Metabolic and hormonal responses of growing modern meat-type chickens to fasting.

1. The present study compared the effects of fasting on circulating concentrations of glucose, insulin and glucagon in male and female modern meat-type chickens (Ross 708) at three ages (19 d, 33 d and 47 d). 2. Plasma concentrations of glucose were reduced by fasting with reductions of 24.9% (19-d-old), 22.6% (33-d-old) and 17.9% (47-d-old) in broiler chickens fasted for 12 h. 3. Plasma concentrations of insulin decreased with fasting. For instance, circulating concentrations of insulin declined after 6 h of fasting by 45.7%, 54.7% and 50.0%, respectively, in 19-d-old, 33-d-old and 47-d-old broiler chickens. 4. Plasma concentrations of glucagon were increased by fasting. Plasma concentrations of glucagon were elevated by 3.79% (19-d-old), 3.51% (33-d-old) and 3.79% (47-d-old) with 6 h of fasting and remained elevated with 12 h, 18 h and 24 h of fasting.

Changes in body temperature during growth and in response to fasting in growing modern meat type chickens.

1. Rectal or core body temperature was determined in a study to examine the effects of fasting in modern meat type broilers at three stages of growth, namely d 19, 33 and 47. 2. There were two treatment groups: fed with feed available ad libitum and fasted. Rectal temperatures were determined at noon (1200 h). At that time, feed was removed from the fasted group. The body temperatures were then determined again after 6, 12, 18 and 24 h. 3. Core body temperatures decreased with fasting. The decrease was evident after as little as 6 h of fasting with a further decline evident by 12 h. 4. Accompanying the decrease in body temperature with fasting there were decreases in the venous concentrations of carbon dioxide in the blood and sodium in the plasma. 5. The decrease in both body temperature and carbon dioxide presumably reflects depressed metabolic rate. 6. Unexpectedly, the core body temperature increased progressively with age in the control fed group (d 19 = 41·04 ± 0·02°C, d 33 = 41·65 ± 0·05°C, d 47 = 42·21 ± 0·12°C). 7. In the fed control group, core body temperatures were reduced at night, when feeding activity would be anticipated to be greatly reduced.

Effect of pullet body weight and hen dietary amino acid treatments on their progeny fed high and low amino acid diets.

Four studies were conducted on Cobb 700 broilers to evaluate the dietary protein and any maternal effects on live production and processing parameters. Day-old Cobb 700 broiler breeder pullets were reared to conform to 2 different BW curves (control BW and increased BW) with 8 replicate pens per treatment. Birds were fed common diets from 1 d of age until first egg (24 wk). At 24 wk, 12 pens of each pullet treatment were given different amino acid (AA) diets (low = 14% CP, high = 15% CP). The performance of female and male progeny from 32 and 45 wk hens were evaluated on low AA and high AA density diets. The 4 progeny trial designs were identical factorial 2 × 2 × 2 designs, with 2 pullet BW curves (control BW and increased BW), 2 dam CP diet levels (low and high), and 2 progeny CP diets (low and high), with 6 replicates each containing 18 birds, for a total of 108 broiler progeny per treatment. Broiler chickens on the higher AA density feed exhibited consistent improvement in mid-growth BW and FCR and white meat yield percentage. Some maternal effects were noted, including increased carcass yield in female broilers from 32 wk old hens. There were 3-way interactions of pullet BW × hen dietary AA × progeny dietary AA treatments for female progeny carcass yield (from 32-week-old hens) and male tender yield (from 45-week-old hens). There were 2-way interactions of pullet BW x hen dietary AA treatments effect on female and male progeny drumstick yield from 32-week-old hens, pullet BW × progeny dietary AA treatments effect on male 27 d BW from 32-week-old hens, and hen dietary AA × progeny dietary AA treatments effect on male thigh yield from 45-week-old hen. The epigenetic effects of maternal pullet BW and dietary AA treatments were seen in processing yields suggesting, the need of dietary CP changes of the progeny.

