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At least 577 records · Page 32Linked to original sources
PubMed1983

Effect of luteinizing hormone on progesterone production by the follicular granulosa in the ovarian hierarchy of the domestic fowl (Gallus domesticus).

A LH function test was used to assess the effect of a previously administered dose of ovine LH on the granulosa from the four largest preovulatory follicles, F1-F4, of laying hens. At intervals of 1, 3, and 6 hr after intravenous ovine LH (40 micrograms; a dose previously shown to cause atresia) or carrier solution (1% bovine serum albumin solution, BSA), a second dose of LH or carrier was injected. The progesterone contained in the dissected granulosa of the F1-F4 follicles 45 min after the second injection was measured by radioimmunoassay. With birds injected with BSA, the mean basal levels ranged from 17 to 59 ng progesterone per granulosa, irrespective of the follicular type. In short-term experiments, i.e., 45 min after LH, the mean progesterone contents of F1 (262 ng) and F2 (137 ng) were significantly higher than their controls, whereas those of F3 (59 ng) and F4 (21 ng) did not change. The response per cell was greater in the F1 granulosa than in that of F2-F4; other evidence is presented to support a hypothesis that the F1 granulosa contains a larger LH receptor population. The effect of LH over a longer period (6 hr) was shown by a decline in the steroidogenic response of the F1 granulosa only. The kinetics of this decline (estimated t1/2 13.7 hr) resembled that previously reported for adenylate cyclase activity in granulosa cells from postovulatory follicles (POF) (t1/2 about 14.4 hr).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Stimulatory and inhibitory effects of prostaglandin E2 on prolactin release in the domestic fowl.

In vivo prolactin secretion was increased in immature cockerels 20-30 min after the intravenous administration of prostaglandin (PG) E2 at a dose of 200 micrograms/kg. The addition of PGE2 to incubation medium had no direct effect on the release of pituitary prolactin during short-term (3-hr) culture, but augmented the stimulatory effect of hypothalamic tissue on prolactin secretion. The stimulatory effect of serotonin, noradrenaline, acetylcholine, and histamine on hypothalamus-induced prolactin release was also increased when pituitaries were coincubated with 10(-7)M PGE2, as was the stimulatory effect of thyrotrophin-releasing hormone (TRH) and hypothalamic extract (HE). The long-term (24-hr) preincubation of pituitaries with 10(-7)M PGE2 reduced the responsiveness of the prolactin-secreting cells to TRH or HE stimulation. PGE2 treatment also reduced the stimulatory effect of hypothalamic tissue on prolactin release and diminished the stimulatory effect of serotonin on hypothalamus-induced prolactin secretion. A 24-hr preincubation of hypothalamic tissue with 10(-7)M PGE2 also reduced its stimulatory effect on prolactin release when subsequently incubated with control pituitary glands. These results demonstrate that PGE2 initially stimulates in vivo and in vitro prolactin secretion in the fowl, possibly by increasing the release of hypothalamic prolactin-releasing activity and/or by increasing pituitary sensitivity to provocative stimuli. Chronic PGE2 stimulation appears to result in a reduction in pituitary responsiveness to stimulatory influences and in the release of hypothalamic-releasing activity.

Acetylcholine↗
PubMed1985

Some new observations on the binding of thyroxine and triiodothyronine to plasma proteins and lipoproteins in the domestic fowl.

In addition to the previously recognised thyroid hormone-binding proteins, three plasma components possibly involved in T3 and T4 transport have been identified in chicken plasma using gel filtration at pH 7.4. In mature female, though not male and immature female birds, a significant amount of T3 (11%) is bound to very-low- and low-density lipoproteins. These could mediate transport of the hormone into the egg. Similarly vitellogenin appears to bind small quantities of both T3 and T4. Selective precipitation of the lipoproteins and vitellogenin from laying-hen plasma produces a binding profile identical to that observed in male and juvenile female birds. Treatment of adult male birds with oestrogen induces a binding profile for T3 similar to that observed in adult females. Also a low-molecular-mass protein (9 X 10(3) D) which preferentially binds thyroxine in substantial amounts (20-30%) was found in plasma from adult male and female and immature female birds. The technique employed allows detection of plasma thyroid hormone-binding proteins which have not previously been resolved by simple electrophoretic procedures.

Animals↗
PubMed1985

The effect of exposure to 40 degrees on the heat production and the serum concentrations of triiodothyronine, thyroxine, and corticosterone in immature domestic fowl.

