas the steers had 1.8-fold (P less than 0.05) greater IGF-1 mRNA in liver than heifers. Production of IGF-1 by liver slices was greater (P less than 0.05) in bulls than steers or heifers. Bulls had 1.3-fold greater plasma IGF-1 than steers (P less than 0.01), whereas steers had 1.8-fold greater plasma IGF-1 than heifers (P less than 0.01). There were no significant differences in concentrations of skeletal muscle IGF-1 mRNA between the three groups of animals. Liver IGF-1 mRNA, liver IGF-1 production, and plasma IGF-1 were all significantly correlated with gain and mean GH peak amplitude, but not with GH baseline, GH peak frequency, or concentrations of T3 and T4. Concentrations if IGF-1 mRNA in skeletal muscle were not correlated to gain or any parameter of the GH profile. Plasma concentrations of T3 were significantly (P less than 0.05) negatively correlated to plasma GH baseline concentrations. Muscle IGF-1 mRNA concentration was negatively related to plasma T4 and T3. The results of this study suggest that the cascade of events starting with secretion of GH from the pituitary, expression of liver IGF-1 mRNA, and secretion of IGF-1 by the liver are important phenomena for growth of cattle.     

A decreased capacity of hepatic growth hormone (GH) receptors and failure of thyrotrophin-releasing hormone to stimulate the peripheral conversion of thyroxine into triiodothyronine in sex-linked dwarf broiler hens

The effect of two different doses of thyrotrophic releasing hormone (TRH) upon the plasma levels of growth (GH) and thyroid hormones in both sex-linked dwarf (dw) and normal (Dw) broiler hens was determined. In normal hens, 1.5 and 24 microg TRH/kg increased the GH plasma concentrations after 15 min. Plasma concentrations of T3 increased significantly 1 h after TRH injection, whereas T4 concentration decreased after 2 following injection of 24 microg/kg TRH. In dwarf hens both doses of TRH increased the plasma concentrations of GH and the GH response lasted longer. However, TRH was ineffective in raising T3 and T4 levels. Saline-injected dwarf birds showed no differences in plasma T4 and T3 levels in comparison with normal hens. A smaller number of hepatic cGH receptors was found in dwarf hens, whereas the affinity of the hepatic GH receptor was not influenced by the genotype. It is concluded that the sex-linked dwarf broiler hen is unable to respond to a TRH-induced GH stimulus probably because of a deficiency in hepatic GH receptors resulting in a failure to stimulate the T4 to T3 converting activity.     

Abnormalities of the thyroid hormone negative feedback regulation of TSH secretion in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) are characterized by several neuroendocrine abnormalities including a chronic hypersecretion of thyrotropin (TSH) of unknown etiology. We hypothesized that the inappropriately high TSH secretion in SHR may be the result of an impaired thyroid hormone negative feedback regulation of hypothalamic thyrotropin-releasing hormone (TRH) and/or pituitary TSH production. To test this hypothesis, SHR or their normotensive Wistar-Kyoto (WKY) controls were treated with either methimazole (0.02% in drinking water) to induce hypothyroidism or administered L-thyroxine (T4) at a dose of 0.8 or 2.0 micrograms/100 g body weight/day to induce hyperthyroidism. All treatments were continued for 14 days after which animals were killed under low stress conditions. TSH concentrations in plasma and anterior pituitary tissue were 2-fold higher (P less than 0.01) in euthyroid SHR compared to WKY control rats while thyroid hormone (T3 and T4) levels were in the normal range. Hypothyroidism induced by either methimazole or thyroidectomy caused a significant (P less than 0.01) rise of plasma TSH levels in both WKY and SHR rats. However, relative to the TSH concentrations in control animals, the increase of plasma TSH in SHR was significantly blunted (P less than 0.01) in comparison to the WKY group. Hypothyroidism caused a significant depletion of TRH in stalk-median eminence (SME) tissue in both groups of rats. However, no differences between SHR and WKY rats were observed. The administration of thyroid hormone caused a dose dependent suppression of plasma TSH levels in both strains of rats. However, at both doses tested plasma TSH concentrations in SHR rats were significantly less suppressed (P less than 0.05) than those in WKY animals. Under in vitro conditions basal and potassium induced TRH release from SMEs derived from SHR was significantly (P less than 0.05) higher than that from WKY rats, whether expressed in absolute terms or as percent of content. These findings suggest that the thyroid hormone negative feedback regulation of TSH secretion may be impaired in SHR rats. Our data do not allow conclusions as to whether defects in the regulation of TSH production are located exclusively at the hypothalamic level. Since the overproduction of hypothalamic TRH and hypophysial TSH should lead to an increased thyroid hormone biosynthesis other defects in the hypothalamus-pituitary-thyroid-axis may contribute to the abnormal regulation of TSH secretion in SHR rats.     