Light intensity preferences of broiler chickens: implications for welfare.

There is considerable debate as to the optimal light intensities for growing chickens. This is influencing regulations and industry practices. The present study examines the preference of broiler chickens for light intensity. A choice system was developed to allow determination of the preferences of broiler chickens for light intensity. This system had three light proof pens each with feeders or waterers but different light intensities. There was a connecting transit pen with a light intensity of 1 to 2 lux. This allowed birds access to the pens each with feeders or waterers. There were markedly more chickens observed in the pens each with feeders or waterers and a light intensity of 20 lux than 5 lux. Moreover, more feed was consumed in the 20 lux pens than 5 pens. There were also high numbers of chickens in the transit compartment with its low light intensity (1 to 2 lux) and no feeders or waterers. Broiler chickens exhibited a preference for 20 lux light intensity for feeding compared to 5 lux light intensity. The present study supports the view that there should be a light intensity of at least 20 lux for the areas around the feeders and also suggests that light intensity may be reduced in other areas for resting and other activities.

Lack of effects of atrazine on estrogen-responsive organs and circulating hormone concentrations in sexually immature female Japanese quail (Coturnix coturnix japonica).

The widely used herbicide, atrazine, has been reported to exhibit reproductive toxicity in rats and amphibians. The present studies investigate toxicity of atrazine in Japanese quail and its ability to influence reproduction in sexually immature females. Atrazine was administered in the diet at concentrations from 0.001 to 1000 ppm (approximately 109 mg kg-1 per day) or systemically via daily subcutaneous injections (1 and 10 mg kg-1) or Silastic implants. Atrazine did not cause overt toxicity in sexually immature female quail (no effects on change in body weight, feed intake, mortality or on circulating concentrations of the stress hormone, corticosterone). It was hypothesized that if atrazine were to have estrogenic activity or to enhance endogenous estrogen production, there would be marked increases in the weights of estrogen sensitive tissues including the oviduct, the liver and the ovary together with changes in gonadotropin secretion. However, atrazine had no effect on either liver or ovary weights. Atrazine in the diet increased oviduct weights at 0.1 and 1 ppm in some studies. These effects were not consistently observed and were not significant when data from studies were combined. Systemic administration of atrazine had no effect on oviduct weights. Dietary (concentrations from 0.001 to 1000 ppm) and systemically administered atrazine had no effect on circulating concentrations of luteinizing hormone (LH). The present studies provide evidence for a lack of general or reproductive toxicity of atrazine in birds.

Lack of estrogenic or antiestrogenic actions of soy isoflavones in an avian model: the Japanese quail.

Isoflavones are soy compounds that possess weak estrogenic and antiestrogenic activities. In addition, phytochemicals, including isoflavones, may play a role in regulating seasonal reproductive cycles. As soy is a common constituent in poultry diets, the effect of these compounds on the reproductive system of production birds may be of concern. The present study examined the putative effects of soy isoflavones supplemented into the diet at 1 and 5% using endpoints of growth and reproduction in the Japanese quail. Isoflavones did not exert an effect on growth, feed intake, growth:feed, or the weight of the estrogen-sensitive immature oviduct in female quail. Furthermore, isoflavones did not influence the growth of the oviduct stimulated by exogenous estradiol. Similarly, isoflavones did not influence growth, feed intake, or growth:feed in male quail. However, isoflavones at 1%, but not 5%, in the diet reduced photoperiod-induced testis development 40% vs. control. In contrast, isoflavones did not influence testis regression stimulated by exogenous estradiol in sexually maturing male quail. The present results suggest that isoflavones may exert modest endocrine disruptor-like effects on reproduction in male, but not female, quail.

Changes in tissue nitrite concentration in the crop of the turkey poult in response to Salmonella typhimurium challenge.

