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.     

Impaired peripheral T3 production but normal induced thyroid hormone secretion in the sex-linked dwarf chick embryo

Plasma concentrations of thyroxine (T4), triiodothyronine (T3) and chicken GH (cGH), together with hepatic 5'-monodeiodination (5'-D) activity, were measured in normal (Dw) and dwarf chick (dw) embryos at incubation d 18. An injection of 10 micrograms of ovine GH (oGH) raised plasma concentrations of T3 in Dw embryos after 1 and 2 h and stimulated hepatic 5'-D activity after 2 h. A non-specific increase in T4 was also observed after 1 h in Dw animals probably due to the heterologous nature of the injection. These effects were not observed in dw embryos. An injection of 1 microgram of TRH was able to increase cGH levels after 15 min in Dw embryos, whereas the the observed increase in the dw group was not significant. In Dw embryos, 0.01, 0.1 and 1 microgram of TRH increased plasma concentrations of T3 in a dose-dependent way, whereas in dw embryos, no reaction to the TRH injections was seen, except for the highest dose used. Contrary to this observation, T4 was increased to the same level in both Dw and dw embryos following TRH injections. An injection of 1 microgram of ovine CRH increased corticosterone after 0.5 h and elevated T3 and T4 after 2 h to the same extent in Dw and dw embryos. It is concluded that the thyrotrophic activities of TRH and oCRH and the corticotropic activity of oCRH do not differ between normal and sex-linked dwarf embryos. However TRH and GH were unable to stimulate the T4-T3 conversion in the liver of dw embryos, presumably due to the lack of hepatic GH receptors in these animals.     

Food intake after hatching inhibits the growth hormone induced stimulation of the thyroxine to triiodothyronine conversion in the chicken.

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.     

Influence of pimozide on a TRH induced TSH secretion in the rat during food deprivation.

Adult Wistar rats food deprived for 3 days had lower basal levels of TSH compared to normal fed animals. An increase of these lower levels to normal values was obtained following a prolonged (injections during 3 consecutive days) or acute treatment (single injection) with pimozide (1 mg/injection). Blood samples obtained after the last or an only injection of pimozide contained profound increased prolactin levels. Prolactin increase was more than 100-fold in fed and more than 30-fold in starved rats following prolonged pimozide treatment and more than 25-fold and 10-fold following a single injection of pimozide. An injection of 250 ng of TRH increased plasma concentrations of TSH in all groups, but this increase was more pronounced in fasted rats injected with pimozide during 3 consecutive days. It is concluded that fasting results in a dopaminergic inhibition of the sensitivity of the thyrotrophs to a TRH challenge.     

Effect of Ambient Salinity,Food-deprivation and Prolactin on the Thyroidal Response to TSH,and in vitro Hepatic T4 to T3 Conversion in Yearling Coho Salmon,Oncorhynchus kisutch

This study examines the effect of food deprivation, increased ambient salinity and prolactin administration on the thyroidal response to ovine TSH, and in vitro hepatic monodeiodination of T4 to T3 in coho salmon, Oncorhynchus kisutch. Fed fish and fish food-deprived for 18 days showed similar significant increases in plasma T4 9 and 24 h after a single injection of TSH. Plasma T3 levels were also elevated in both fed and food-deprived fish 9 h after the TSH injection but plasma T3 levels in the food-deprived fish were markedly lower than in the fed salmon. The increase in T4 and T3 evident in freshwater-acclimated fish after TSH administration was not found in salmon acclimated to 65% sea water. Prolactin, given alone (either as a single injection or a series of three daily injections) had no effect on plasma T4 or T3 levels. When given together with TSH prolactin prolonged the T4 and T3 elevating effect of TSH. Food-deprived salmon had lower in vitro hepatic T4 to T3 conversion rates than fed groups but T4 to T3 conversion did not appear to be affected by increased ambient salinity, or by prolactin and/or TSH administration.     

