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Biomedical subjects

C G Scanes

Publications and source records attributed to C G Scanes.

At least 91 records · Page 5Linked to original sources

Thyroid function in sex-linked and autosomal dwarf chickens.

Thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) elevated plasma thyroxine (T4) and triiodothyronine (T3) concentrations in a (euthyroid) control line of chickens and in an autosomal dwarf strain. These agents were ineffective in sex-linked dwarf (SLD) chickens. Similarly, while somatostatin (SRIF) lowered plasma T4 and T3 concentrations in autosomal dwarf (ADW) chickens and controls, it had no inhibitory effect in the SLD strain. These results suggest that an impairment in the hypothalamus-pituitary-thyroid axis is at least partly responsible for hypothyroidism in the SLD strain.

Animals↗

Effect of estrogen on calcium homeostasis and pituitary hormones in the growing chick.

An experiment was carried out to investigate the effect of a range of estradiol (E2) doses (0.1-6.5 micrograms/g body wt/day) on vitamin D metabolism and the plasma levels of growth hormone (GH) and prolactin (PRL) in the growing chick. Doses of 0.5-0.7 microgram/g E2, which are insufficient to raise the plasma calcium level, did induce an increase in growth rate, an increase in 25-hydroxyvitamin D 1 alpha-hydroxylase (1-hydroxylase) and 24-hydroxylase activities, and an increase in plasma GH level. These parameters leveled off or fell over the dose range 1-2 micrograms/g E2 but there was evidence of a second peak in 1-hydroxylase activity at 6 micrograms/g E2. At this high dose rate, the plasma Ca level rose to 8 mM, as it does in the laying hen; 24-hydroxylase activity, growth rate, and plasma GH and plasma PRL levels all decreased. It was concluded that the dose response to estrogen in the growing chick is not linear and, in the case of 1-hydroxylase activity, may even be biphasic.

Animals↗

Possible participation of calcium in growth hormone release and in thyrotropin-releasing hormone and human pancreatic growth hormone-releasing factor synergy in a primary culture of chicken pituitary cells.

We previously reported that thyrotropin-releasing hormone (TRH) and human pancreatic growth hormone-releasing factor (hpGRF) exert synergistic (greater than additive) effects on growth hormone (GH) release from chicken pituitary cells in primary culture. In the present studies the possible participation of calcium in GH release and in TRH and hpGRF synergy was investigated. Following dispersion with collagenase, cells were cultured for 48 hr prior to exposure (2 hr) to test agents. Cultured cells were exposed to a range of calcium concentrations (0, 0.02, 0.2, and 2.0 mM) in the presence and absence of secretagogues. These results demonstrated that basal GH release was not altered by the concentration of calcium in the medium: however, secretagogue-induced GH release required calcium. Thus, TRH, hpGRF, 8 Br-cAMP, or forskolin stimulated GH release in the absence of calcium. Furthermore, synergistic GH release evoked by TRH and hpGRF, 8 Br-cAMP, or forskolin was observed only at the highest calcium concentration (2.0 mM). In other studies, ionomycin (10(-5) M), a calcium ionophore, stimulated GH release to a value about 125% over the basal (absence of test agent) value. Ionomycin-induced GH release was not affected by TRH (5.0 ng/ml); the combined effects of ionomycin (10(-7)-10(-5) M) and hpGRF (5.0 ng/ml) on GH release were less than additive. However, ionomycin (10(-5) M) further increased GH release over that resulting from the synergistic action of TRH and hpGRF (5.0 ng/ml each). Verapamil (a calcium channel blocker) did not affect GH release induced by either TRH or hpGRF (5.0 ng/ml each). However, this agent did inhibit synergistic GH release evoked by TRH and hpGRF, 8 Br-cAMP, forskolin, or isobutylmethylxanthine. These results suggest that calcium participates in secretagogue-induced GH release from chicken somatotrophs in vitro.

Animals↗

Seasonal changes in body weight, fat depots, and plasma levels of thyroxine and growth hormone in free-living great tits (Parus major) and willow tits (P. montanus).