The present study examines whether Salmonella typhimurium colonization of the crop of young turkeys influences nitrite concentration in the component tissues of the crop. Nitric oxide (NO) is the principal compound in biological samples that is converted into nitrites and NO is known to be a component of the early host response to infection. Challenge with S. typhimurium increased the concentration of nitrite in the crop wall of 3-wk-old turkey poults. The magnitude of the response was reduced at 8 h and absent at 48 h after challenge. As would be expected, S. typhimurium concentrations in the crop were markedly increased following challenge, and were nondetectable in control poults.

Evaluation of corn furan fatty acid putative endocrine disruptors on reproductive performance in adult female chickens.

Based on evidence from rodent models, it was hypothesized that furan fatty acids found in corn would inhibit reproduction in the laying hen. An isomeric mixture of furan fatty acids [9, (12)-oxy-10,13-dihydroxystearic acid and 10, (13)-oxy-9,12-dihydroxystearic acid] was administered for a period of 3 wk via the diet (1 and 3 ppm) at levels greater than those in corn to 20-wk-old pullets. There were no overt indications of acute or chronic toxicity (no effects on mortality, feed intake, or average daily gain). Similarly, there was no dose-dependent effect on reproductive parameters [egg production, egg weight, shell thickness, ovarian weight, number or weight of large yolky preovulatory follicles, and number of small yellow follicles (4-8 mm in diameter)]. The present data do not suggest that furan fatty acids are a cause of concern to the poultry industry.

The anterior pituitary gland: lessons from livestock.

There has been extensive research of the anterior pituitary gland of livestock and poultry due to the economic (agricultural) importance of physiological processes controlled by it including reproduction, growth, lactation and stress. Moreover, farm animals can be biomedical models or useful in evolutionary/ecological research. There are for multiple sites of control of the secretion of anterior pituitary hormones. These include the potential for independent control of proliferation, differentiation, de-differentiation and/or inter-conversion cell death, expression and translation, post-translational modification (potentially generating multiple isoforms with potentially different biological activities), release with or without a specific binding protein and intra-cellular catabolism (proteolysis) of pituitary hormones. Multiple hypothalamic hypophysiotropic peptides (which may also be produced peripherally, e.g. ghrelin) influence the secretion of the anterior pituitary hormones. There is also feedback for hormones from the target endocrine glands. These control mechanisms show broadly a consistency across species and life stages; however, there are some marked differences. Examples from growth hormone, prolactin, follicle stimulating hormone and luteinizing hormone will be considered. In addition, attention will be focused on areas that have been neglected including the role of stellate cells, multiple sub-types of the major adenohypophyseal cells, functional zonation within the anterior pituitary and the role of multiple secretagogues for single hormones.

Physiology of ghrelin and related peptides.

Growth hormone (GH) released from pituitary under direct control of hypothalamic releasing (i.e., GHRH) and inhibiting (i.e., sst or SRIF) hormones is an anabolic hormone that regulates metabolism of proteins, fats, sugars and minerals in mammals. Cyril Bowers' discovery of GH-releasing peptide (GHRP-6) was followed by a search for synthetic peptide and nonpeptide GH-secretagogues (GHSs) that stimulate GH release, as well as a receptor(s) unique from GHRH receptor. GHRH and GHSs operate through distinct G protein-coupled receptors to release GH. Signal transduction pathways activated by GHS increase intracellular Ca2+ concentration in somatotrophs, whereas GHRH increases cAMP. Isolation and characterization of ghrelin, the natural ligand for GHS receptor, has opened a new era of understanding to physiology of anabolism, feeding behavior, and nutritional homeostasis for GH secretion and gastrointestinal motility through gut-brain interactions. Other peptide hormones (i.e., motilin, TRH, PACAP, GnRH, leptin, FMRF amide, galanin, NPY, NPW) from gut, brain and other tissues also play a role in modulating GH secretion in livestock and lower vertebrate species. Physiological processes, such as neurotransmission, and secretion of hormones or enzymes, require fusion of secretory vesicles at the cell plasma membrane and expulsion of vesicular contents. This process for GH release from porcine somatotrophs was revealed by atomic force microscopy (AFM), transmission electron microscopy (TEM) and immunohistochemical distribution of the cells in pituitary during stages of development.