Four-week-old fowl were exposed to 40 degrees for 35 days and the effects on the serum concentrations of triiodothyronine (T3), thyroxine (T4), and corticosterone were investigated. Changes in resting heat production, food intake, body temperature, body weight gain, and growth (both in terms of skeletal growth and weight of selected organs) were also measured. Body temperature was increased at 40 degrees, and body weight gain and skeletal growth were both reduced. The serum concentrations of T3 and T4 were reduced at 40 degrees. The decrease in serum T3 was more strongly correlated with the reduction in food intake than was the reduction in T4. Resting heat production was decreased by exposure to 40 degrees; the reduction in heat production was correlated with serum T3 and serum T4 concentrations. Exposure to 40 degrees had no effect on adrenal weight or on serum corticosterone concentration but weights of the bursa, spleen, and thymus glands were decreased. These results suggest that (a) T3 is the principle metabolically active thyroid hormone in the chicken and that the reduction in heat production at 40 degrees is related to the decline in T3; (b) the reduction in T3 is a consequence of the reduction in food intake; and (c) the response to a stressor need not involve increased adrenocortical activity.

Animals↗
PubMed1986

In vitro release of triiodothyronine and thyroxine from thyroid glands of the domestic fowl (Gallus domesticus).

Basal and thyrotrophin (TSH)-stimulated release of iodothyronines (triiodothyronine, T3, and thyroxine, T4) from intact chicken thyroid glands was determined in vitro. In the absence of TSH, T3 and T4 were released in measurable amounts in the incubation media. The release of both iodothyronines was directly related to the media TSH concentrations and incubation period. Lineweaver-Burke analysis revealed that the Vmax for T3 was 99.4 pg/gland, with an apparent Km of 17.8 mU TSH, and that the Vmax for T4 was 323.35 ng/gland, with an apparent Km of 51.5 mU TSH, demonstrating that T4 is the major iodothyronine released by avian thyroid glands. The basal release of T4 was suppressed by the addition of a calcium chelator (ethyleneglycol-bis-(beta-aminoethylether)-N,N,N', N'-tetraacetic acid; EGTA), a calcium antagonist (cobalt chloride, CoCl2), or prostaglandin E1 (PGE1) to the incubation media. Basal T4 released was increased in the presence of a calcium agonist (lanthanum chloride, LaCl3), a calcium ionophore (A23187), dibutyryl cyclic adenosine 3'3'-monophosphate (dbcAMP), isobutylmethylxanthine (IBMX), indomethacin, magnesium chloride (MgCl2), and potassium iodide (KI). Thyrotrophin-stimulated T4 release was reduced by CoCl2, PGE1, and indomethacin but enhanced by LaCl3, MgCl2, and KI. These results demonstrate that it is possible to measure the release of thyroid hormones in an in vitro system in the chicken. Basal and stimulated iodothyronine release from the chicken thyroid gland appears to be mediated by calcium- and cAMP-dependent mechanisms.

Animals↗
PubMed1987

The ontogenesis of reproductive hormones in the female embryo of the domestic fowl.

The ontogenesis of sexual hormones and the responsiveness of both ovaries to LH were studied during the last third of incubation of chick embryos. Pituitary LH and FSH and serum 17 beta-estradiol increase through development to reach a plateau near hatching. Serum LH and the ovarian progesterone content show maxima on Day 19 of incubation. Serum progesterone levels are highly variable, with apparently unchanged values during development. Ovine LH was able to stimulate progesterone secretion in vitro in the left ovary at all times during development. LH stimulation of 17 beta-estradiol secretion in vitro is high on Day 13 in both ovaries but lower at later stages.

Animals↗
PubMed1987

Effects of insulin-like growth factor I (IGF-I) on growth hormone-releasing factor (GRF) and thyrotropin-releasing hormone (TRH) stimulation of growth hormone (GH) secretion in the domestic fowl (Gallus domesticus).

