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Glucocorticoids as well as thyroid hormones are essential for normal brain development. Exogenous glucocorticoids stimulate 3,3',5-triiodothyronine (T(3)) availability in circulation of birds and similar effects have been observed in sheep. Chicken data indicate that glucocorticoid administration also stimulates thyroid hormone metabolism in brain but the effects on local thyroid hormone concentrations are not known. Therefore, the current study: (1) determined local thyroid hormone availability in separate brain areas of 18-day-old embryonic chickens (E18) after injection of dexamethasone (DEX), and (2) investigated the impact on the thyroid hormone metabolic pathways in these brain parts and compared the results with the hepatic situation. For this, E18 chicken embryos were treated with a single intravenous dose of DEX (25 microg). Despite the decreased 3,5,3',5-tetraiodothyronine (T(4)) availability in the liver of the DEX treated embryos, the T(3) content was strongly increased, parallel to the plasma T(3) surge. This T(3) surge was primarily related to a fall in hepatic T(3) breakdown through a downregulation of the type III deiodinase (D3). The sulfation pathway in liver seems not to be affected by DEX. In all brain parts, DEX affects the T(3) production capacity by upregulation of the type II deiodinase (D2). This enables the brain to compensate for the decrease in T(4) availability, although the T(3) concentrations are not consistently increased like in plasma and liver. This observation points to the existence of a fine-tuning mechanism in brain that enables the brain to keep the T(3) concentrations within narrow limits.

The intracellular thyroid hormone (TH) availability is influenced by different metabolic pathways. We investigated the relationship between tissue and plasma TH levels as well as the correlation with changes of deiodination and sulfation during chicken embryonic development. From day 14 until day 19, T3 remains unchanged in liver and kidney in spite of increasing plasma T4 and T3 levels and a slightly increased T4 availability in these tissues. During this period, the T3 breakdown capacity by type III deiodinase (D3) is high in liver but low in kidney. The TH inactivation capacity of type I deiodinase (D1), with production of inactive rT3 instead of T3, in kidney seems to be potentiated by the sulfation pathway. A sharp rise in T3 and T4 is detected in all tissues examined when the embryo switches to lung respiration. The same day, T4 content in liver is sharply enhanced and sulfation activity is decreased. So, T4 availability in liver is increased while a declined D3 activity allows for the accumulation of hepatic T3. The increase in renal T3 and T4 are more closely related to plasma TH profiles and a lack of correlation with the changes in renal D1 and D3 activity suggests that T4 and T3 content in this organ is strongly dependent on direct uptake from the blood. Despite much lower T4 levels, T3 levels in brain are in the same range as in liver and kidney and intracellular T3 even exceeds the T4 levels towards the end of development. The rise in TH content coincides with a drop in D3 activity, low sulfation activity and an increased T3 production capacity via type II deiodinase (D2). In conclusion, the current study describes the dynamics of intracellular TH concentrations in liver, kidney, and brain during chicken development and investigates their relationship with circulating TH levels and changes of deiodinases and sulfotransferases. The clear differences in intracellular TH profiles among the different tissues demonstrate that circulating levels are not necessarily representative for the local TH changes. Some of the changes in intracellular TH availability can be linked to changes in local deiodination and sulfation capacities, but the importance of these enzyme systems in relation to other factors, such as hormone uptake, differs between liver, kidney, and brain.

In chickens, fasting results in increased plasma thyroxine (T(4)) levels and decreased plasma 3,5,3'-triiodothyronine (T(3)) levels. Refeeding, in turn, restores normal plasma T(3) and T(4) levels. The liver is an important tissue for the regulation of circulating thyroid hormone levels. Previous studies demonstrated that the increase in hepatic type III deiodinase in fasted chickens plays a role in the decrease of plasma T(3). Another factor that could be important is the level of T(4) and T(3) uptake by the liver. In mammals, caloric restriction is known to diminish transport of T(4) and T(3) into tissues. The present study examines whether this is also the case in chicken. Four-week-old chickens were subjected to a 24-h starvation period followed by refeeding. Blood and liver samples were collected at the start of refeeding and at different times of refeeding. Thyroid hormone levels were measured directly in plasma and in tissues following extraction. The results demonstrate that intrahepatic T(4) levels are increased and T(3) levels are decreased in fasted compared to ad libitum fed chickens. The parallel changes in plasma and hepatic T(3) and T(4) content demonstrate that T(4) availability in liver tissue is not diminished during fasting, suggesting that in chicken thyroid hormone uptake by the liver is not affected by nutritional status.

