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Biomedical subjects

C G Scanes

Publications and source records attributed to C G Scanes.

At least 127 records · Page 7Linked to original sources
PubMed1986

Somatostatin inhibits thyroid function in fowl.

Plasma concentrations of thyroxine (T4) and triiodothyronine (T3) were marginally (less than 25%) lowered 10 and 60 min, respectively, following somatostatin (SRIF) administration (at doses of 10-30 micrograms/kg) in immature domestic fowl. When plasma iodothyronine levels were elevated by the administration of anti-SRIF (1.0 ml/kg) 10 min prior to SRIF challenge, the inhibitory effect of SRIF on T4 and T3 concentrations was greatly augmented. The relative reduction in the T3 concentration was greater than the decline in the T4 level, resulting in a decline in the T3:T4 ratio. These data indicate that SRIF inhibits thyroid function in fowl, possibly by direct effects on the thyroid gland and by effects on the peripheral conversion of T4 to T3.

Animals↗
PubMed1986

Seasonal changes in some plasma hormones in pigeons: diurnal variation under natural photoperiods with constant or seasonally changing ambient temperature.

The diurnal variations of several plasma hormones and free fatty acids (FFA) were studied during periods in summer and winter for pigeons reared either outdoors or indoors. The latter were subjected to constant temperature and naturally varying photoperiods. A significant seasonal variation in the mean daily levels of triiodothyronine (T3), thyroxine (T4), corticosterone (B), lutropin (LH) and FFA was seen in the outdoor birds and in the T4 and B levels of indoor birds. The diurnal variation of hormone levels was generally more pronounced in winter in both groups. Cold ambient temperature significantly decreased the plasma LH level and potentiated the increasing effect of short photoperiod on plasma B level. Diurnal variation of plasma FFA level seems to be under the control of photoperiod, without any effects due to the ambient temperature. No significant correlation was found between FFA and GH concentrations.

Acclimatization↗
PubMed1986

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.

Aging↗
PubMed1986

Stimulation of in-vivo growth hormone secretion in young chickens by rat hypothalamic growth hormone-releasing factor and synthetic analogues.

Rat hypothalamic GH-releasing factor (rhGRF), at doses between 0.1 and 10 micrograms/kg, increased plasma GH concentrations in immature domestic fowl 5-10 min after i.v. injection. Sodium pentobarbitone anaesthesia blunted the GH responses to rhGRF, although in both conscious and anaesthetized chicks the maximal responses were induced by a dose of 1 microgram rhGRF/kg. The stimulatory effect of rhGRF on in-vivo GH secretion was less than that provoked by corresponding doses of human pancreatic GRF, but greater than that elicited by two rhGRF analogues, (Nle27)-rhGRF(1-32) and (Nle27)-rhGRF(1-29). These results demonstrate that the chicken pituitary is responsive to mammalian GRF and provide evidence of structure-activity relationships of GRF in the domestic fowl.

Animals↗
PubMed1986

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.

Adipose Tissue↗
PubMed1986

Effect of thyroid hormones on growth hormone secretion in broiler chickens.

Plasma concentrations of growth hormone (GH) were observed to be significantly elevated following the administration of thyrotropin-releasing hormone (TRH) in young (4- to 12-week-old) but not in adult (20-week-old) broiler chickens. However, adult sex-linked (dw) dwarf hens did respond to TRH. Treatment with triiodothyronine (T3) but not thyroxine (T4) (at 1 ppm in the diet from hatch) consistently and significantly reduced the growth rate and decreased the plasma concentrations of GH following TRH injection in normal (DwDw males or Dw-females), hemizygous dwarf (dw-) female, and heterozygous (Dwdw) male lines of broiler chickens. Similarly, T3 was significantly more effective than T4 in inhibiting the increase in plasma concentrations of GH following TRH injection in broiler chicks made hypothyroid by methimazole administration.

Animals↗
PubMed1986

Effect of chicken growth hormone, triiodothyronine and hypophysectomy in growing domestic fowl.

Hypophysectomy in growing chicks was followed by reduced body and skeletal (shank-toe length) growth. In addition decreases were observed in tibia length and weight (although the proximal growth plate often contained more cartilage and was less uniform in its thickness), the plasma concentrations of immunoreactive-Somatomedin C (IR-SmC) and free fatty acids and weight for the heart, liver, pectoralis, thymus, and bursa Fabricus. The effect of triiodothyronine (T3) and purified chicken growth hormone (GH) on body and other growth was examined in hypophysectomized chicks. Body and skeletal growth (as estimated by respectively the increases in body weight and shank toe length in 24 days) were increased by the administration of T3 (either as injections or in the diet). T3 also increased tibia weight and length and returned the proximal growth plate thickness to that found in intact controls. Similarly T3 administration was followed by increases in the weights of the heart, liver, thymus, and bursa Fabricus. However plasma concentrations of IR-SmC were unaffected by T3 treatment. Chicken GH at a dose of 100 micrograms/kg stimulated aspects of growth somewhat with injections of chicken GH being followed by a slight increase in tibia length and a substantial increase in thymus weight. Chicken GH also increased plasma concentrations of IR-SmC and free fatty acids. Combination T3 and chicken GH treatment did not cause greater growth than observed with T3 alone. An exception to this being the greater weight of the bursa Fabricus in the chicks receiving T3 and GH than T3 alone. Intact male chicks which received injections of chicken GH (10 micrograms) between 1 and 14 day old had slightly greater body weight at 31, 38 and 44 days old relative to vehicle injected chicks.