Recent studies in mammalian species indicate that IGF-I may act as a negative feedback inhibitor of GH release through alteration of pituitary secretion or sensitivity to hypothalamic regulatory factors. Although avian GH secretion appears to be regulated by the differential release of hypothalamic inhibitory (somatostatin) and stimulatory (GRF and TRH) factors, feedback effects of IGF-I on in vivo GH release in birds have not been investigated. To study the effects of elevated IGF-I concentration on GRF- and TRH-stimulated GH secretion, 4-week-old chickens received an intravenous injection of recombinant human IGF-I either 15 min prior to (6 micrograms, study 1), or simultaneous with (10 micrograms, study 2). GRF (hGRF44NH2, 5 micrograms/kg) or TRH (0.5 microgram/kg) administration. Radioimmunoassay analysis of plasma collected prior to and following peptide treatment indicated that circulating IGF-I concentrations were elevated 83.9, 60.6, 77.9, and 88.8% at the time of TRH and GRF administration in studies 1 and 2, respectively. Peak GH concentrations (mean of +5- and +15-min samples) subsequent to TRH injection were significantly (P less than 0.01) depressed 45.1 and 48.2% in IGF-I-treated as compared with control chicks in the first and second studies, respectively. GRF-stimulated GH secretion was significantly (P less than 0.01) decreased by IGF-I administration in study 2 (41.3%) but not in study 1. An estimated half-life for IGF-I in the chicken is less than 15 min based on the disappearance rate of the elevation produced by exogenous IGF-I injections. Thus, IGF-I exerts a negative feedback effect on pituitary hormone secretion in avian as well as mammalian species.

Animals↗
PubMed1989

Increases in calbindin D 28K mRNA in the uterus of the domestic fowl induced by sexual maturity and shell formation.

Uterine concentrations of calbindin D 28K mRNA were measured in immature pullets and laying hens by dot-blot hybridization using a [32P]cRNA probe prepared from the calbindin cDNA. In immature pullets, estrogen increased the calbindin mRNA level and the plasma concentration of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. When testosterone was administered with estrogen there was a further increase in calbindin and its mRNA and an increase in the free 1,25-(OH)2D3 index calculated as the ratio of the molar concentrations of total 1,25-(OH)2D3 and vitamin D-binding protein (DBP). In laying hens the uterine concentration of calbindin mRNA was low 4 hr after ovulation, but increased most markedly 12 and 18 hr later, when shell calcification took place. Calbindin concentration remained unchanged during the different stages of egg formation but was much higher in laying hens than in pullets treated with sex steroids. Suppression of shell formation by premature expulsion of the egg decreased the concentrations of calbindin mRNA and uterine calbindin and the free 1,25-(OH)2D3 index in the plasma. A concomitant increase in calbindin and its mRNA was observed at resumption of shell formation in hens previously laying shell-less eggs. Withdrawal of food for 44 hr decreased the uterine concentration of calbindin and its mRNA without a change in the free 1,25-(OH)2D3 index in the blood. It is concluded that the synthesis of uterine calbindin is stimulated primarily at sexual maturity and at calcification of the first shell by transcriptional processes. The daily increase in calbindin mRNA associated with shell formation and the absence of a concomitant change in calbindin concentration suggest that post-transcriptional processes exist and that stimuli other than the sex steroid or the 1,25-(OH)2D3 are involved in regulation of calbindin synthesis in the uterus.

Animals↗
PubMed1992

Influence of chicken and human lipoproteins on steroidogenesis in granulosa cells of the domestic fowl (Gallus domesticus).

When freshly dispersed granulosa cells from the largest preovulatory follicle were incubated in the presence of very low density (VLDL), low density (LDL), or high density (HDL) lipoproteins isolated from sera of laying hens, production of both basal and LH-stimulated progesterone was significantly increased in a dose-related manner. VLDL, the principal transporter of cholesterol to the ovum, appeared to be the most efficacious. A highly significant potentiation of the steroidogenic action of 8-bromo-cyclic adenosine monophosphate and forskolin was also observed. Human LDL, and especially HDL, caused significant stimulation of progesterone production by these cells. It is suggested that the release of cholesterol from lipoproteins taken up by granulosa cells raises the precursor pool for steroidogenesis. This mechanism is further enhanced by a cyclic AMP-mediated mechanism.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

Thinning of articular cartilage in the domestic fowl.

Thinning of articular cartilage was identified in pelvic limb joints of broiler and Leghorn-type fowls. Almost all of 100 fowls examined showed cartilage thinning or loss in hip and knee joints. Particular attention was paid to proximal femora; in these, the principal mechanism of cartilage loss involved processes described as "peripheral remodelling". From the edge of cartilage sheets, fibrovascular tissue removed articular cartilage by two mechanisms. Either a pannus of fibrovascular tissue covered the articular surface or non-osseous tissue invaded through discontinuities in the bone plate. As in man, peripheral remodelling appears to be age-related and unrelated to regressive or destructive cartilage loss.

Animals↗