Comparison between constant-protein, calorie-restricted and protein-restricted, calorie-restricted diets on growth, in vitro lipogenesis and plasma growth hormone, thyroxine, triiodothyronine and somatomedin-C (Sm-C) of young chickens

1. We studied the effects of calorie-restricted, constant-protein and calorie-restricted, protein-restricted diets on growth and in vitro metabolism of male chickens from select (Cobb Line 500) and byproduct (Cobb female line) lines of broiler chickens. 2. Chickens consumed 40, 60, 80 or 100% of a prescribed formula for dietary energy (body weight in g0.70 x 16.7 kJ) in the presence of set (CEP) or varied dietary protein (VEP). 3. Chickens fed VEP were heavier (P less than 0.05) at all energy intakes than chickens fed CEP. Slope analysis of data for in vitro lipogenesis showed a significant difference between the two treatment series. 4. Plasma growth hormone was inversely related (P less than 0.05) to Sm-C. Growth hormone levels were greater in chickens on a low plane of energy nutrition (40%) than on the maximum plane (100%). 5. Plasma Sm-C levels (pooled across energy series) were greater in the select than in the byproduct line. There were no differences in plasma T3 between the two lines. There was a significant increase (P less than 0.05) in T3 and a decrease in the T4/T3 ratio accompanying an increase in dietary energy. 6. Restricting dietary carbohydrate and protein compromises anabolic processes more than restricting carbohydrate alone.     

Thyrotropin-releasing hormone (TRH) is not thyrotropic but somatotropic in fed and starved adult chickens.

Adult fed and starved Warren chickens, 2 yr of age, and approaching the end of the second laying year, were injected iv with 1 of the following products: 10 micrograms of thyrotropin releasing hormone (TRH); 100 micrograms of bovine thyrotropin (bTSH); 100 micrograms of ovine growth hormone (oGH); saline. The influence on plasma concentrations of thyroxine (T4), triiodothyronine (T3) or chicken GH (cGH) were followed. Prior to injection, it was clear from the control values that starvation for 3 d decreased plasma levels of T3 and increased cGH, whereas 7 d of fasting increased T4 and cGH. The plasma levels of cGH were elevated greater than 10-fold at 15 min following the TRH challenge in food-deprived chickens compared to a less than 4-fold increase in normal fed hens. This increase was followed by a rise in T3 after 1 h, which was also more pronounced in the starved animals, whereas T4 decreased or remained unaffected. Increases in T4 can, however, be obtained with 100 micrograms TSH in normal fed (2-fold) or starved animals (greater than 3-fold). Following injection of 100 micrograms oGH, a significant increase in T3 levels was observed which in fed animals was already present at 30 min, but the higher levels persisted for 1 and 2 h in fed and starved hens. At the same time, a decrease in T4 was observed in both groups of GH-treated chickens. It is concluded that TRH at the dose used is not thyrotropic but has a somatotropic effect and is responsible for the peripheral conversion of T4 into T3.     

Effects of triiodothyronine treatments on body and organ growth and the development of immune function in dwarf chickens