Aging↗
PubMed1985

Growth hormone secretion in anaesthetized fowl. 1. Refractoriness to repeated stimulation by human pancreatic growth hormone-releasing factor (hpGRF) or thyrotrophin releasing hormone (TRH).

The intravenous (iv) administration of thyrotrophin releasing hormone (TRH, at 1.0 or 10.0 micrograms/kg) or human pancreatic growth hormone-releasing factor (hpGRF(1-44)NH2, at 10 micrograms/kg) markedly increased the growth hormone (GH) concentration in the plasma of immature or adult cockerels anaesthetized by sodium pentabarbitone (30 mg/kg, iv). A second injection of either TRH or hpGRF failed to increase the GH concentration in immature chicks when administered 15, 30, or 60 min after the first injection. However, significant GH responses to TRH or hpGRF were observed when the interval between injections was either 120 or 240 min. The magnitude of the GH responses to TRH were, however, diminished by 83.3 and 26.7% when given 120 or 240 min after the initial TRH injection, and the responses to hpGRF were similarly reduced by 68.3 and 33.6%. A similar period of GH refractoriness to TRH or hpGRF stimulation was also observed in adult birds, although the recovery of GH responsiveness occurred earlier. While a second injection of hpGRF was ineffective in increasing the plasma GH concentration if given within 30 min of the first, it was fully effective when the interval between injections was greater than 60 min. In response to a second injection of TRH, the GH concentration was elevated when the interval between injections was greater than 120 min, after which the magnitude of the response evoked was greater than that induced by the initial injection. Growth hormone secretion secretion in immature and adult fowl is therefore refractory to repeated provocative stimuli, although the mechanism involved is unknown.

Anesthesia↗
PubMed1985

Growth hormone secretion in anaesthetized fowl. 2. Influence of heterologous stimuli in birds refractory to human pancreatic growth hormone-releasing (hpGRF) or thyrotrophin releasing hormone (TRH).

In anaesthetized young (6 weeks old) and adult (22-30 weeks old) domestic fowl, the administration of thyrotrophin releasing hormone (TRH; 1.0 micrograms/kg in young birds; 10.0 micrograms/kg in adults) or human pancreatic growth hormone-releasing factor (hpGRF(1-44)NH2; 10.0 micrograms/kg in both cases) markedly increased the growth hormone (GH) concentration in plasma samples collected 10 min later. In birds injected with TRH, this stimulation of GH secretion attenuated the GH response to a second TRH challenge (given 15 or 60 min after the first in adult or young birds, respectively); similarly, hpGRF pretreatment blunted the GH response to a further hpGRF injection. However, the administration of hpGRF to both immature and adult birds made refractory to TRH challenge was followed by increased GH secretion and vice versa. Moreover, the GH secretory response to hpGRF in birds pretreated with TRH was greater (1.99-fold in young birds, 1.52-fold in adults) than the increase in plasma GH concentration following hpGRF administration in untreated birds. Similarly, prior exposure to hpGRF also increased the GH response to TRH stimulation (by 2.24-fold in the young, 3.56-fold in the adults). These results demonstrate that TRH not only overcomes GH refractoriness to hpGRF and vice versa, but the GH response to heterologous provocative stimuli is potentiated in birds refractory to TRH or hp GRF challenge.

Anesthesia↗
PubMed1985

Isolated adrenocortical cells of the domestic fowl (Gallus domesticus): steroidogenic and ultrastructural properties.

Isolated adrenocortical cells from White Leghorn chickens (Gallus domesticus) were compared to those from rats (Rattus norvegicus). Cells were prepared from collagenase-dispersed adrenal glands of sexually mature male animals. Corticosterone was measured by radioimmunoassay after incubation for 2 h with steroidogenic agents. Of the four ACTH analogues used, three were 6-17 times more potent with rat cells than with fowl cells (potencies were indicated by half-maximal steroidogenic concentrations). However, 9-tryptophan (O-nitrophenylsulfenyl) ACTH was 8 times more potent with fowl cells than with rat cells, thus suggesting that ACTH receptor differences exist between the two cell types. In addition, cAMP analogues were 10 times more potent with rat cells than with fowl cells suggesting that fowl corticosteroidogenesis is less dependent on cAMP than is rat corticosteroidogenesis. At equal cell concentrations, rat cells secreted 20-40 times more corticosterone than did chicken cells when they were maximally stimulated. Although rat cells converted 8 times more pregnenolone to corticosterone than did fowl cells, the half-maximal steroidogenic concentration for pregnenolone-supported corticosterone synthesis was the same for both cell types (about 5 microM). This suggests that fowl cells have lower steroidogenic enzyme content rather than lower steroidogenic enzyme activity. An unusual feature seen in the isolated fowl adrenocortical cells was an abundance of intracellular filaments.

