Biomedical subjects

C G Scanes

Publications and source records attributed to C G Scanes.

At least 109 records · Page 6Linked to original sources

PubMed1988

Influence of age, strain, and beta-adrenergic agonist on insulin sensitivity in chicks as determined by an adaptation of the euglycemic clamp technique.

The euglycemic clamp technique has been widely used to examine changes in in vivo insulin sensitivity during physiological changes in mammals. The technique offers the advantage that the tissue uptake of glucose induced by a set dose of insulin is determined at the normal (steady state) circulating concentration of glucose (euglycemia). The euglycemic clamp technique has been modified to examine in vivo sensitivity to insulin in chickens. Insulin sensitivity is determined by the rate of infusion of exogenous glucose required to maintain euglycemia. Young (6 to 8-wk-old) male chickens (White Leghorn) are more sensitive to insulin than adult males of the same strain. There is, however, no difference in insulin sensitivity between young male chicks of broiler and White Leghorn strains. Chronic administration of beta-adrenergic agonist (L-640,033, donated by Merck, Sharp, and Dohme Research Laboratories, Rahway, NJ) in the diet, at levels of 0, .25, 1.0, and 4.0 ppm for 3 to 5 days also did not influence in vivo insulin sensitivity.

Adrenergic beta-Agonists↗

PubMed1987

Growth hormone secretion from chicken adenohypophyseal cells in primary culture: effects of human pancreatic growth hormone-releasing factor, thyrotropin-releasing hormone, and somatostatin on growth hormone release.

A primary culture of chicken adenohypophyseal cells has been developed to study the regulation of growth hormone (GH) secretion. Following collagenase dispersion, cells were exposed for 2 hr to vehicle (control) or test agents. Human pancreatic (tumor) growth hormone-releasing factor (hpGRF) and rat hypothalamic growth hormone-releasing factor stimulated GH release to similar levels. GH release was increased by the presence of dibutyryl cyclic AMP. Thyrotropin-releasing hormone (TRH) alone did not influence GH release; however, TRH plus hpGRF together exerted a synergistic (greater than additive) effect, increasing GH release by 100 to 300% over the sum of the values for each secretagogue acting alone. These relationships between TRH and hpGRF were further examined in cultured cells exposed to secretagogues for two consecutive 2-hr incubations. TRH pretreatment enhanced subsequent hpGRF-stimulated GH release by about 80% over that obtained if no secretagogue was present during the first incubation. In other experiments, somatostatin (SRIF) alone did not alter GH secretion. However, SRIF reduced hpGRF-stimulated GH release to levels found in controls. Furthermore, GH release stimulated by the presence of both TRH and hpGRF was lowered to control values by SRIF. The results of these studies demonstrate that a primary culture of chicken adenohypophyseal cells is a useful model for the study of GH secretion. Indeed, these results suggest that TRH and hpGRF regulate GH secretion by mechanisms which are not identical.

Animals↗

PubMed1987

Opiate inhibition of growth hormone secretion in young chickens.

Plasma concentrations of growth hormone (GH) were decreased following the intravenous administration of morphine sulfate. Maximum inhibition of GH secretion was observed 40 min after morphine sulfate challenge. At this time, doses of morphine sulfate (at 5 mg and 50 mg/kg) reduced the GH concentrations by 86 and 90%, respectively, in comparison with those in the vehicle-injected controls. An opiate antagonist, naloxone, had no stimulatory effect on basal GH concentrations, but attenuated the GH response to morphine. Neither morphine nor naloxone had any significant effect on circulating luteinizing hormone (LH) levels. These results indicate an inhibitory opiate pathway in the control of GH release and demonstrate effects on GH and LH secretion contrary to those observed in mammalian species.

Animals↗

PubMed1987

Polyhormonal regulation of avian and mammalian corticosteroidogenesis in vitro.