The effects of triiodothyronine (T3) treatments on general body growth, long bone growth, primary lymphoid organ development, antibody production, and serum growth hormone (GH) and thyroid hormone levels were examined in two dwarf strains (sex-linked dwarf--SLD, and autosomal dwarf--ADW) and in a normal-growing control strain (K) of White Leghorn chickens. One-day-old male chicks from each of these strains were assigned to either an untreated control group or to one of the groups receiving a T3 supplement ranging from 0.01 to 1.0 ppm. General body growth and long bone growth were significantly (P less than 0.05) stimulated only within the SLD strain by the intermediate T3 dosages. The 1.0-ppm T3 dosage level resulted in depressed body weights within both the K and ADW strains but produced no significant changes within the SLD strain. Thymic growth was significantly stimulated due to treatments of 0.1 ppm T3 in the SLD strain (P less than 0.05) and 1.0 ppm T3 in both the SLD and ADW strains (P less than 0.001 and P less than 0.05, respectively). Bursal growth was significantly depressed (P less than 0.05) at all T3 dosage levels within the SLD strain while 0.01 and 0.1-ppm T3 treatments resulted in significant bursal growth stimulation in the K and ADW strains, respectively. Concomitant with the depressed bursal growth, antibody production was significantly depressed (P less than 0.05) within the SLD strain at the 1.0-ppm T3 dosage level. Antibody production was not significantly affected by any of the T3 treatments within the control K or ADW strains. Serum T3 levels were significantly increased in all strains by the T3 supplementation but thyroxine (T4) serum levels were affected only within the SLD strain. The 0.01-ppm T3 treatment resulted in a significant increase (P less than 0.05) in serum T4 levels within this strain and treatment group. The only increase (P less than 0.05) in GH levels due to T3 treatments occurred within the same SLD treatment group. The higher T3 treatments resulted in serum GH levels being severely depressed (P less than 0.01) in all strains.     

Increase of IGF I binding to erythrocyte receptors during the TRH-test: correlation between IGF I binding and thyroid hormone values

The effects of TRH on insulin-like growth factor I receptors were investigated on erythrocytes from 7 GH-deficient children having plasma GH levels less than 10 ng/ml during two provocation tests. Intravenous injection of synthetic TRH (0.2 mg/m2) was followed by a marked increase of IGF I binding on erythrocytes, from 3.9% +/- 0.3% to 5.9% +/- 0.3% (P less than 0.005) after 1 hour and 7.3% +/- 0.4% (P less than 0.005) after 2 hours. The IGF I binding variations were due to an increase in both the receptor affinity and the number of sites. The levels of plasma GH, IGF I, T3, T4, free T4, TSH and prolactin having been determined during the TRH test at 0, 1 hour, and 2 hours after the injection, the increase in the IGF I binding to erythrocytes at the same time correlated with the rise of thyroid hormones: triiodothyronine T3 (P less than 0.001) and thyroxine T4 (P less than 0.005) and not with the level of the other hormones. These findings suggest that thyroid hormones play a role in the regulation of insulin-like growth factor I receptors.     

The thyroid reserve in children with chronic lymphocytic thyroiditis revealed by the thyrotropin-releasing hormone and thyroid-stimulating hormone tests

Serum thyroid hormone and TSH concentrations were measured before and after the administration of TRH (10 micrograms/kg body weight) and bovine TSH (10 IU) in 14 children with chronic lymphocytic thyroiditis. The TRH test showed that the responsiveness of TSH was positively correlated with the basal TSH (P less than 0.001) and inversely with the increase in serum thyroid hormones, for delta T3 (P less than 0.05) and for delta T4 (P less than 0.001). Overall, the patients had significantly lower mean values for basal T4, but not for T3. The TSH test revealed that the delta T3 was positively correlated with delta T4 (P less than 0.05). delta T3 after TSH administration was positively correlated with it after TRH (P less than 0.05). The patients were divided into three groups on the basis of their peak TSH values after TRH administration. In Group 1 (peak value below 40 microU/ml; N = 5); T3 increased significantly after TRH and TSH administrations (P less than 0.05 and P less than 0.025, respectively). In addition, delta T4 was significant after TSH administration. In Group 2 (peak TSH above 40 and less than 100 microU/ml; N = 6); only delta T3 after TRH was significant (P less than 0.05). In Group 3 (peak TSH above 100 microU/ml; N = 3); the response of thyroid hormones was blunted. Thus, the thyroid hormone responses to endogenous TSH coincided with that to exogenous TSH, and the exaggerated TSH response to TRH indicates decreased thyroid reserve.     