The influence of a recombinant chicken prolactin (rcPRL) preparation on thyroid function was studied in 18- and 19-day-old chicken embryos. Displacement studies on hepatic microsomes indicate that this preparation does not compete with radiolabeled chicken growth hormone (cGH) for hepatic GH-receptor binding. In a first series of experiments rcPRL or immunoaffinity-purified cGH was injected intravenously in 19-day-old chicken embryos. After 2 hr, cGH increased plasma T3 in a dose-dependent way by inhibiting hepatic inner ring type III deiodination (IRD-III) and consequently T3 degradation. Outer ring deiodination (ORD-I) was not influenced confirming previous results. The rcPRL preparation (2 and 10 microg) did not influence plasma T3, but depressed T4 and raised hepatic IRD-III activity simultaneously, whereas no influence on hepatic ORD-I activity could be found. In a second experiment on 18-day-old embryos, it could be demonstrated that the effect of 2.5 microg cGH on plasma T3 and liver IRD-III lasted up to 6 hr after injection, whereas 2.5 microg cPRL affected plasma T4 and liver IRD-III up to 2 hr. Both rcPRL and cGH depressed rT3 up to 6 hr, whereas an injection of rcPRL, but not of cGH, elevated plasma concentrations of corticosterone. These results indicate that prolactin may have a role, together with GH, in controlling peripheral thyroid hormone metabolism.

Male and female broiler chicks were raised separately in nearly continuous lighting [23 h light (L):1 h dark (D), CL] and consumed feed ad libitum. At 7 d of age, the intermittent lighting schedule (1L:3D, IL) was imposed on half of the chicks, whereas the other chicks remained under CL. In addition to performance characteristics, several parameters of the somatotrophic and thyrotrophic axes were studied together with plasma concentrations of testosterone. Males had a higher growth rate than females regardless of the imposed lighting schedule and this pronounced growth difference is reflected by higher plasma concentrations of growth hormone (GH), and a better GH receptor occupancy. Differences in growth rate between sexes could not be attributed to differences in circulating 3,3',5-triiodothyronine (T3) levels or to hepatic deiodination activities. However, from 3 wk of age onwards, males had significantly higher plasma testosterone levels than females. Plasma GH and T3 levels decreased whereas plasma insulin-like growth factor-I and thyroxine levels increased with age in all experimental groups. The age-related decline in plasma GH levels were less pronounced for males than for females. No major changes in other hormonal parameters or deiodination activities could be observed as a result of imposing IL, except for the higher plasma GH levels of IL chickens, and for plasma testosterone concentrations in IL males at Day 41, which were twice the levels found in their CL counterparts. These results therefore suggest that the somatotrophic axis as well as circulating testosterone levels mediate the sex-related differences in growth rate and the compensatory growth as present in males.