1. The combined actions of ACTH, corticosterone and prolactin (PRL) in the acute regulation of corticosteroidogenesis were investigated using isolated adrenocortical cells from intact and hypophysectomized (hypox) rats (Rattus norvegicus) and from intact male domestic fowl (Gallus gallus domesticus). 2. Exogenous corticosterone suppressed to about 50% ACTH-induced corticosterone production of cells from either species. This suppression, in part, was due to corticosterone degradation. 3. oPRL, in the presence or absence of ACTH, raised corticosterone production of hypox rat cells, but not intact rat and domestic fowl cells. 4. In addition, oPRL counteracted the corticosterone-induced suppression of net ACTH-stimulated corticosterone production of hypox rat and intact domestic fowl cells, but not intact rat cells. 5. The potency of oPRL with domestic fowl cells was 4 times that with hypox rat cells. 6. Furthermore, in domestic fowl cells, the effect of oPRL was Ca2+-dependent.

Adrenal Cortex↗

PubMed1987

Somatostatin inhibition of growth hormone secretion in an adult bird: the domestic fowl.

1. The intravenous (i.v.) infusion of somatostatin (SRIF, 1.0 microgram/kg per min) promptly (within 5 min) reduced the growth hormone (GH) concentration in the plasma of conscious adult chickens. 2. The GH concentration progressively declined throughout a 60-min period of SRIF infusion, but was dramatically increased above pre-infusion levels within 5 min of SRIF withdrawal and maintained at an elevated level for at least 30 min afterwards. 3. Sodium pentobarbitone-anaesthesia lowered the basal GH concentration to levels comparable with those in conscious birds infused with SRIF. When administered to anaesthetized birds, exogenous SRIF was unable to further reduce the GH concentration and unable to induce 'rebound' GH release. 4. While thyrotropin releasing hormone (TRH, 10 micrograms/kg) increased the GH concentration in both conscious and anaesthetized birds, only the GH response in the anaesthetized birds was diminished by SRIF infusion. 5. Rebound GH secretion following the termination of SRIF infusion was observed in both conscious and anaesthetized birds injected with TRH. 6. These results demonstrate that SRIF can inhibit basal and TRH-stimulated GH secretion in adult domestic fowl and indicate that anaesthesia disrupts the normal control of GH releases.

Animals↗

PubMed1987

Influence of triiodothyronine and growth hormone on growth of dwarf and normal chickens: interactions of hormones and genotype.

The effects of dietary triiodothyronine (T3), injections of a preparation of growth hormone (GH) (purified from chicken pituitary tissue) and their combination on growth were investigated in three lines of chickens. The three lines were the Cornell K strain (K) (a single Comb White Leghorn strain), the Cornell K strain hemizygous for the sex-linked dwarfing gene (SLD), and the Cornell K strain homozygous recessive for the autosomal dwarfing gene (ADW). A dietary T3 treatment by genotype interaction was observed. Dietary T3 (0.1 ppm) decreased growth in the K line, tended to decrease growth in the ADW line while it tended to increase growth in the SLD line. Chicken growth hormone (100 micrograms/kg body wt) alone did not affect growth in any of the lines studied. There was, however, a GH treatment by T3 treatment interaction. Chicken GH overcame the growth-depressing effects of T3 in the K and ADW lines while it tended to promote growth in T3 treated SLD birds. Dwarf (SLD) chickens had higher basal circulating GH concentrations, lower circulating immunoreactive somatomedin C concentrations, and lower circulating T3 concentrations than the K or ADW chickens.

Aging↗

PubMed1987

Opiate participation in thyroid hormone regulation in domestic fowl.