Thyroid hormone action on ACTH secretion

Thyroid hormone effects on pituitary ACTH have not been well established. Adult male Sprague-Dawley rats were rendered hypo- and hyperthyroid while undergoing treatment with 6-Propylthiouracil (PTU) and L-Thyroxine (T4). At the time of decapitation, plasma values for T4 (micrograms/100 ml) were 3.9 +/- 0.4 in the control, 17.3 +/- 2.2 in the T4 and less than 2 in the PTU treated group; plasma T3 and TSH confirmed hyper- and hypothyroidism in the T4 and PTU treated groups respectively. Plasma immunoassayable ACTH and corticosterone were significantly increased in hyperthyroid and decreased in the PTU treated animals. Pituitaries were removed and incubated in DMEM. After 3 h incubation, ACTH content and secretion to the medium were significantly lower in the PTU group. As expected, pituitary TSH content and secretion were decreased in the T4 treated animals. These data indicate that thyroid hormones influence pituitary-adrenal function by increasing ACTH secretion and consequently corticosterone production.     

Effects of TRH on circulating growth hormone, prolactin and triiodothyronine levels in the bovine.

The effects of administration of synthetic thyrotropin-releasing hormone (TRH) on circulating growth hormone (GH), PROLACTIN (PRL) and triiodothyronine (T3) levels of lactating dairy cows, non-lactating dairy heifers, and beef cows were studied. Intravenous administration of 0.1, 1, and 5 microgram of TRH per kg of body weight (bw) elevated plasma GH and PRL levels of lactating cows within 5 min. The plasma GH and PRL levels increased in proportion to the dose of TRH and reached a peak 10 to 30 min after TRH injection. Intravenous administration of 1 microgram of TRH per kg of bw to 7 non-lactating heifers, 14 lactating dairy cows, and 5 non-lactating beef cows elevated plasma GH level to peak values after 15 min, the increase rates being 6.9, 5.6, and 3.8 times as high as those in the pretreatment levels. The mean maximum vale was also in that order. Plasma T3 levels of non lactating dairy heifers at pre- and post-injection of TRH were significantly higher than those of lactating cows. The peak values of plasma PRL were obtained between 5 to 30 min after TRH administration. The increase rates of lactating dairy cows, heifers, and beef cows were 19.2, 13.9, and 20.9 times as high as those in the pretreatment. In contrast to GH and T3, plasma PRL levels of both pre- and post-injection with TRH in lactating cows and heifers were significantly higher in May than in October, though the increase rates were similar. Plasma PRL levels of lactating dairy cows at pre- and post-injection with TRH were significantly higher than those of non-lactating heifers. Subcutaneous administration of TRH was also effective to increase plasma TH, rl, and T3 levels in lactating cows. No significant change of GH or PRL response to TRH was observed after a short-term pretreatment of thyroid hormones.     

The pituitary-thyroid axis in acromegaly

The pituitary-thyroid axis of 12 acromegalic patients was evaluated by measurement of the serum concentrations (total and free) of thyroxine (T4), triiodothyronine (T3) and reverse T3 (rT3) and thyrotropin (TSH), growth hormone (GH) and prolactin (PRL) before and after iv stimulation with thyrotropin releasing hormone (TRH). Using an ultrasensitive method of TSH measurement (IRMA) basal serum TSH levels of the patients (0.76, 0.07-1.90 mIU/l) were found slightly, but significantly (P less than 0.01), lower than in 40 healthy controls (1.40, 0.41-2.50 mIU/l). The total T4 levels (TT4) were also reduced (84, 69-106 nmol/l vs 100, 72-156 nmol/l, P less than 0.01) and significantly correlated (P less than 0.02, R = 0.69) to the TSH response to TRH, suggesting a slight central hypothyroidism. The acromegalics had, however, normal serum levels of TT3 (1.79, 1.23-2.52 nmol/l vs 1.74, 0.78-2.84 nmol/l, P greater than 0.10), but significantly decreased levels of TrT3 (0.173, 0.077-0.430 nmol/l vs 0.368, 0.154-0.584 nmol/l, P less than 0.01) compared to the controls. The serum concentration of the free iodothyronines (FT4, FT3, FrT3) showed similar differences between acromegalics and normal controls. All the acromegalics showed a rise of serum TSH, GH and PRL after TRH. Positive correlation (P less than 0.05, R = 0.59) was found between the TSH and GH responses, but not between these two parameters and the PRL response to TRH. These findings may be explained by the existence of a central suppression of the TSH and GH secretion in acromegalic subjects, possibly exerted by somatostatin. Euthyroidism might be maintained by an increased extrathyroidal conversion of T4 to T3.     