Sex-linked dwarf chickens have in plasma low triiodothyronine (T3) levels and slightly raised thyroxine (T4) concentrations and are functional hypothyroid. The kinetic parameters of T4 and T3 were investigated using 125I-labeled hormones. In addition the nuclear T3-receptors in the liver were examined using a radioreceptorassay and Scatchard analysis. Four-week-old dwarf (dw) and normal (Dw) chickens were injected with 125I-labeled T3 or T4 and blood samples taken 60, 120, 180, and 300 min after 125I-T3 injection and 120, 240, 360, and 480 minutes after 125I-T4 treatment. Labeled T4 and T3 and the degradation products were separated by paper chromatography. After the paper strips were dried, the iodinated compounds were visualized and counted in the gamma counter. The kinetic parameters, the half-life time (T1/2), the apparent distribution volume (Vd) and the metabolic clearance rate (MCR) were calculated using the natural base logarithm values of the measured radioactivity plotted against time and used for linear regression. T4 was cleared from circulation more slowly in dwarf than in control chicks and reflected a longer T1/2 (21.8%) and a reduced MCR (45%). The Vd tended to be lower (34.7%) in dwarfs. While the T1/2 of T3 was longer (28.1%) in dwarf chickens than in control animals, the MCR for T3 was considerably increased (31.8%). This results from an increased Vd (63.1%) in the dwarf chicks. The T3-receptor study in the liver of dwarf and non-dwarf chickens from Week 1 to Week 4 posthatching revealed that the total capacity and the affinity constant of the binding sites were comparable in dwarf and normal chickens. However, the occupancy of the receptors was higher in the dwarf animals.

The disappearance rates for glycosylated (GcGH) and non-glycosylated chicken growth hormone (NGcGH) were compared following their intravenous injection into anaesthetized adult laying hens. The metabolic clearance rate of GcGH was about 20% lower (P = 0.13) compared to NGcGH. Similarly, there was a tendency towards a longer half-life for GcGH. No major physiological significance could be attributed to the glycosylation state of the preparations as far as their effects on circulating insulin-like growth factor I and iodohormone levels were concerned.

Osmotic minipumps were implanted in 4-wk-old female broiler chickens to supply a 2-wk continuous infusion of recombinant human insulin-like growth factor-I (rhIGF-I) in three doses (.03, .1, and .3 mg/kg BW per day). At the end of the experimental period no differences in BW were detected, although abdominal fat was significantly reduced in the highest dose group. Measurement of fat content in both breast and thigh muscle indicated a different effect of IGF-I treatment on these parameters, as no reduction was observed. Determination of circulating IGF-I levels revealed a twofold increase in the .3-mg group whereas the lowest dose did not increase circulating plasma levels. The changes in IGF-I levels did not influence growth hormone levels whereas thyroxine levels were significantly decreased both in the .03- and .3-mg groups after 1 wk of treatment. At the same time plasma triiodothyronine levels were increased in the .1- and .3-mg/kg groups. These results indicate that a continuous infusion of IGF-I did not increase weight gain but may play a role as a fat repartitioning agent.

The effect of a single injection of 10 micrograms chicken GH on circulating thyroid hormones as well as in vitro liver 5'-monodeiodination (5'-D) activity was studied in posthatch chicks submitted to different feeding conditions. One group was normally fed after hatching, a second group was only fed after three days and a third group was food deprived after 2 days of feeding. Combination of all results indicates that the start of food intake abolishes the stimulatory effect of a GH injection on circulating T3 and liver 5'-D activity. Food deprivation after a period of food intake restores the GH effect on plasma T3 but not on liver 5'-D.

An injection of ovine growth hormone, porcine follicle stimulating hormone, and bovine thyrotropin stimulating hormone increased in Tilapia nilotica plasma concentrations of thyroxine (T4) and reverse triiodothyronine (rT3) after 4 and 8 hr, whereas plasma concentrations of T3 were unaffected. An injection of somatostatin (SRIF) alone did not influence thyroid hormone levels. If, however, SRIF was injected together with these hormones, which raised plasma T4, or together with T4 itself, an increase in plasma concentrations of T3 could be observed, whereas the increase in rT3 was less pronounced. It is concluded that SRIF may change the normal 5-deiodinase (5-D) activity and increased rT3 during hyperthyroxinemia into a 5'-D activity and a rise in T3, respectively, in T. nilotica.