Administration of morphine sulfate (at 5 and 50 mg/kg) to immature domestic fowl lowered the circulating thyroxine (T4) concentration in a dose- and time-dependent manner. The inhibitory effect of morphine on T4 secretion was mediated via opiate receptors, since it was completely blocked in the presence of naloxone (50 mg/kg). The possibility that T4 secretion may be under tonic opioid inhibition was suggested by a stimulatory effect of naloxone on plasma T4 concentrations. Morphine sulfate (50 mg/kg) enhanced plasma triiodothyronine concentrations, an effect that was completely suppressed in the presence of naloxone. These results demonstrate differential effects of opiates on T4 and T3 concentrations and suggest that opiates tonically inhibit T4 release and accelerate its rate of peripheral monodeiodination.

Animals↗

PubMed1987

Postnatal changes in circulating concentrations of growth hormone, somatomedin C and thyroid hormones in pigs.

Plasma concentrations of growth hormone (GH), somatomedin (SmC), thyroxine (T4) and triiodothyronine (T3) were determined from birth to post weaning in pigs (Yorkshires). Plasma samples were obtained from the smallest, median and largest piglet from 11 litters. No differences in the circulating concentrations of any of the hormones were observed between piglets of different sizes. However, there were changes in circulating concentrations of hormones during postnatal development. Plasma concentrations of GH decreased between 2 and 8 to 10 days of age. A progressive increase in the circulating concentrations of SmC was observed with concentrations rising (3.83-fold between 2 days and 40 days of age). Plasma concentrations of T4 and T3 were maximal at 23 and 16 days of age, respectively.

Aging↗

PubMed1987

Plasma concentrations of growth hormone and somatomedin C in dwarf and normal chickens.

Sex-linked dwarf chicks, offspring from the mating of heterozygous sires with dwarf females, were used in this study. On days 18 and 20 of incubation, plasma concentrations of growth hormone (GH) and somatomedin C (Sm-C) did not differ between normal chicks and those of the dw-dwdw genotype. After hatching, Sm-C concentrations in normal chicks remained comparable to the embryo values for up to 1 week, but those in dwarf chicks were lower. After 3 weeks Sm-C increased greatly in the controls, whereas in dwarf birds it was far less pronounced up to 18 weeks of age and only increased to control levels on week 12. GH was low during incubation and increased sharply after hatching in normal and dwarf chicks. After 3 weeks and up to 18 weeks, GH levels were higher in dwarf chicks, except at week 12 when they decreased to control concentrations.

Animals↗

PubMed1987

Effects of hyper- or hypothyroid status on growth, adiposity and levels of growth hormone, somatomedin C and thyroid metabolism in broiler chickens.

Relatively few methods involving dietary manipulation of thyroid status have been used to study the effect of that status on growth and body composition as well as on changes in hormone levels and metabolism. The present work examines the influence of either a hyperthyroid status (induced by feeding triiodothyronine: T3 or thyroxine: T4) or a hypothyroid status (induced by feeding methimazole: MMI) on growth, feed consumption and body composition as well as on changes in thyroid hormone levels and metabolism and in hormone levels of the somatotroph axis of broiler chickens. MMI depressed growth but increased fatness. Long-term administration of thyroid hormones decreased both growth and fat deposition, T3 being more effective than T4. The reduced growth of MMI-treated birds was not only related to the hypothyroid state but also to decreased somatomedin C (Sm-C) production, although growth hormone (GH) levels remained high. Thyroid hormone-treated birds showed slightly depressed GH levels but unchanged Sm-C levels. MMI induced an increase in hepatic 5'-monodeiodination activity, while T3 and T4 reduced that activity. The T4 administered was largely eliminated as inactive reverse T3. Both of the statuses (hypothyroid and hyperthyroid) profoundly changed peripheral thyroid hormone metabolism and influenced GH/Sm-C relationships, but in the opposite way. Hormonal changes could be related to the observed changes in growth and adiposity of broiler chickens and illustrate the negative correlation between T3 and body fat.

Adipose Tissue↗

PubMed1987

Control of energy balance during egg production in the laying hen.