Adrenal Cortex↗
PubMed1985

Effect of androgens and gonadotropins on progesterone secretion of chicken granulosa cells.

A culture system has been used to study the effect of PMSG in vivo pretreatment and androgens on the in vitro secretion of progesterone from avian granulosa cells. PMSG in vivo pretreated cells secreted greater amounts of progesterone than did cells obtained from untreated hens. Testosterone and 5-alpha-dihydrotestosterone significantly increased basal progesterone secretion in PMSG pretreated cells as well as in granulosa cells harvested from non-treated hens. Testosterone or 5 alpha-dihydrotestosterone in combination with FSH or LH were additive and never resulted in a synergistic stimulation of progesterone secretion.

Animals↗
PubMed1985

Adrenergic control of lipogenesis and lipolysis in the chicken in vitro.

The adrenergic inhibition of lipogenesis and stimulation of lipolysis in the avian has been examined using chicken hepatocytes and adipose tissue explants in vitro. Lipogenesis was inhibited by adrenergic agonists: epinephrine (alpha + beta) greater than isoproterenol (beta 1/beta 2) greater than norepinephrine (alpha 1/alpha 2, beta 1) greater than metaproterenol (beta 2), phenylephrine (alpha 1). Dobutamine (beta 1 agonist) and dopamine (dopaminergic agonist) did not significantly affect [14C]acetate incorporation into lipid, while clonidine and para-aminoclonidine (alpha 2 agonists) were slightly stimulatory. Lipolysis in young and adult chicken adipose tissue was stimulated by epinephrine, isoproterenol, phenylephrine, dobutamine and metaproterenol, but was inhibited by clonidine and para-aminoclonidine. Both the antilipogenic and lipolytic effects of epinephrine were partially blocked by phentolamine (alpha 1 = alpha 2 antagonist) or propranolol (beta 1 = beta 2 antagonist), but completely inhibited by phentolamine and propranolol administered together.

Adipose Tissue↗
PubMed1985

Effects of prostaglandin F2 alpha on prolactin secretion in the fowl.

The plasma concentration of prolactin in immature cockerels was increased between 10 and 40 min after the intravenous administration of prostaglandin (PG) F2 alpha (200 micrograms/kg body weight). Lower doses had no effect on plasma prolactin concentration. The addition of PGF2 alpha (10(-9) to 10(-6) M) to incubation media had no effect on the basal release of pituitary prolactin but reduced the release of prolactin from pituitary-hypothalamus co-incubations. The addition of noradrenaline (10(-7) M), serotonin (10(-7) M), acetylcholine (10(-6) M) or histamine (10(-6) M) to the co-incubation increased the hypothalamus-induced prolactin release, although these effects were not observed in the presence of 10(-7) M PGF2 alpha. The in vitro release of pituitary prolactin was increased by adding chicken hypothalamic extract in the presence or absence of PGF2 alpha. These results suggest a dual effect on PGF2 alpha of prolactin secretion in the fowl; its stimulation in vivo may result from a peripheral action.

Animals↗
PubMed1985

TRH stimulation of in vivo GH release in the domestic fowl. Influence of TRH metabolites and effect of age on in vitro degradation of TRH.

Thyrotropin-releasing hormone (TRH) stimulated in vivo growth hormone (GH) release in conscious and anesthetized young domestic fowl. The administration of the presumed metabolites of TRH, deamido-TRH (TRH-OH) and histidyl-proline diketopiperazine (HPD), was followed by small but significant (p less than 0.05) increases in the plasma concentrations of GH in both conscious and anesthetized chicks. However, the ability of TRH-OH or HPD to stimulate GH secretion was less than that observed with a 100-fold lower dose of TRH. The administration of either TRH-OH or HPD with TRH increased the GH response over that observed with TRH alone. The ability of chicken plasma to degrade exogenous TRH in vitro was determined by measuring immunoreactive TRH (IR-TRH) content and by assessing the ability of the incubated samples to increase the plasma concentration of GH when administered to young fowl. The in vitro half-life of TRH was estimated to be 9.8 (by immunoassay) and 9.6 (by a biological index) min for plasma from adult male chickens and 23.9 (by immunoassay) and 20.2 (by biological index) min for plasma from 6-week-old chicks. This difference in degradation may account, at least in part, for the observed age-related decrease in the plasma concentration of GH in birds and for the diminished GH responsiveness of adult birds to exogenous TRH.

Age Factors↗