Fed and food deprived (7 days) adult dwarf goats were injected intravenously with 75 micrograms/kg b. w. of ovine growth hormone (o-GH). Blood samples were collected from the jugular vein -2, -1 and 0 hr prior to and 30, 60, 90 and 120 min after injection and assayed for thyroxine (T4) and triiodothyronine (T3) concentrations. The 5'-monodeiodination (5'-D) activity was consequently determined in liver and kidney samples following slaughtering. Fasting alone increased plasma concentrations of T3 and T4, whereas injection of o-GH raised T3 additionally and more profoundly in food deprived animals compared to fed ones. A small increase in plasma T4 was also observed following o-GH injection, but only in starved goats. At the same time the hepatic, but not the kidney, 5'-D activity was stimulated in food deprived and GH injected animals. It is concluded that during prolonged fasting an increased peripheral T4 to T3 conversion is occurring contrary to the known decrease in T3 production during short periods of food deprivation. This increased conversion may be under the control of GH.

In this study, intravenous injection of several doses of porcine follicle stimulating hormone (pFSH: 0.002, 0.01, 0.05, and 0.5 micrograms/g body wt), bovine TSH (bTSH: 0.5 micrograms/g body wt), and ovine growth hormone (oGH: 0.04, 0.02, and 0.4 microgram/g body wt) stimulated an increase in plasma thyroxine (T4) and reverse triiodothyronine (rT3) in tilapia. This effect occurred in a dose-dependent manner. pFSH was the most potent in stimulating thyroid function. The dose of 0.002 microgram pFSH/g body wt increased plasma levels of T4 over control levels (2.59 +/- 0.16 ng/ml) about 2.5-fold within 4 hr, whereas a concentration of 0.5 micrograms/g body wt caused a great and prolonged increase of T4 and rT3 levels. Control levels (2.59 +/- 0.16 ng/ml for T4 and 40.37 +/- 8.60 pg/ml for rT3) were increased 19- and 22-fold respectively, over 24 hr. An increase of T4 and rT3 levels occurred also after injection of total hypophyseal extract and Con A II glycoprotein fraction of a tilapia pituitary homogenate, whereas the protein fraction failed to alter plasma concentrations of T4 and rT3. rT3 levels were also significantly increased at 2 hr, but not at 1 hr, after injection of T4. Basal T3 levels (1.90 +/- 0.22 ng/ml) were reduced by half over 24 hr in all experiments. These results suggest the existence, in tilapia, of a 5-D pathway deiodination of T4 which is pituitary independent. Stimulation of T4 release is always followed by an increase in plasma rT3 levels.

Circulating levels of T3 and T4, as well as T3 and T4 content of the thyroid glands were measured by radioimmunoassay in the neotenic and metamorphosed axolotl Ambystoma mexicanum. In the two experiments which were performed plasma T4 concentrations were more elevated in metamorphosed axolotls, especially in the first experiment (2.12 +/- 0.40 ng/ml vs. 369 +/- 30 pg/ml). T3 plasma values which were only estimated in the second experiment were about five times higher in metamorphosed animals (63.2 +/- 7.4 pg/ml vs. 12.5 +/- 0.8 pg/ml). Also the thyroid hormone content of the glands was higher after metamorphosis. Nevertheless the neotenic gland still contained considerable amounts of T3 (14.7 +/- 1.8 ng and 48.3 +/- 4.8 ng/thyroid, respectively, in the first and second experiment) and T4 (530 +/- 61 ng; 2173 +/- 291 ng/thyroid). Because of the higher T3/T4 ratio found in the plasma compared to the thyroid gland, it was suggested that circulating T3 may be derived partly from peripheral T4 conversion, mainly after metamorphosis. An intravenous injection of 10 micrograms synthetic TRH was able to induce a very significant increase of the plasma T4 concentration (which was maintained during 24 hr) in the metamorphosed axolotls of the first experiment, however, not in those of the second experiment nor in the neotenic animals. Following an injection of 10 mU bovine TSH (first experiment) circulating levels of T4 were raised in both groups. The opposing TRH results could be related with the different control levels of T4 in the two experiments. However, the results indicate that TRH is capable of functioning as a possible thyrotropin-releasing factor in the metamorphosed axolotl.