Oral thyrotropin-releasing hormone (TRH) test in acromegaly

The effects of 40 mg oral and 200 microgram intravenous TRH were studied in patients with active acromegaly. Administration of oral TRH to each of 14 acromegalics resulted in more pronounced TSH response in all patients and more pronounced response of triiodothyronine in most of them (delta max TSh after oral TRh 36.4 +/- 10.0 (SEM) mU/l vs. delta max TSH after i.v. TRH 7.7 +/- 1.5 mU/l, P less than 0.05; delta max T3 after oral TRH 0.88 +/- 0.24 nmol/vs. delta max T3 after i.v. TRH 0.23 +/- 0.06 nmol/l, P less than 0.05). Oral TRH elicited unimpaired TSH response even in those acromegalics where the TSH response to i.v. TRH was absent or blunted. In contrast to TSH stimulation, oral TRH did not elicit positive paradoxical growth hormone response in any of 8 patients with absent stimulation after i.v. TRH. In 7 growth hormone responders to TRH stimulation the oral TRH-induced growth hormone response was insignificantly lower than that after i.v. TRH (delta max GH after oral TRH 65.4 +/- 28.1 microgram/l vs. delta max GH after i.v. TRH 87.7 +/- 25.6 microgram/l, P greater than 0.05). In 7 acromegalics 200 microgram i.v. TRH represented a stronger stimulus for prolactin release than 40 mg oral TRH (delta max PRL after i.v. TRH 19.6 +/- 3.22 microgram/, delta max PRL after oral TRH 11.1 +/- 2.02 microgram/, P less than 0.05). Conclusion: In acromegalics 40 mg oral TRH stimulation is useful in the evaluation of the function of pituitary thyrotrophs because it shows more pronounced effect than 200 microgram TRH intravenously. No advantage of oral TRH stimulation was seen in the assessment of prolactin stimulation and paradoxical growth hormone responses.     

Rapid modulation of TRH-like peptides in rat brain by thyroid hormones

Recent identification of membrane receptors for T4, T3, 3,5-T2, and 3-iodothyronamine that mediate rapid physiologic effects of thyroid hormones suggested that such receptors may supplement the regulation of TRH and TRH-like peptides by nuclear T3 receptors. For this reason 200 g male Sprague-Dawley rats received daily i.p. injections of PTU or T4. Levels of TRH and TRH-like peptides were measured 0, 2 h or 1, 2, 3, or 4 days later. Rapid increases or decreases in TRH and TRH-like peptide levels were observed in response to PTU and T4 treatments in various brain regions involved in mood regulation. Significant effects were measured within 2 h of T4 injection. Nuclear T3 receptor-mediated changes in gene expression altering translation, post-translational processing and constitutive release of peptides require more than 2 h. We conclude that non-genomic mechanisms may contribute to the psychiatric effects of thyroid disease and thyroid hormone adjuvant treatment for major depression.     

Effects of xylazine immobilization on biochemical and endocrine values in white-tailed deer

The effect of xylazine hydrochloride on biochemical and endocrine parameters in plasma was examined in adult white-tailed deer (Odocoileus virginianus (Zimmermann]. In the first experiment, seven animals were injected intramuscularly via a blowgun dart with 0.65 mg/kg xylazine (100 mg/ml) and were bled 10, 20, 30, and 60 min post-injection. In the second experiment, eight animals were manually restrained for the first blood sampling and then injected manually and bled as before. Plasma calcium (Ca), inorganic phosphorus (P), and alkaline phosphatase (AP) were measured spectrophotometrically. Plasma parathyroid hormone (PTH), calcitonin (CT), thyroxine (T4), triiodothyronine (T3), and cortisol were measured by radioimmunoassay. Plasma PTH, CT, T4, T3, and AP activity did not differ (P greater than 0.05) during the 1 hr period studied in either experiment. Plasma Ca and P decreased significantly (P less than 0.05) in the second experiment, whereas cortisol levels increased significantly (P less than 0.05) 10 min post-injection in both experiments. The results may have been due to a drug effect or a combined drug and stress effect. It is suggested that xylazine may be safely used as an anesthetic in measuring PTH, CT, T4 and T3, and plasma AP up to 60 min post-injection in deer. Caution should be taken in using xylazine as an anesthetic to study adrenocortical function.     