Annual changes in body weight, fat depots, and plasma levels of thyroxine (T4) and growth hormone (GH) were studied in free-living great tits and willow tits. Birds were collected during six ecologically well-defined periods of the year. Special attention was given to the nonreproductive part of the year. T4 showed simple unimodal cycles in both species and both sexes, with high levels during the warmer part of the year, and low levels during the winter and spring periods. Although increasing levels were temporarily separated between the two species, they were in both cases correlated with the onset of gonadal regression and moult. Plasma levels of GH fluctuated in a much more complex pattern, and no obvious and consistent correlation to any extrinsic or intrinsic factor was found. Body weights and fat depots both showed seasonal variations that varied slightly between the two species. Values, with the exception for breeding females, were generally the highest during the autumn, winter, and spring periods.

Adipose Tissue↗

Triiodothyronine inhibition of thyrotropin-releasing hormone- and growth hormone-releasing factor-induced growth hormone secretion in anesthetized chickens.

The ability of triiodothyronine (T3) to reduce basal and secretagogue-induced growth hormone (GH) release was examined in anesthetized young and adult male chickens. Infusion of T3 had no effect on basal plasma concentrations of GH in either young or adult chickens. However, GH secretion following challenge with either thyrotropin-releasing hormone (TRH) or growth hormone-releasing hormone (GRF) was reduced, in a dose-dependent manner, by the infusion of T3. In vivo sensitivity to T3 inhibition was greater with TRH- than GRF-stimulated GH release in either young (ED50 for TRH-induced GH release, 0.34 microgram T3/kg/min; ED50 for GRF-induced GH release, 0.49 microgram T3/kg/min) or adult chickens (ED50 for TRH-induced GH release, 0.11 microgram T3/kg/min; ED50 for GRF-induced GH release 1.89, micrograms T3/kg/min). Moreover, there was an increase in sensitivity of TRH-induced GH release to T3 with age.

Animals↗

Heterogeneity of chicken growth hormone (cGH). Identification of lipolytic and non-lipolytic variants.

The identification and biological activity of chicken growth hormone (cGH) charge variants is described. On the basis of electrophoresis and immunoreactivity chicken pituitary glands contain at least two "charge" variants (Rf = 0.22 and 0.3) which have different net charge but similar molecular weight (26,300 d). Both are immunoreactive but show different bioactivity with adipose explants, band 0.22 being lipolytic whereas band 0.3 appears to be inactive. The abundance of these cGH bands vary with age, both being higher in young birds and lower in adults. These results suggest that cGH variants may have different biological actions.

Aging↗

Influence of beta-agonist on plasma concentrations of growth hormone in broiler chickens on a low plane of nutrition.

The effect of the chronic administration of a beta-agonist (L-640,033; donated by Merck, Sharp and Dohme, Research Laboratories, Rahway, NJ) on both the plasma concentration of growth hormone (GH) and the episodic pattern of GH secretion was examined. Administration of .25, 1.0, or 4.0 ppm beta-agonist in the diet for only 3 to 5 days did not affect the overall mean plasma concentration of GH. These treatments also did not influence the frequency of GH secretory pulses. However, the amplitude of the GH secretory pulses was reduced. In contrast, administration of 1.0 ppm beta-agonist for the 10 to 12-day period increased the mean plasma concentration of GH, the amplitude of the GH secretory pulses, the basal (between pulses) plasma concentration of GH, and the interpeak interval. No effect of in vivo GH secretion was found with .25 ppm beta-agonist treatment for 10 to 12 days. Chicks receiving 4.0 ppm beta-agonist for 10 to 12 days had GH secretory pulses with increased amplitude, but no other differences in GH secretory characteristics were observed.

Adrenergic beta-Agonists↗

Plasma concentrations of insulin like growth factors (IGF-)I and IGF-II in dwarf and normal chickens of high and low weight selected lines.