Circulating levels of T4 are measured by radioimmunoassay after intravenous injection of TRH, bovine (b) TSH, and pituitary extracts in the Mexican axolotl (Ambystoma mexicanum). Very low control levels of T4 are found (53 +/- 3 pg/ml (n = 27), but they are increased sevenfold following injection of 1/2 pars distalis extract or 1/2-1/10 IU b-TSH. Increased levels following these injections are found in plasma up to 48 hr after the injection. An in vitro assay also indicates that a 1/2 pars distalis of the axolotl is able to release T4 from the thyroid of R. ridibunda somewhat less effectively than a 1/50 pars distalis of the same size of R. ridibunda itself. TRH (50 and 100 micrograms) is unable to stimulate the release of T4 when injected intravenously into the axolotl. It is concluded that both the hypophysis and the thyroid gland of A. mexicanum may release optimal amounts of hormones necessary for metamorphosis following proper stimulation, but that TRH cannot function as a releasing hormone in this respect.

In the chicken the transition of a poikilotherm to a homeotherm reaction upon cold exposure takes place in the perinatal period between pipping and hatching. However, newly hatched chicks cannot maintain their body temperature within narrow limits after cold exposure. The fact that relatively little attention was payed on the role of thyroid hormones in the thermoregulatory reaction to cold of young chicks was probably due to the hypothetically long latention time that was thought to be necessary to bring about changes in secretory activity by cold stimulation. However, more recently, rapid changes (within hours) of thyroid hormone concentrations upon cold exposure were described in the chickens and the quail. In this study, changes in circulating T3 and T4 concentrations upon cold exposure of young chicks during the first two weeks were followed, that means during the period wherein NST (non-shivering thermogenesis), if it exists at all, should be progressively replaced by ST (shivering thermogenesis). Because of the importance of feeding condition on thyroid hormone levels, the experiments were carried out with and without a preceeding fasting period. In all experiments a short-term cold exposure of young chickens (1-11 days) fed ad lib decreased T3 but increased T4 levels while a reversed picture was found after short cold exposure of the fasted animals. However, after prolonged cold stimulus (15 degrees C) of young chickens fed ad lib, plasma T3 was also significantly elevated over that of controls whereas T4 levels returned to normal values. A prolonged warm treatment (37 degrees C) of young chickens fed ad lib resulted in significantly lower T3 and higher T4 concentrations. After a prolonged cold treatment no differences in T4 or T3 response upon TRH were found whereas the warm treatment abolished these responses upon TRH. However, a cold treatment at the stage of incubation during which the hypothalamo-hypophyseal control of thyroid function is established (dag 10-14) enhanced the T4 response to TRH with a long lasting effect extending to the posthatch period. Since T3 is thought to be the active form of thyroid hormones with regard to thermopoiesis we have studied more specifically the effect of blocking peripheral conversion of T4 on thermoregulatory abilities in young chicks and the influence of temperature treatment on monodeiodination capacity. The lower rectal temperatures following the interference with the peripheral monodeiodination of T4, the effect being more pronounced at the lower ambient temperature, are indicative for a preponderant role of T3 on thermogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)

The administration of either glucocorticoids (dexamethasone or corticosterone) or adrenocorticotropic hormone (ACTH) to chicken embryos was followed by increase in the circulating concentration of triiodothyronine (T3), the T3 to thyroxine (T4) ratio and the activity of liver T4-5' monodeiodinase. No consistent changes in plasma concentrations of T4 or GH were observed. In post-hatching chicks, corticosterone and dexamethasone depressed the circulating concentrations of both T4 and T3. Iopanoc acid, an inhibitor of liver T4-5' monodeiodinase, elevated plasma concentrations of T4 and depressed those of T3 in both chicken embryos and young chicks. It is suggested that glucocorticoids affect circulating concentrations of T4 and T3 both by affecting the activity of the liver T4-5' monodeiodinase and by influencing the hypothalamo-pituitary axis.