The energetic costs of egg production are considered, as is the relationship between egg production and feed intake. Hens feed during the photophase with a peak in consumption prior to the scotophase. This pattern of intake, followed by nocturnal fast, would be expected to lead to an energy deficit at night. However, much of the energy requirement of the night is met by utilization of feed stored in the upper gastrointestinal tract. It is presumed that some nocturnal energy deficit occurs and is met by changes in metabolism and endocrine balance. The hormonal involvement in these changes in avian metabolism is discussed.

Animal Feed↗

PubMed1987

Hormonal responses to protein restriction in two strains of chickens with different growth characteristics.

The hormonal response to protein restriction was studied in breeds of chickens with different rates of growth and body size. Fast-growing (broiler) chicks and lighter-weight (White Leghorn) birds were fed isoenergetic 5% (low) and 20% (control) protein diets ad libitum starting at 2 wk of age. At 4 wk of age, one-half of each group continued receiving the initial diet, while the other half was fed the alternate diet for two additional weeks. Growth was decreased in birds fed the low protein diet due to restriction of protein, sustained low feed intake and hence possibly insufficient energy for growth. Birds fed low protein diets had higher plasma growth hormone (GH) concentrations (325% in Leghorns and 233% in broilers) compared with controls. Plasma concentrations of somatomedin-C in protein-restricted Leghorn and broiler chicks were only 50 and 34% of those of controls, respectively. Similarly plasma concentrations of thyroxine (T4) and triiodothyronine (T3) were reduced in protein-deprived birds compared with those fed adequate protein. Plasma T3 concentrations of restricted birds were 48 (Leghorns) and 47% (broilers) of those of controls, whereas plasma T4 concentrations were 44 (Leghorns) and 41% (broilers) of those of controls.

Animals↗

PubMed1987

Cimaterol-induced muscle hypertrophy and altered endocrine status in lambs.

The objectives of this study were 1) to determine how cellular growth of skeletal muscle is altered by the repartitioning agent cimaterol and 2) to determine if cimaterol alters endocrine status in association with its repartitioning effects. Thirty Dorset wether lambs were randomly assigned to a pre-treatment baseline group or received 0 or 10 ppm cimaterol in a complete, mixed, high-concentrate diet for 7 or 12 wk. Weights of biceps femoris (BF), semimembranosus (SM) and semitendinosus (ST) muscles were 32.8, 27.1 and 31.5% greater, respectively, in treated lambs at 7 wk, and were 22 to 24% greater at 12 wk. Longissimus (LD) cross-sectional area was 26 and 32% greater at these treatment intervals. Percent type I fibers declined significantly over the course of the experiment in ST, SM and LD, and cimaterol caused a small but significant reduction in percent type I fibers in the ST at 7 and 12 wk. Muscles from lambs fed cimaterol contained 50 and 75% more fibers that exhibited negative staining for phosphorylase activity. Mean cross-sectional area of type I and type II fibers in the combined portions of the ST were 30.4 and 29.3% greater, respectively, in cimaterol-fed lambs after 12 wk, while type I and type II fiber areas in the longissimus were only 13 and 15% greater, respectively. Cimaterol-induced hypertrophy of the ST resulted in both protein and RNA content being 30 to 35% greater (P less than .01) at 7 and 12 wk, while DNA concentration was 22% less (P less than .01) at 7 wk. DNA concentration returned to normal by 12 wk. These results indicate that cimaterol elicits a rapid increase in muscle RNA and protein accretion without concurrent incorporation of satellite cell nuclei. Plasma insulin and insulin-like growth factor-1 (IGF-1) concentrations were 55 and 34% lower, respectively, in cimaterol-fed lambs. Plasma somatotropin concentration and area under the curve were 2.3 times greater (P less than .01) in lambs fed cimaterol for 6 wk, while plasma cortisol, prolactin and glucose concentration were unaffected at 6 or 12 wk. The significant changes in endocrine status may be important in the mechanism(s) of cimaterol in altering muscle accretion.