Insulin dependence of the actions of growth hormone and somatostatin on splanchnic biogenic amines of the dog

It is known from studies previously conducted in this laboratory that an iv injection of ovine growth hormone (GH, 100 micrograms/kg BW) or an equimolar amount of somatostatin (SRIF, 7.5 micrograms/kg BW), given to normal conscious dogs into a saphenous vein, leads to a significant increase in hepatic portal plasma serotonin and a simultaneous decrease in the concentrations of dopamine, norepinephrine and epinephrine. The changes take place within 12 minutes after the injection and are observed only in the portal circulation. The purpose of the present experiment was to investigate whether or not similar results could be obtained in diabetic animals. Mongrel dogs were rendered diabetic by surgical pancreatectomy and fitted with an indwelling hepatic portal catheter. Radioenzymatic methods were employed for quantitative measurements of plasma free serotonin and catecholamines. No response was noted when the same type of experiments as those conducted in normal dogs were now carried out in trained, fully conscious totally pancreatectomized dogs deprived of exogenous insulin supply. When the same animals were given an injection into a peripheral vein of 50 mU/kg BW regular crystalline insulin (a small dose that affected neither plasma glucose nor biogenic amine levels) 10 minutes prior to the administration of the other hormones, the usual response to both GH and SRIF was restored, i.e. the data were comparable to those of normal dogs. It is concluded that the GH/SRIF effect on gut biogenic amines is insulin dependent.     

Effects of growth hormone administration on wool growth in merino sheep

The effects of daily administration of 10 mg of highly purified ovine growth hormone (GH) for a period of 4 weeks on wool growth have been measured in 12 Merino ewes fed either a calculated maintenance energy intake or 1.6 times this amount (six on each ration). Concentrations of hormones, glucose, urea, alpha-amino N and amino acids in the blood were monitored and faeces and urine collected for measurement of nitrogen balance. Wool growth rate decreased by 20% during the 4 weeks of GH treatment in sheep fed the high energy diet, largely because of reduced wool fibre diameter. This was followed by restoration of normal growth and then an increase of up to 20% above control levels, a response which persisted for 12 weeks following cessation of GH administration, and which was due to increases in both fibre length and diameter. GH administration caused marked increases in plasma concentrations of GH, insulin and somatomedin C, glucose and free fatty acids, all of which returned to basal levels following cessation of GH administration. No consistent changes in plasma concentration of T3, T4, cortisol, prolactin or alpha amino N were detected. Plasma urea and methionine levels decreased during GH treatment and returned to, or were raised above, basal levels after the GH treatment period. GH injection also resulted in a net retention of N during treatment, followed by a transient period of net N loss. The GH-induced changes in wool growth may be caused by a change in the partitioning of amino acids between the muscle mass and the skin. No other contributing factor(s) were identified.     

Effect of mammalian growth hormone and prolactin on the growth of hypophysectomized chickens

Body weight gain and shank-toe growth during a 26-day treatment period following hypophysectomy were 55 and 46%, respectively, of control values, but the body weight gain was unaffected and bone growth only slightly reduced when the hypophysectomized chickens were fed a low dose of corticosterone (5 ppm). Bovine growth hormone (0.5 mg GH/kg body wt/day for 18 days) enhanced body weight gain and shank-toe length increase (an estimate of bone growth) by 46 and 33%, respectively, compared to the growth of hypophysectomized chickens receiving only corticosterone. These same endpoints were increased approximately 24% after ovine growth hormone treatment in hypophysectomized chickens not receiving corticosterone. Body weight gain during 18 days of treatment with bovine prolactin (0.5 mg PRL/kg/day) was 27% greater than the value for corticosterone-treated hypophysectomized chickens, but bone growth was unaffected. The mammalian GH preparations increased heart weight of the hypophysectomized chickens (25-29%), but pectoralis muscle weight was unaffected. GH treatment enhanced thymal weights by 71% in corticosterone-treated hypophysectomized chickens, and by 93% in hypophysectomized animals not receiving corticosterone. GH had no significant effect on bursal weights, and PRL had no effect on either of these lymphoid organ weights in corticosterone-treated hypophysectomized chickens. GH increased liver and adipose tissue weights considerably more than the large increases that followed treatment of hypophysectomized chickens with corticosterone alone (69 and 126% greater, respectively), but had no effect on these endpoints in hypophysectomized chickens not receiving corticosterone. PRL also greatly increased liver and adipose tissue weights in corticosterone-treated hypophysectomized chickens (79 and 75%, respectively). These results provide evidence that mammalian GH enhances body weight gain, bone growth, and the growth of several organs in the hypophysectomized chicken. Mammalian PRL increased body weight gain, liver weight, and adipose tissue weight in corticosterone-treated hypophysectomized chickens, but did not influence bone growth or the weights of the heart, pectoralis, thymi, or bursa.     