The influence of an intravenous injection of chicken growth hormone (cGH), a total chicken pars distalis (PD) extract, and a PD extract depleted of cGH by immunoadsorption was studied in the 18-d-old chick embryo. Plasma concentrations of triiodothyronine (T3), thyroxine (T4), and hepatic 5'-monodeiodination (5'-D) activity were measured. An injection of total PD extract raised plasma T3, T4, and 5'-D activity, whereas a PD extract depleted of GH only increased plasma T4. The amount of cGH present in the PD extracts, as measured by homologous cGH radioimmunoassay, increased T3 and raised liver 5'-D, but had no effect on plasma T4. The effect on liver 5'-D was more pronounced with cGH than with a total PD extract, whereas the effect on plasma T3 was somewhat less pronounced. It was concluded that cGH increased the peripheral conversion of T4 into T3 in the chick embryo, whereas a PD extract depleted of cGH was purely thyrotropic. The PD extract also seemed to have 5'-D-suppressing activity.

Normal fed and 2 days fasted Warren chickens were injected intravenously with 100 micrograms of ovine growth hormone (GH) and ovine prolactin and plasma concentrations of thyroid hormones were assayed prior and up to 2 h after injection. Fasting alone decreases T3, but increases T4. An injection of GH resulted in increases of plasma T3 concentrations in two fasting experiments by 40% (after 3/4 h) and 104% (after 1 h). In normal fed animals no increase is observed in the first experiment, whereas a 35% increase occurs in the second one. An injection of 100 micrograms prolactin does not influence T3 in normal fed or fasting animals. Both GH and prolactin, however, may decrease plasma concentrations of T4. In a separate experiment 50 micrograms and 200 micrograms of GH raised the decreased T3 levels after fasting by 39% and 60% respectively 1 h after injection and by 24 and 61% respectively in normal fed chicken, whereas prolactin was ineffective in this regard. Using Hisex chickens, the influence of an injection of 100 micrograms GH on plasma concentrations of thyroid hormones could be confirmed. At the same time GH increases the liver 5'-monodeiodinase activity by 330% after 1 h and by 147% after 2 h. The peroxidase activity is not influenced in normal fed chickens, but GH decreases this activity in food deprived animals after 1 h and 2 h. It is concluded that ovine GH, but not prolactin, stimulates the peripheral conversion of T4 into T3 in both normal fed and food deprived chicken and that this effect is dose dependent.

In male neotenic axolotls Ambystoma mexicanum plasma concentrations of thyroxine (T4) and testosterone were increased following intravenous injection of 10 micrograms luteinizing hormone-releasing hormone. A dose of 50 micrograms influenced only plasma T4 levels. This observation suggests for the first time that a hypothalamic hormone is capable of stimulating the thyroidal axis in the neotenic axolotl.

Basal and TSH-induced plasma concentrations of T4 have been measured by radioimmunoassay in the neotenic and metamorphosed male axolotl Ambystoma mexicanum both before and after an ovine prolactin pretreatment. All injections are made into the vena abdominalis. Basal levels of T4 are low in neotenes (85 +/- 19 pg/ml) and somewhat higher in metamorphosed Ambystoma (171 +/- 39 pg/ml), but are increased during metamorphosis (1094 +/- 138 pg/ml). Following injection of 5 mU bovine TSH circulating levels of T4 are raised about 4 times in neotenes, but more than 50 times in metamorphose animals. Three intravenous injections, each of 640 mU prolactin and given, respectively, 24 and 13 hr before and simultaneously with 5 mU TSH, do not inhibit the TSH-induced release in both experimental groups. In the metamorphosed Ambystoma again a more than 50-fold T4 increase is present, whereas in neotenes a 10-fold TSH-induced T4 release is seen, which is more pronounced than before the prolactin treatment. It is concluded that in A. mexicanum ovine prolactin does not block a TSH-induced T4 release and that any antagonistic action with thyroid hormones is not mediated through the thyroid gland.