Plasma concentrations of hormones related to growth and development were determined in normal and in dwarf chickens from lines selected for high or low juvenile body weight. In young (51 days of age) chickens, plasma concentrations of insulin like growth factor (IGF-) I were lower in the low than high weight lines and were reduced in dwarf compared with in normal birds. However, no differences in plasma concentrations of IGF-I were observed between adults from low and high growth lines. Plasma concentrations of IGF-II were lower in the low growth line irrespective of age and, also were reduced in dwarf birds. No line differences were observed with either thyroxine (T4) or triiodothyronine (T3). Dwarf chickens had reduced plasma concentrations of T3 but not T4. Correlations between and amongst hormone concentrations and body weights were observed. The present studies provide evidence for a role of IGF-I, IGF-II and T3 in poultry growth.

Animals↗

Immunogold identification of the somatotrophs of domestic fowl of different ages.

The somatotrophs of the pituitary gland of the male domestic fowl were identified by means of an immunoelectron-microscopic method based on gold as the electron-opaque label and an antibody to growth hormone. Gold particles indicating sites of growth hormone were restricted to cells in which virtually all of the granules were labelled. Little, if any, gold label was found outside the granules in these cells designated as somatotrophs, or at sites outside these cells. The size of these gold-labelled secretory granules presumed to contain growth hormone decreased with age, from a mean sectional diameter of 256 +/- 6.2 nm (SEM) at 4-6 weeks to 221 +/- 5.7 nm at 11-18 weeks and 205 +/- 8.6 nm at 24-30 weeks of age. On the basis of these values for mean sectional diameters the change between the first two periods represents a decrease in granule volume of about 36%. However, during the same period the growth hormone concentration of the granules increased. Accordingly, growth hormone content per granule changed little if at all. In contrast, from 11-18 weeks to 24-30 weeks of age there was a decrease of 31% in growth hormone content per granule. These data indicate that growth hormone packaging in the chicken somatotroph changes with age. The first change results in the production of smaller granules of higher growth hormone concentration. During this period growth hormone content per granule remains relatively constant. The later change results in the production of granules of lower growth hormone content than that of younger animals.

Animals↗

Thyrotrophin-releasing hormone induces growth hormone secretion in adult hypothyroid fowl.

While thyrotrophin-releasing hormone (TRH) stimulated growth hormone (GH) secretion in adult anesthetized cockerels, the GH response was blocked in anesthetized birds pretreated with thyroxine (T4) or triiodothyronine (T3). Moreover, whereas GH secretion in conscious adult birds was poorly responsive to TRH stimulation, conscious birds made hypothyroid by goitrogen pretreatment (with propylthiouracil, methimazole, or thiourea) were responsive to TRH challenge. Basal circulating GH concentrations in the goitrogen-pretreated birds were also higher than in the vehicle-injected controls. Surgical thyroidectomy similarly increased the basal GH concentration in adult birds and promoted TRH-induced GH secretion. These results demonstrate inhibitory effects of the thyroid hormones on basal and stimulated GH secretion in adult domestic fowl and suggest that GH release in adults is partly under tonic thyroidal inhibition.

Animals↗

Acute effects of hypophysectomy and administration of pancreatic and thyroid hormones on circulating concentrations of somatomedin-C in young chickens: relationship between growth hormone and somatomedin-C.

The short-term control of plasma concentrations of somatomedin C (SmC) in young chicks was examined by either surgical removal of the pituitary gland or by the administration of hormones which affect plasma concentrations of growth hormone (GH). As expected, removal of the source of GH by hypophysectomy reduced plasma concentration of GH, these being suppressed by 95.7% within 1 hour. Hypophysectomy was rapidly followed by reductions in the plasma concentration of SmC. For instance, plasma concentrations of SmC were decreased to 53% of pretreatment one hour following hypophysectomy. This suggests both that SmC has a short half life and that the release of SmC into the circulation is tightly coupled to the presence of pituitary hormone(s), presumably including GH. Sham surgery also decreased plasma concentrations of GH but were without effect on plasma concentrations of SmC. The short term control of plasma concentrations of SmC was also examined by the acute administration of hormones, which affect GH secretion in vivo. Injections of thyroxine or triiodothyronine decreased the plasma concentration of GH but were without effect on the plasma concentration of SmC. On the other hand, the administration of either glucagon or insulin decreased the plasma concentration of both GH and SmC. The present data suggest that plasma concentrations of SmC do not simply reflect the GH status in young chickens.