Self-suppression of corticosteroidogenesis: evidence for a role of adrenal 5 alpha-reductase.

Exogenous corticosterone (B), the natural glucocorticoid product of rats, suppressed endogenous B production of isolated rat adrenocortical cells induced by alpha ACTH-(1-24), [9-tryptophan (O-nitrophenylsulfenyl)]ACTH-(1-24) [( Trp (Nps)9]ACTH-(1-24], and cAMP as well as pregnenolone supported-steroidogenesis. This self-suppression occurred within 2 h. It was dependent on the concentration of exogenous B. However, self-suppression did not alter the half-maximal steroidogenic concentration (ED50) of each steroidogenic agent. In addition, exogenous B did not suppress ACTH-induced cAMP production or gross protein synthesis, as measured by leucine incorporation into bulk cellular proteins. These results with isolated cells suggested at least two mechanisms for self-suppression: 1) exogenous B inhibited steroidogenic steps in a noncompetitive manner, and/or 2) exogenous B induced B degradation. In this study we examined the effect of exogenous B on the degradation of B. Accordingly, we measured the adrenal 5 alpha-reductase activity (5 alpha RA) of cell homogenates prepared from treated cells. Isolated adrenocortical cells were incubated for 2 h with alpha ACTH-(1-24), ovine PRL (oPRL), and B. They were then homogenized and assayed for 5 alpha RA, as indicated by the disappearance of exogenous B, as shown by RIA. In addition, the percentage of exogenous tritium-labeled B [( 3H]B) converted to 5 alpha-dihydrocorticosterone (DHB), the principal reduced metabolite of B, was determined by TLC. Isolated adrenocortical cells from intact rats showed insignificant 5 alpha RA and DHB formation when incubated with or without alpha ACTH-(1-24) and with or without oPRL. However, with exogenous B, there was significant 5 alpha RA and DHB formation. oPRL plus B decreased DHB formation. The effects of B and oPRL were more demonstrable with cells from hypophysectomized rats. These cells exhibited high 5 alpha RA and DHB formation; exogenous B increased these values, whereas oPRL acutely reversed the effects of hypophysectomy and exogenous B. In other work avoiding cell homogenization, exogenous B suppressed ACTH-induced B accumulation and increased DHB formation in intact cell suspensions from intact rats and intact male domestic fowl. Furthermore, exogenous B increased the conversion of [3H] pregnenolone to DHB in intact cell suspensions from intact rats, showing that B synthesized de novo as well as exogenous B can be degraded during self-suppression. These data indicate that acute self-suppression of corticosteroidogenesis is at least partly mediated by an increase in 5 alpha RA.

Adrenocortical cell function in the hypophysectomized domestic fowl: effects of growth hormone and 3,5,3'-triiodothyronine replacement.