Adrenergic beta-Agonists↗

PubMed1987

Growth hormone inhibition of glucagon- and cAMP-induced lipolysis by chicken adipose tissue in vitro.

The ability of growth hormone (GH) to inhibit the early (first hour) lipolytic response to glucagon and cAMP was investigated using chicken adipose tissue explants in vitro. In the first hour of incubation, GH inhibited glucagon, 8-bromo-3',5'-cyclic adenosine monophosphate (8-bromo-cAMP), and 1-isobutyl-3-methyl-xanthine (IBMX) induced glycerol release. The antilipolytic effect of GH was dose dependent, with inhibition of glucagon and 8-bromo-cAMP observed in the presence of as little as 100 ng/ml GH. In the fourth hour of incubation (late lipolytic response), GH (10, 100, or 1000 ng/ml) enhanced the lipolytic action of glucagon.

1-Methyl-3-isobutylxanthine↗

PubMed1987

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.

Animals↗

PubMed1987

Effects of slaframine on circulating concentrations of growth hormone and glucose.

The ability of slaframine (SF), a parasympathomimetic, to alter blood growth hormone (GH) and glucose concentrations in broiler chicks was investigated. Eighty male broiler chicks (average weight 225 g) were divided into 10 groups and dosed with either saline (control) or 1 mg SF/kg of body weight by oral intubation. Plasma samples were obtained from separate groups of chicks at 1, 2, 4, 8, and 12 hr after SF administration and analyzed for growth hormone and glucose. One hour after SF administration, glucose increased (P less than .05) 21.4% compared with controls. Growth hormone increased (P less than .05) 449 to 948% from 8 to 12 hr after SF administration. Administration of SF at 1 mg/kg of body weight was associated with increased plasma GH.

Alkaloids↗

PubMed1987

Thyroid function, growth hormone, and organ growth in broilers deficient in phosphorus.

The effects of a dietary P deficiency on thyroid function, serum growth hormone, and growth parameters in 10 to 29-day-old broiler cockerels was determined. Chicks fed severely P-deficient diets (.05% or .10% available P) grew more slowly and ate less feed than controls fed .65% P. The deficiency was also accompanied by hypercalcemia, hypophosphatemia, and decreases in percent bone ash, fat-free tibial weight, and tibial length and width. Increases in the relative weights of kidneys, hearts, and pituitary glands (.05% P only) occurred as well. Most of these changes occurred to a lesser extent or not at all in pair-fed controls, showing that they resulted specifically from the P deficiency and were not simply a result of reductions in feed intake. Phosphorus deficiency also was accompanied by peripheral edema and hydropericardium. Relative thyroid weight was unaffected. Serum triiodothyronine was consistently lower in the P-deficient chicks, although effects were significant only in one experiment. Thyroxine levels tended to be low also, but not consistently so. Serum growth hormone in P-deficient chicks in both studies was consistently lower than that in pair-fed controls, but this was significant only when .10% but not .05% available P was fed. The findings suggest that serum levels of both thyroid hormone and growth hormone are altered by P deficiency, but the results were not clearly definitive.

Animals↗

PubMed1987

Endocrinology of the avian embryo: an overview.

The full endocrine system is developed during the embryonic stages of the domestic fowl and probably in all avian species. This involves the genesis and differentiation of endocrine cells and progressive acquisition of interactions between endocrine tissues leading to integrated series of control systems. The embryonic endocrine organs produce hormones with a variety of physiological roles (including homeostatic, homeorhetic, and anticipatory). The present chapter provides an overview of the recent advances in the endocrinology of the avian embryo. Particular attention is focused on the general phenomenon of endocrine development and on the ontogeny of the hypothalamo-pituitary (growth hormone)-somatomedin-growth axis, the hypothalamo-pituitary-thyroid axis, and the hormones of calcium homeostasis.

Animals↗