The regulation of ovine placental lactogen the role of the fetal hypothalamic-pituitary axis

The possible r?le of the fetal hypothalamic-pituitary axis in regulating the secretion of ovine placental lactogen (oPL) was investigated in chronically-catheterised ewes and fetuses in late pregnancy. Intravascular administration of agents to fetuses that significantly increased fetal prolactin concentrations (chlorpromazine 6.25 mg;thyrotrophin releasing hormone, 10 micrograms), significantly reduced fetal prolactin concentrations (bromocriptine, 0.033 mg/h), or significantly reduced fetal growth hormone (GH) concentrations (somatostatin, 2.5 micrograms/min), had no effect on maternal or fetal oPL concentrations. Mean fetal levels of prolactin or GH in late gestation could not be correlated with oPL concentrations, although fetal hypophysectomy prevented the normal prepartum fall in oPL concentrations.     

Catecholamine secretion from the adrenal medulla of the fetus, regulation by hormones

In the ovine fetus, the adrenal medulla activity secretes catecholamines into the circulation under normal and stress conditions. Little is known regarding the endocrine regulation of adrenal medullary catecholamine secretion in the fetus. The present study was undertaken to investigate the direct effects of the hormones prolactin, angiotensin II and cortisol on catecholamine release from fetal adrenal medulla, and to determine whether the effect of the hormones change during development into adulthood. Adrenal medulla from fetal, newborn and adult pregnant sheep was collected, dispersed into single cells and plated. Following preincubation, the cells were treated with ovine prolactin or angiotensin II at 8, 40 and 200 micrograms/ml; or cortisol at 10(-8), 10(-7) and 10(-6)M for 24 h. Catecholamine release into the medium were measured at 3, 6, 12 and 24 h. Ovine prolactin at 8 to 200 micrograms/ml significantly stimulated the release of total catecholamines after 12 h of incubation. The effect of prolactin was dose-dependent such that the magnitude of the response increased and the response time shortened with increasing concentrations of prolactin. In addition, the release of all three catecholamines--dopamine, norepinephrine and epinephrine--was significantly elevated. In newborn cells, only the highest concentration of 200 micrograms/ml ovine prolactin stimulated total catecholamine release at 6 h and 12 h, with significant increases of the three catecholamines at 12 h. In maternal cells, stimulation of catecholamine release was observed also with the highest concentration of prolactin tested (200 micrograms/ml) and after 12 h of incubation, when only the release of epinephrine was significantly enhanced by 324%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyrotropic and peripheral activities of thyrotrophin and thyrotrophin-releasing hormone in the chick embryo and adult chicken