Possible role of pancreatic insulin and glucagon in the hyperlipidemia and obesity of obese strain of chicken

Circulating levels of insulin, glucagon, thyroid hormones as well as lipid levels were determined in an obese strain of chicken and their lean controls. Hepatic and muscle glycogen and lipids were also measured. Obese birds had higher plasma lipids accompanied by significantly higher insulin and lower glucagon levels compared to lean controls. Hepatic and muscle triglycerides were also higher in obese birds. Plasma T4 level was significantly higher in obese but T3 was not different in the two groups. Results suggest that genetically obese birds have significantly increased insulin/glucagon ratios as previously reported in the PTU induced hypothyroid-obese chicks (Horm. Metab. Res. 12: 51, 1980) and this could have causal relationship to hyperlipidemia and obesity observed in these birds.     

Effect of active and passive immunization with TRH on plasma TSH response to propylthiouracil.

The role of thyrotropin-releasing hormone (TRH) in the secretion of TSH from the anterior pituitary was investigated in rats by active and passive immunization with TRH. The plasma TSH response to propylthiouracil (PTU) in TRH-bovine serum albumin (BSA)-immunized rats was significantly lower than that of BSA-immunized or non-immunized rats. Similarly, the increased plasma TSH level following PTU treatment was significantly suppressed after iv injection of antiserum to TRH. However, the decline in plasma TSH levels was not complete. The results of the present study indicate, at least in part, the physiological significance of endogenous TRH in the regulation of pituitary TSH secretion.     

Influence of D-thyroxine on plasma thyroid hormone levels and TSH secretion.

Triiodothyronine (T3), thyroxine (T4), basal TSH and TSH after stimulation with TRH were determined in healthy subjects and patients treated with D-thyroxine (DT4). After a dosage of 6 mg DT4 the D/L T4 plasma concentration rose about 4-fold 4 hours after application and was only moderately elevated 14 hours later. To achieve constantly elevated T4 levels 3 mg DT4 were applied in the further experiment every 12 hours. The D/L T4 plasma concentration rose 2.5-4-fold and there was a small but significant increase of the D/L T3 plasma concentration. 74 hours after onset of treatment basal TSH was below detectable limits and the increase of TSH 30 min after injection of 200 mug TRH (TRH test) was only about 15% compared to zero time. The time course of TSH suppression was investigated after treatment with DT4 and LT4 (single dosage of 3 mg). TRH-tests were performed before, 10, 26, 50 and 74 hours after the first dosage of D or LT4. There was no difference in the time course of basal TSH and TSH stimulated by TRH. In 10 patients on DT4 long-term therapy, basal and stimulated TSH were found to be below the detectable limits of 0.4 mug/ml. Our results show that (1) plasma half-life of DT4 is less than 1 day, (2) TSH suppression after D and LT4 treatment is very similar, and (3) in patients on long-term DT4 treatment, TSH plasma concentration is below detectable limits even after stimulation with TRH.     

Effects of streptozotocin-induced diabetes mellitus on hypothalamic-pituitary-thyroid axis in rats

The effects of streptozotocin-induced diabetes mellitus on the hypothalamic-pituitary-thyroid axis in rats were studied. Streptozotocin (60 mg/kg) was injected ip. Rats were decapitated at two and four weeks after the streptozotocin treatment. Thyrotropin releasing hormone (TRH), thyrotropin (TSH), thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2) and 3',5'-diiodothyronine (3',5'-T2) were measured by means of the specific radioimmunoassay for each. Immunoreactive TRH (ir-TRH) contents in the hypothalamus significantly decreased at four weeks (p less than 0.02). Basal TSH levels in plasma significantly decreased (p less than 0.005, p less than 0.001), and plasma ir-TRH and TSH responses to cold were significantly inhibited after the streptozotocin treatment (p less than 0.001). The plasma TSH response to TRH was decreased, but not significantly. The plasma T4 and T3 levels fell significantly. RT3 did not change throughout the experiment. 3,3'-T2 levels in plasma fell significantly, whereas 3',5'-T2 increased. Blood glucose levels rose significantly after streptozotocin treatment, but insulin treatment led to partial restoration. The findings suggest that streptozotocin-induced diabetes mellitus affects various sites of the hypothalamic-pituitary-thyroid axis in rats.     