The control of adrenocortical function in the domestic fowl (Gallus domesticus) was investigated using adrenocortical cells isolated from hypophysectomized (hypox) and intact cockerels and from hypox cockerels injected with T3, purified chicken GH (cGH), and T3 plus cGH. Corticosterone in plasma and cell incubations was measured by RIA. Cellular responses to varying concentrations of steroidogenic agents were fitted and statistically analyzed by computer. Hypophysectomy reduced the basal plasma corticosterone (B) concentration to 53% of the value in intact birds and eliminated a stress response. Although hypophysectomy reduced adrenal weight by 20%, it did not change relative adrenal weight (milligrams per 100 g BW). However, replacement with cGH increased relative adrenal weight by 24%, whereas replacement with T3 or T3 plus cGH reduced relative adrenal weight by 16%. In the absence of steroidogenic agents, there were no detectable differences in B production by adrenocortical cells isolated from various experimental groups. However, with a maximal steroidogenic concentration of ACTH, B production by isolated adrenocortical cells from hypox birds was 61% of that by cells from intact birds. The ED50 of ACTH for cells from hypox cockerels was 2.7 times greater than that of cells from intact cockerels, thus indicating a loss of cell sensitivity to ACTH after hypophysectomy (the greater the ED50, the lesser the cell sensitivity). Although cGH replacement increased maximal B production (Bmax) induced by ACTH to 329% that by cells from hypox cockerels, it increased the ACTH ED50 3.6 times, thus decreasing cell sensitivity more than hypophysectomy alone. In contrast to cGH, T3 replacement maintained the cell sensitivity to ACTH at the level of cells from intact birds, but lowered Bmax to 54% that of cells from hypox cockerels. The combination of cGH and T3 administered to hypox cockerels both maintained cell sensitivity to ACTH and raised the Bmax to 358% that of cells from hypox animals. These treatments also affected 8-bromo-cAMP-induced Bmax and pregnenolone-supported Bmax, but did not significantly alter the ED50 of these agents.(ABSTRACT TRUNCATED AT 400 WORDS)

Phosphorylation of prolactin and growth hormone.

To determine whether GH and prolactin could be phosphorylated, turkey GH, chicken GH, chicken prolactin and turkey prolactin were incubated in vitro with the catalytic subunit of protein kinase A and [gamma-32P]ATP. Phosphorylation was assessed after sodium dodecyl sulphate-polyacrylamide gel electrophoresis, Western blotting and autoradiography. Polyacrylamide electrophoresis showed that both purified native chicken GH and turkey GH were phosphorylated under the conditions employed. However, the glycosylated variant of chicken GH did not appear to be labelled. Chicken prolactin, turkey prolactin and the glycosylated variant of turkey prolactin were all intensely phosphorylated by protein kinase A. Ovine and rat prolactins could also be phosphorylated by protein kinase A. The phosphate content of different native prolactin (turkey, ovine and rat) and GH (ovine and chicken) preparations was also determined and found to be significant. Chicken pituitary cells in primary culture incorporated 32P in GH- and prolactin-like bands isolated by non-denaturing polyacrylamide gel electrophoresis, and this was stimulated by phorbol myristate acetate. Phosphorylation of GH and prolactin may thus explain some of the charge heterogeneity of these hormones.

Effect of triiodothyronine and in vitro growth hormone on avian interleukin-2.

One-day-old chickens were treated with varying levels of triiodothyronine (T3) added to the diet. At 28 days of age, the IL-2-like activity in the splenocyte culture supernatants were assessed. The lowest dose of T3 (0.1 ppm) enhanced IL-2-like activity while the highest dose (1.0 ppm) was significantly suppressive. The intermediate dose elicited varying effects. Recombinant chicken growth hormone (rcGH) was added to some cultures 24 h prior to IL-2 assay. In vitro rcGH significantly depressed the IL-2-like activity of splenocytes from animals given the low T3 diet. The addition of varying concentrations of T3 in vitro to splenocytes from non-T3-supplemented chickens had no effect on the IL-2-like activity. These results indicate that in vivo supplementation of low dietary T3 but not in vitro T3 is effective in enhancing avian IL-2-like activity. The addition of rcGH in vitro can modify this response.

Effect of growth hormone and thyroid hormone on autoimmune thyroiditis in obese chickens.