Using Japanese catching nets a total of 77 males and 37 females of the fruit eating bat Epomops franqueti (Megachyroptera) were captured during a period of 1 year around Kisangani (Zaïre). Adult males with white epaulets weighing 143 +/- 3.6 g (18) had their testes present in the scrotum and higher plasma concentrations of thyroxine (T4) and testosterone than adult males without epaulets and with abdominal testes (weight 107.5 +/- 2.0 g (39)) or juveniles (72.7 +/- 2.8 g (20)). Mean embryo weight of pregnant bats was 4.26 +/- 1.09 g (12) ranging from 1.8 to 14.8 g whereas body weight of mothers (+ embryos) was 117.0 +/- 3.6 g (12). Body weight of nonpregnant bats was 107.3 +/- 2.1 (10) and of female juveniles 74.6 +/- 4.3 (15). Plasma concentrations of triiodothyronine (T3) were lowest in nonpregnant adults and comparable in juveniles and pregnant bats. No difference in plasma T4 concentrations was found between all groups. Estradiol-17 beta concentrations were three times higher in pregnant bats compared to nonpregnant ones or juveniles. A possible relationship between these high figures and elevated T3 values has been discussed.

Annual variations in plasma concentration and thyroid gland content of thyroid hormones were studied in male Rana ridibunda during 2 consecutive years together with in vitro capacity of the thyroid gland to release thyroxine (T4) following stimulation with bovine thyrotropin (b-TSH). A low thyroidal content of triiodothyronine (T3) (2-4 ng) and T4 (300-400 ng) is found during winter and increases rapidly after hibernation to maximal values of +/- 50 ng T3 and 2000-2500 ng T4 in May-July. Plasma levels of T3 vary between 10 and 15 pg/ml for all months studied except for a low of 5.4 and 5.7 pg/ml in December and March, respectively. Plasma concentrations of T4 are low in winter (100-200 pg/ml) but increase in January, reaching maximal levels in February-March (700-1000 pg/ml). In the first year levels decrease again until August (last observation month) to about 250 pg/ml, whereas in the second year this decrease is more sudden, reaching winter values of 100-200 pg/ml as early as May-June. Thereafter a second increase in plasma concentrations of T4 is observed again with maximal values of 800 pg/ml obtained in October. This biphasic circannual pattern, from two different observations, is also found in the in vitro T4 release capacity of the thyroid glands following stimulation with 100 mU of b-TSH. The maximal release capacity of the thyroid glands following stimulation with 100 mU of b-TSH. The maximal release capacity of the thyroids is present in March and July-August. Minimal release capacities are present in winter but also in April-June.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma concentrations of thyroxine (T4), triiodothyronine (T3), reversed triiodothyronine (rT3), and insulin-like growth factors I and II (IGF-I, IGF-II) together with peripheral 5'-monodeiodination activity were measured in both normal and sex-linked dwarf embryos between day 14 of incubation and day 1 posthatch. Plasma T4 levels increased gradually during embryonic development while T3 concentrations remained low until day 20, when a sharp increase was observed. rT3 levels also increased from day 14 and dropped on day 20 when T3 levels started to increase. 5'-monodeiodination activity was high on day 14 of incubation, decreased thereafter, and showed an increase at the time of air sac penetration together with increased T3 levels. At this stage, differences between normal and dwarf embryos were observed; the latter had lower nonsignificant 5'-Monodeiodination activity and lower (P less than 0.01) plasma T3 levels. Plasma IGF-II levels were high during the whole embryonic period studied. Dwarf embryos had lower (P less than 0.05) IGF-II levels at the time of hatching. IGF-I levels were high on days 14 and 16, declined afterwards, and started to increase again around hatching. With the exception of T3 and IGF-II levels, introduction of the dwarf gene did not cause major changes in the hormonal parameters studied. This may explain the identical body weight at hatching.

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.

Chick embryos were injected with iopanoic acid (IOP) on either day 17 or 18 of incubation, and radioimmunoassays of triiodothyronine (T3) and thyroxine (T4) in serum and thyroid glands were performed from day 19 on through pipping and hatching and 1 day after hatching. The IOP was able to block T4 to T3 conversion in chick embryos from day 19 of incubation. Blocking T4 conversion did not delay hatching significantly, nor did it affect embryonic mortality significantly. Yolk sac retraction was not affected at hatching. A rise in serum reverse T3 (rT3) and T4 was observed after IOP administration. The rise in T4 could not be explained solely by a decreased T4 conversion. The results indicated that peripheral monodeiodination occurs in the late chick embryo.