Animals↗

Flight effects on plasma levels of free fatty acids, growth hormone and thyroid hormones in homing pigeons.

Significant increases in circulating levels of free fatty acids (FFA) and growth hormone (GH), were observed in homing pigeons after a flight of 48 km, lasting 60-80 min. No significant change in plasma levels of thyroxine (T4) and triiodothyronine (T3) was observed. Nor was there any change in T3/T4 ratio. The increase in plasma FFA is attributed to the increased release into circulation of at least one adipokinetic hormone, GH. It may be concluded that in free sustained homing flight under normal weather conditions and within the specific distance and duration, metabolic fuel and hormonal homeostasis is maintained.

Animals↗

Growth hormone secretion induced by thyrotropin-releasing hormone in adult chickens: evidence of dose-dependent induction of either refractoriness or sensitization.

Thyrotropin-releasing hormone (TRH) has been previously demonstrated to both stimulate growth hormone (GH) secretion and induce refractoriness to subsequent TRH provocation in vivo in chickens. Challenges with TRH at intervals of 1 h evoked different patterns of GH release in anesthetized adult chickens dependent upon TRH dosage. Initially, the administration of TRH at 10 micrograms/kg increased the plasma concentration of GH. However, the second and subsequent, through to the sixth challenges with TRH did not affect GH release. Plasma concentrations of GH were elevated by repeated injections of TRH (1.0 micrograms/kg). The magnitude of the response was reduced for the second and third challenges with full recovery of the GH response to the fifth challenge and an enhanced response to the sixth challenge. Similar GH secretory responses to TRH (at 0.1 micrograms/kg) were observed with the first through fourth challenge but the magnitude of response was again increased for the fifth and sixth challenge. At a lower dose (0.01 microgram/kg), TRH did not initially affect plasma concentrations of GH. However, GH release was increased by the third challenge, and subsequent TRH administration evoked progressively larger increases in plasma concentration of GH. It would appear that only high doses of TRH induce refractoriness to subsequent challenge, while lower doses presensitize the pituitary to TRH. If TRH challenges at a dose which provokes the complete refractoriness (10 micrograms/kg) are administered at intervals of 2, 3 or 4 h, the GH secretory response is consistent for each challenge. The refractoriness to TRH is thus overcome within a period of 2 h.

Animals↗

The role of thyroid hormones in the growth hormone response to protein restriction in the domestic fowl (Gallus domesticus).

The possible role of thyroid hormones in the rise in plasma GH observed in protein-restricted chicks was examined. Increased sensitivity of protein-restricted chicks to secretagogue challenge (TRH or GH-releasing factor) appears to account, at least in part, for increased GH concentrations in protein-restricted chicks. Thyroid hormones administered acutely were able to suppress plasma GH concentrations in protein-restricted chicks. Further, chronic thyroid hormone supplementation to low protein diets normalized circulating thyroid hormone concentrations and also normalized the response to GH secretagogue challenge. This decreased sensitivity to TRH provocation occurred without an accompanying change in plasma concentrations of insulin-like growth factor-I, a reputed inhibitor of GH secretion in the chicken.

Animals↗

Pharmacological investigations on the lipolytic and antilipolytic effects of growth hormone (GH) in chicken adipose tissue in vitro: evidence for involvement of calcium and polyamines.