The influence of an intravenous injection of thyrotrophin-releasing hormone (TRH) and bovine thyrotrophin (TSH) on circulating levels of thyroid hormones and the liver 5'-monodeiodination (5'-D) activity is studied in the chick embryo and the adult chicken. In the 18-day-old chick embryo, an injection of 1 microgram TRH and 0.01 I.U. TSH increase plasma concentrations of triiodothyronine (T3) and of thyroxine (T4). TRH, however, preferentially raises plasma levels of T3, resulting in an increased T3 to T4 ratio, whereas TSH preferentially increases T4, resulting in a decreased T3 to T4 ratio. The 5'-D-activity is also stimulated following TRH but not following TSH administration. The increase of reverse T3 (rT3) is much more pronounced following the administration of TSH. In adult chicken an injection of up to 20 micrograms of TRH never increased plasma concentrations of T4, but increases T3 at every dose used together with 5'-D at the 20 micrograms dose. TSH on the other hand never increased T3 or 5'-D, but elevates T4 consistently. It is concluded that TSH is mainly thyrotropic in the chick embryo or adult chicken whereas TRH is responsible for the peripheral conversion of T4 into T3 by stimulating the 5'-D-activity. The involvement of a TRH induced GH release in this peripheral activity is discussed.     

Time course of changes in plasma concentrations of the growth related hormones during protein restriction in the domestic fowl (Gallus domesticus)

Experiments were conducted to evaluate the possible role of circulating growth hormones triiodothyronine (T3), thyroxine (T4), and insulin-like growth factor I (somatomedin-C; IGF-I) in the elevation of plasma growth hormone (GH) which occurs in protein-restricted chickens. Plasma hormone changes were determined over a 2-week period of protein depletion by feeding a 5% protein diet as well as a similar period of protein repletion with a 20% protein diet. The rise in plasma GH was observed in two separate studies. Plasma concentrations of T4, T3, and IGF-I were all depressed in protein-restricted chicks prior to or concurrent with the GH elevation. In the protein repletion time course study, T4 and T3 concentrations were normalized prior to or concurrent with plasma GH normalization. However, IGF-I concentrations in repleted chicks did not return to control levels until after normal levels of GH were observed. These data suggest that thyroid hormones may play a greater role in the regulation of GH secretion during periods of malnourishment than IGF-I; the latter being currently thought to be a peripherally circulating inhibitor of GH release in animals.     

Central somatostatinergic regulation of growth hormone secretion in dwarf chickens.

1. Basal circulating growth hormone (GH) concentrations in sex-linked-dwarf (SLD) chickens were unaffected by the intracerebroventricular (icv) injection of 10, 50 or 100 micrograms somatostatin (SRIF). 2. The GH response to systemic thyrotropin-releasing hormone (TRH; 10 micrograms/kg, iv) was, however, 'paradoxically' enhanced 20 min after icv SRIF administration. 3. A lower dose (1.0 micrograms) of SRIF had no effect on basal or TRH-induced GH release. 4. High-titre SRIF antisera (4 microliters) also had no acute effect on basal plasma GH concentrations, but augmented the GH response to TRH challenge. 5. SRIF would appear to act at central sites to modulate stimulated GH secretion in SLD chickens.     

Induction of responsiveness of rat diaphragm to ovine growth hormone after administration of reserpine.

The diaphragm of the pituitary intact rat is insensitive to the insulin-like effects of growth hormone unless weanling animals are used, and even then these effects are not achieved reliably. We report here that an intraperitoneal injection of reserpine is able to induce consistent responsiveness to ovine growth horomone (oGH) in hemidiaphragms from 20-27 day old rats as assessed by stimulation of 3H-AIB transport and 14C-phenylalanine incorporation into protein. Maximal stimulation of 3H-AIB transport (approximately 40%) can be elicited by addition of oGH (5 micrograms/ml) to hemidiaphragms after a 2 mg/kg injection of reserpine given 5 h prior to sacrifice. The degree of stimulation does not alter significantly if the rats are sacrificed 3, 5 or 12 h after administration of reserpine, although it decreases by 24 h. Administration of reserpine 3 h before sacrifice also leads to a 50% increase in 14C-phenylalanine incorporation into protein in rat diaphragms in response to the addition of oGH (5 micrograms/ml). The induced sensitivity to oGH is not due to inhibition of GH secretion by reserpine as demonstrated by RIA of plasma GH. Addition of a monoclonal antibody to the GH receptor (MAb263) did not result in a stimulation or inhibition of 3H-AIB uptake or stimulation of protein synthesis in reserpinized rat hemidiaphragms. These results suggest that reserpine can induce tissue responsiveness in rats 20-27 d.o. independent of plasma GH levels. Our results also imply that the type 1 GH receptor of Barnard, Bundesen, Rylatt and Waters (1985) does not mediate the insulin like actions of GH on rat diaphragm.     