Females of the giant swamp frog Dicroglossus occipitalis were captured in the tributaries of the Zaïre River near Kisangani, a town situated close to the equator (00 degree 31' N) with virtually constant conditions as to photoperiod, temperature, precipitation, and relative humidity. An annual variation in the reproductive capacity of this species could be demonstrated. A reproductive quiescence with a low gonadal somatic index (GSI), undeveloped eggs, and minimal plasma concentrations of estradiol-17 beta (E2) and progesterone (P4) was found from October to January. E2 and P4 and thyroxine (T4) contents of the thyroids were positively correlated with GSI and egg size. Plasma T4 concentrations, however, were negatively correlated with GSI, whereas variations in corticosterone correlated only with E2. No correlation between plasma concentrations of glucose and GSI or all other hormonal parameters could be found. It is concluded that during egg maturation, increased amounts of E2 and P4 are produced. The observed variations in thyroidal and plasma T4 may be the result of an activation of thyroid function by the peripheral conversion of T4 into triiodothyronine.

Rhode Island Red eggs were incubated at 33.8 and 376.8 C from day 17 until hatching under a photoperiod of 12L:12D. After hatching, the same light schedule was maintained, and all chicks were raised at 25 +/- 1 C and 50% relative humidity. Infrared lamps were used up to 7 days. Pipping and hatching occurred significantly later in chicks incubated at 33.8 C, and the interval between events was prolonged. Chicks of the 33.8 C group had a lower body weight on day 3 posthatch, but relative growth was accelerated from the 2nd week on, resulting in equal weights on day 36 for males and day 43 for females. Circadian mean serum levels of triiodothyronine (T3) during a 24-hr period (blood sampling every 4 hrs) were positively correlated with relative growth rate in both temperature groups, whereas thyroxine (T4) correlated with weight and age. Body weight of females remained lower from day 9 (33.8 C) and 22 (37.8 C) on. In the 37.8 C group, a significant fit of serum T4 to a sinusoidal curve (observed during a 24-hr cycle) was present for both sexes from day 16 on; this was true from day 32 on in the lower incubation temperature group. The acrophases of this rhythm occurred at about 0500 hr (1100 hr after onset of the dark period) and did not differ between temperature groups of sexes. A significant fit to a sinusoidal curve for the T3 data was only possible for both sexes and temperature groups on days 112 and 128 with an acrophase at about 1700 hr. Differences in growth rate between temperature groups can be related to differences in mean serum levels of T3. Differences in growth rate between sexes were not parallelled by differences in levels of thyroid hormones or acrophases, but males did not have a higher amplitude in the sinusoidal T4 rhythm compared to females. This difference was more pronounced in the 37.8 C group.

The in vivo release of thyroxine (T4) in the carp (Cyprinus carpio) and the in vitro release of T4 in the frog (Rana ridibunda) from isolated thyroids were used as a bioassay to study the thyrotropic activity of carp hypophyses. The addition of up to 1 hypophyseal equivalent to the medium did not increase the in vitro release of T4 from isolated frog thyroids in November whereas 3 mU of bovine thyrotropin (b-TSH) was effective. However, when this experiment was repeated at the end of February, the responsiveness of frog thyroids was increased since the addition of 0.5 carp hypophyseal equivalent did stimulate the release of T4. When Winter carp alone were used in an in vivo bioassay, an intracardial injection of up to a dilution of 1/64 hypophyseal equivalent increased plasma concentrations of T4 after 2 and 4 hr. However, 3 mU of b-TSH was ineffective in this regard. Affinity chromatography of b-TSH indicated that all thyrotropic activity as tested in the frog bioassay was retained on a concanavalin (Con A)-Sepharose column. Following Con A separation of a carp hypophyseal homogenate it was finally demonstrated that the unadsorbed protein fractions did not increase plasma concentrations of T4, whereas the adsorbed glycoprotein fraction did. No influence on circulating triiodothyronine (T3) levels was noted with both fractions. These results indicate that the thyrotropic activity of a carp hypophysis is of a glycoprotein nature.