The involvement of RNA/protein synthesis, calcium, calmodulin, protein kinase C, and polyamines in the lipolytic and antilipolytic (inhibition of glucagon-stimulated lipolysis) responses to GH have been investigated employing chicken adipose tissue in vitro. The lipolytic, but not the antilipolytic, effect of GH was blocked by inhibitors of RNA/protein synthesis (actinomycin D, cycloheximide, and puromycin) and calcium uptake (verapamil) and low calcium concentrations (0.28 mM CaCl2). The antilipolytic, but not the lipolytic, effect of GH was blocked by alpha-difluoromethylornithine (DFMO), a polyamine synthesis inhibitor. DFMO-induced blockade of the antilipolytic GH response was reversed by the addition of spermidine. The lipolytic and antilipolytic effects of GH were not influenced by chlorpromazine (a calmodulin inhibitor) or phorbol 12-myristate 13-acetate (PMA) (an activator of protein kinase C).

Adipose Tissue↗

Inhibition of growth hormone-stimulated lipolysis by somatostatin, insulin, and insulin-like growth factors (somatomedins) in vitro.

The effects of somatostatin, insulin, insulin-like growth factor I (IGF-I), and insulin-like growth factor II (IGF-II)/MSA on growth hormone (GH) (1 microgram/ml)-induced lipolysis were examined employing chicken adipose tissue in vitro. Basal and GH-stimulated glycerol release were inhibited by somatostatin (1 ng/ml) and by IGF-II/MSA (10 and 100 ng/ml). Insulin and IGF-I (10 and 100 ng/ml) completely inhibited the lipolytic response to GH without affecting basal glycerol release. Insulin and IGF-I were equipotent in inhibiting GH-induced lipolysis while IGF-II is only 16% as potent as insulin.

Adipose Tissue↗

Inhibition of growth hormone-induced lipolysis by 3',5'-guanosine monophosphate in chicken adipose tissue in vitro.

The influence of cyclic 3',5'-guanosine monophosphate (cGMP) on the lipolytic and antilipolytic (inhibition of glucagon-stimulated lipolysis) responses to GH (1 microgram/ml) was examined in chicken adipose tissue in vitro. Both 8-bromo-cGMP (0.1 mM) and sodium nitroprusside (1 mM) (a guanyl cyclase stimulator) completely inhibited the lipolytic effect of GH. A cGMP-lowering agent, LY83583 (10 microM), reversed the inhibitory effect of sodium nitroprusside on GH-stimulated lipolysis. Furthermore, the suppressive effects of insulin (100 ng/ml), insulin-like growth factor I (IGF-I) (100 ng/ml), or insulin-like growth factor II (IGF-II/MSA) (100 ng/ml), but not somatostatin (1 ng/ml), on GH-stimulated lipolysis were prevented by LY83583 addition. Neither 8-bromo-cGMP, sodium nitroprusside, nor LY83583 altered GH-induced inhibition of glucagon (1 ng/ml)-stimulated lipolysis. It is proposed that cGMP may mediate inhibitory control of GH-stimulated lipolysis by insulin, IGF-I, and IGF-II in chicken adipose tissue.

Adipose Tissue↗

Effect of age and protein restriction on the clearance and secretion of growth hormone in the domestic fowl.

Metabolic clearance rates (MCR) and secretion rates for growth hormone (GH) were determined in young (6-wk-old) chicks and adults (1 yr old) as well as in chicks fed low protein diets for 2 wk. Birds were either conscious or anesthetized during these determinations in the latter study. Age-related differences in plasma concentrations of GH reflect greater secretion of GH in younger chicks (3.5-fold increase). The MCR was reduced by 35% in chicks compared with adults, but when expressed per unit metabolic body weight, was higher in the young chickens. The MCR in protein-restricted chicks was 28% lower than in that of controls. However, when the MCR was calculated on a metabolic body weight basis, protein-restricted and control chicks did not differ in MCR. Elevated plasma concentrations of GH in unanesthetized, protein-restricted chicks were due to greater GH secretion (2.4-fold) of these chicks compared with secretions of chicks fed control diets. Basal secretions of GH, determined in the anesthetized chicks, did not differ between dietary treatments. These results indicate that secretion of GH but not clearance was affected by protein restriction in conscious birds.

Age Factors↗