Responses of plasma adrenocorticotropin and cortisol to intravenous injection of synthetic ovine corticotropin releasing factor in the morning and early evening in normal human subjects

This study was designed to compare the responsiveness of adrenocorticotropin (ACTH) and cortisol secretion to corticotropin-releasing factor (CRF) in the morning and early evening in normal human subjects. Synthetic ovine CRF (1.0 micrograms/kg) or normal saline, was administered as an i.v. bolus injection to six normal males at 900 h and 1700 h. Blood samples were obtained before and 15, 30, 60, 90 and 120 min after CRF or saline injection. Significant increases in plasma ACTH and cortisol levels were observed in all subjects at the both time of testing after CRF injection. The net increments in the areas under the concentration curve (areas in the CRF experiment minus those in the saline control experiment) were not statistically different for both ACTH (mean +/- SEM: 41.0 +/- 10.6 pg/ml h in the morning: 51.1 +/- 8.9 pg/ml h in the evening) and cortisol (mean +/- SEM: 28.5 +/- 5.0 micrograms/dl h in the morning; 36.2 +/- 4.0 micrograms/dl h in the evening). Also no significant difference was observed in net increment, peak level and the ratio of peak level to the basal level of ACTH and cortisol after CRF injection. There were no appreciable changes in plasma concentrations of growth hormone, thyroid-stimulating hormone or prolactin, although slight but statistically significant rises in plasma levels of luteinizing hormone and follicle-stimulating hormone were observed. These results suggest that there is no significant difference in responsiveness of the pituitary-adrenal axis to CRF in the morning (900 h) and early evening (1700 h), and thus the time of day will not necessarily have to be considered when CRF is used between these times in a clinical test to evaluate pituitary ACTH reserve.     

Growth, protein synthesis and plasma concentrations of growth hormone, thyroxine and triiodothyronine in dwarf, control and growth-selected strains of broiler-type domestic fowl

Body weight, tissue weight and plasma hormone concentrations were determined at 1, 3, 6, 12 and 21 weeks of age in two dwarf strains and one control strain of broiler chickens. Protein synthesis, accretion and degradation rates were determined in the control strain with age. Within each strain, plasma growth hormone (GH) concentrations were greater at 1 and 3 weeks of age and consequently decreased with age. Plasma GH concentrations were greater in the sex-linked dwarf chicken during pubescence and maturity (12 and 21 weeks) compared to the autosomal dwarf and control chickens. Circulating concentrations of 3,5,3' triiodothyronine (T3) were depressed by 70% in sex-linked dwarf birds compared to controls, while thyroxine concentrations did not differ at most time points. These findings support the suggestion that sex-linked dwarf chickens have reduced peripheral conversion of T4 to T3.     

Adrenal inhibition of corticotropin-releasing hormone-induced thyrotropin release: a comparative study in pre- and posthatch chicks