The effect of thyroxine (T4) and recombinant (rcGH) or purified pituitary-derived (pcGH) chicken growth hormone on the development of spontaneous autoimmune thyroiditis (SAT) was examined in the Obese strain (OS) chicken. Day-old OS chicks were randomly assigned to a control or 1.0 ppm T4 supplemented diet and a vehicle or 500 micrograms rcGH/kg BW daily injection, using a 2 x 2 factorial design. At 4 weeks, sera were analyzed for anti-thyroglobulin autoantibody (TgAAb) using a kinetics-based ELISA. Leucocytic infiltration of the thyroid was assessed using computer-based video imaging techniques. A close correlation between TgAAb and thyroid infiltration was seen with both being decreased (p < 0.05) by the T4/rcGH treatment. Neither the T4 or rcGH alone produced this effect and the rcGH treatment significantly elevated TgAAb. In a second experiment, all but the control group received 1.0 ppm T4 supplementation and two of the T4-treated groups received either 50 or 200 micrograms pcGH/kg BW by daily injection. As before, T4/pcGH significantly reduced TgAAb and thyroid infiltration. T4 alone produced no significant effects. These data support the conclusion that the combined treatment of T4 and cGH exert an immunomodulatory effect within a strain that is predisposed to autoimmune thyroiditis while GH treatment alone exacerbated the condition. These results also show that video imaging techniques can be used to evaluate the extent of histopathology present within the OS thyroid.

Effect of hypophysectomy and growth hormone on immune development in the domestic fowl.

The effect of hypophysectomy and recombinant growth hormone (rcGH) treatment on the growth and development of the immune system was investigated in young chickens. Flow cytometric analysis of cell surface markers revealed no changes in the proportion of thymocytes expressing CT-1a, CD4, and/or CD8 among any of the treatment groups. In contrast, the proportion of both single positive CD4 and CD8 peripheral blood lymphocytes (PBL) was altered in hypox birds treated with rcGH compared to the vehicle-treated group. Specifically, rcGH treatment produced a decrease in the proportion of CD8+ cells and an increase in the percentage of CD4+ PBL. There was little change in the labeling intensity of PBL or thymocytes associated with any treatment; however, double positive (CD4+CD8+) thymocytes from hypophysectomized chicks that were not given rcGH had increased fluorescence relative to rcGH supplemented hypox chicks. As expected, hypophysectomy reduced body, skeletal, and thymic growth. Treatment of hypox chicks with rcGH enhanced body weight while thymic weights were somewhat increased. Skeletal growth was not significantly altered by rcGH. Bursal growth appeared refractory to either treatment. These studies support the conclusion that growth hormone influences thymic growth and the maturation of thymus-derived lymphocytes. These results also demonstrate a biological activity for chicken growth hormone derived through recombinant technology.

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.

Purification and radioimmunoassay of chicken growth hormone.

Chicken growth hormone has been isolated from adenohypophysial tissue from which the glycoprotein hormones had been removed. The procedure entailed alkali extraction, ammonium sulphate precipitation and ion-exchange chromatography on DEAE-cellulose. The resulting fraction was homogeneous, active in the rat tibia bioassay and had a similar isoelectric point, molecular weight and amino acid composition to mammalian growth hormone. A specific homologous radioimmunoassay has been developed using the avian growth hormone.

Inhibition of growth hormone release by prostaglandins in immature domestic fowl (Gallus domesticus).

The effect of prostaglandin (PG) E1, PGE2 and PGF2 alpha on GH secretion has been assessed in immature domestic fowl. The intravenous or subcutaneous administration of PGE1 and PGE2 (at a dose of approximately 200 microgram/kg) to 2-, 6- and 8-week-old cockerels consistently lowered plasma GH concentrations. This inhibition in GH secretion was observed for at least 40 min after administration of PGE1 and PGE2. The same dose of PGF2 alpha suppressed plasma GH levels in 2- and 6- week-old birds but the magnitude and duration of this response was less than that induced by PGE1 and PGE2. At this dose, administration of PGE1 and PGE2 resulted in overt signs of distress (e.g. gaping, panting, eye closure and postural instability) within 5-10 min of injection and the birds appeared to be sedated thereafter. Prostaglandin F2 alpha and lower doses of PGE1 and PGE2 did not have any apparent effect on behavior. These results suggest that prostaglandins inhibit GH secretion in birds although this may reflect a non-specific stress response.