Hormones of hypothalamic-pituitary-thyroid axis are significant regulators of synthesis and secretion of vitamin K-dependent plasma coagulation factors

Present data about hormonal regulation of haemostasis are often contradictory and are mostly based on clinical observations. The aim of the current research is to study the effects of the hormones of hypothalamic-pituitary-thyroid (HPT) axis on plasma levels (i.e. on the synthesis and secretion) of vitamin K-dependent coagulation factors in rats. The study was carried out on 65 male Wistar rats, divided into five groups. The animals were injected subcutaneously (s.c.) once daily for three consecutive days as follows: the first group was injected with Thyrotropin releasing hormone (TRH), in a dose of 0.06 mg/kg b.w.; the second group by Thyroid stimulating hormone (TSH), with a dose of 1 MU/kg b.w., the third and the fourth group respectively with Liothyroninum (Triiodothyronin ? T3) and Levothyroxinum (Thyroxin ? T4) with a dose of 0.08 mg/kg b.w. each. The control group rats were injected with saline (the solvent of the hormones), following the same schedule and volume per kg b.w. The necessary quantity of blood was acquired by a cardiac puncture under ether narcosis, and antigen levels of plasma factors II, VII, IX and X (FII:Ag, FVII:Ag, FIX:Ag and FX:Ag) were determined by ELISA kits (Diagnostica Stago, France). TRH, TSH, T3 and T4 significantly decreased the plasma antigen levels of FII and FVII (p<0.001). TRH, T3 and TSH reduced significantly FIX:Ag level( p<0.001 for TRH and T3 and p<0.05 for TSH) while T4 did not exert significant changes ( p>0.05). FX:Ag level was also significantly reduced by TRH, T3 (p<0.001), TSH and T4 (p<0.01). Plasma levels of vitamin K-dependent coagulation factors F??:Ag, FV??:Ag, F?Х:Ag and FХ:Ag are significantly reduced under the influence of the hormones of hypothalamic-pituitary-thyroid axis which signifies their decreased synthesis and secretion. T4 does not induce substantial changes in FIX:Ag plasma level.     

Effect of pulsatile or continuous administration of pituitary-derived chicken growth hormone (p-cGH) on lipid metabolism in broiler pullets.

1. The effects of pulsatile and continuous intravenous administration of exogenous, pituitary-derived chicken growth hormone (p-cGH) on lipid metabolism and endocrine/metabolite levels of broiler-strain pullets were studied. 2. Eight-week-old pullets were administered p-cGH or vehicle over a 10 min period every 90 min for 7 days. 3. Pullets were also administered the same daily amount (123 micrograms/kg of body weight/day) continuously for 7 days. 4. Feed intake, body weight gain, in vitro lipogenesis and hepatic enzyme activities were determined with certain hormones identified with the control of growth. 5. Pulsatile p-cGH administration for 7 days lacked effect on weight gain, feed efficiency, muscle or bone development. 6. Abdominal fat pad size was decreased (P less than 0.05) by pulsatile but not continuous administration of p-cGH. Pulsatile p-cGH administration also decreased (P less than 0.05) in vitro lipogenesis. Liver malic enzyme and isocitrate dehydrogenase activities were increased (P less than 0.05) by pulsatile but not continuous administration of p-cGH. In contrast, glutamic oxaloacetic transaminase activity was increased by a continuous infusion of p-cGH. 7. Plasma concentrations of T4 corticosterone and triglycerides were decreased (P less than 0.05) by a pulsatile but not a constant infusion of p-cGH. 8. Plasma T3 and GH were increased (P less than 0.05) by pulsatile p-cGH compared to both a continuous infusion of p-cGH and the saline controls. 9. This study is the first to prove that in the broiler chicken, the pattern of exogenous p-cGH administration is a factor influencing in vitro responses to the hormone.