Recent evidence indicates that corticotropin-releasing hormone (CRH) acts as a potent stimulator of thyrotropin (TSH) release in the chicken. In this study adrenal and thyroidal feedback mechanisms were studied. Administration of corticosterone 30 min prior to an ovine CRH (oCRH) challenge diminished the in vivo sensitivity of thyrotrophs to oCRH in 19-day-old chicken embryos (E19) (20 micrograms corticosterone; 2 micrograms oCRH) but not in 8-day-old chickens (C8) (40 micrograms corticosterone; 4 micrograms oCRH). At both ages studied, corticosterone (0.01 and 1 microM) did not alter the in vitro TSH response to oCRH (100 nM) indicating that an indirect mechanism is involved at the embryonic stage which is no longer present in posthatch chickens. In vitro, 3,5,3'-triiodothyronine (T3) pretreatment (0.01 and 1 microM) resulted at both ages studied in a dose-dependent drop in the in vitro oCRH-induced TSH release. As recorded previously, corticosterone treatment provoked a rise in plasma T3 in embryonic but not in posthatch chickens. The presence of an indirect adrenal feedback mechanism in chicken embryos may therefore be linked to the increase in plasma T3 which will alter the sensitivity of thyrotrophs to hypothalamic releasing factors. In conclusion, corticosterone does not directly modulate the responsiveness of thyrotrophs to CRH, but its feedback mechanism may be dependent on the evoked increase in plasma T3 which is only present in embryonic chickens. Corticosterone may in this regard play an essential role during embryonic development by coordinating thyroidal feedback mechanisms at the level of the chicken pituitary.     

Endocrine response to fasting in the overwintering captive raccoon dog (Nyctereutes procyonoides)

The raccoon dog (Nyctereutes procyonoides) is an omnivorous canid utilizing the passive wintering strategy in the boreal climate. Farmed raccoon dogs (n=12) were randomly assigned into two study groups on 26 November 2003. Between 3 December 2003 and 27 January 2004, half of the animals were fasted for 8 weeks and plasma weight-regulatory hormone concentrations determined on 26 November and 30 December 2003 and on 27 January 2004. The plasma peptide YY, ghrelin, and growth hormone (GH) concentrations increased due to food deprivation, while the T4 and Acrp30 concentrations decreased. Furthermore, the plasma GH concentrations were higher in the fasted raccoon dogs than in the fed animals, which had higher plasma insulin, glucagon, and T4 concentrations. However, fasting had no effect on the plasma leptin concentrations. The results confirm previous findings with unchanged leptin levels in fasting carnivores. Increased GH levels probably contribute to increased lipolysis and mobilization of fat stores. Ghrelin can also enhance lipolysis by increasing the GH levels. The decreased levels of T4 may reduce the metabolic rate. The plasma dopamine concentrations decreased due to fasting unlike observed previously in rats. Together with the unaffected adrenaline, noradrenaline, and cortisol concentrations, this suggests that food deprivation in winter does not cause stress to the raccoon dog but is an integral part of its natural life history.     

Effect of fasting on nychthemeral concentrations of plasma growth hormone (GH), insulin-like growth factor I (IGF-I), and cortisol in channel catfish (Ictalurus punctatus)

This experiment was conducted to characterize the effect of fasting versus satiety feeding on plasma concentrations of GH, IGF-I, and cortisol over a nychthemeron. Channel catfish fingerlings were acclimated for two weeks under a 12L:12D photoperiod, then fed or fasted for 21 d. On day 21, blood samples were collected every 2 h for 24 h. Weight of fed fish increased an average of 66.2% and fasted fish lost 21.7% of body weight on average. Average nychthemeral concentrations of plasma GH were not significantly different between fed (24.7 ng/mL) and fasted (26.8 ng/mL) fish, but average nychthemeral IGF-I concentrations were higher in fed (23.4 ng/mL) versus fasted (17.8 ng/mL) fish. An increase in plasma IGF-I concentrations was observed in fasted fish 2 h after a peak in plasma GH, but not in fed fish. Average nychthemeral plasma cortisol concentrations were higher in fed (14.5 ng/mL) versus fasted (11.0 ng/mL) fish after 21 d. Significant fluctuations and a postprandial increase in plasma cortisol were observed in fed fish and there was an overall increase in plasma cortisol of both fasted and fed fish during the scotophase. The present experiment indicates little or no effect of 21-d fasting on plasma GH levels but demonstrates fasting-induced suppression of plasma IGF-I and cortisol levels in channel catfish.     

Changes in thyroid hormone levels in chicken liver during fasting and refeeding

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.