Intracerebroventricular injection taurine changes free amino acid concentrations in the brain and plasma in chicks.

Brain amino acid metabolism has been reported to regulate body temperature, feeding behavior and stress response. Central injection of taurine induced hypothermic and anorexigenic effects in chicks. However, it is still unknown how the amino acid metabolism is influenced by the central injection of taurine. Therefore, the objective of this study was to investigate the changes in brain and plasma free amino acids following central injection of taurine. Five-day-old male Julia layer chicks (n = 10) were subjected to intracerebroventricular (ICV) injection with saline or taurine (5 µmol/10 µL). Central taurine increased tryptophan concentrations in the diencephalon, and decreased tyrosine in the diencephalon, brainstem, cerebellum, telencephalon and plasma at 30 min post-injection. Taurine was increased in all the brain parts after ICV taurine. Although histidine and cystathionine concentrations were increased in the diencephalon and brainstem, several amino acids such as isoleucine, arginine, methionine, phenylalanine, glutamic acid, asparagine, proline, and alanine were reduced following central injection of taurine. All amino acid concentrations were decreased in the plasma after ICV taurine. In conclusion, central taurine quickly changes free amino acid concentrations in the brain and plasma, which may have a role in thermoregulation, food intake and stress response in chicks.

Intracerebroventricular injection of taurine induces hypothermia through modifying monoaminergic pathways in chicks.

Brain monoamines are reported to regulate body temperature and food intake. The objective of this study was to investigate the mechanism of brain monoamine metabolism in taurine-induced hypothermia and appetite suppression. In Experiment 1, 5-day-old male Julia layer chicks (n = 10) were subjected to intracerebroventricular (ICV) injection with saline or taurine (5 µmol/10 µL). In Experiment 2, the chicks were ICV injected with saline, taurine, fusaric acid (dopamine-ß-hydroxylase inhibitor: 558 nmol), or taurine with fusaric acid. In Experiment 3, the chicks were ICV injected with saline, taurine, para-chlorophenylalanine (PCPA, tryptophan hydroxylase inhibitor: 400 nmol), or taurine with PCPA. In Experiment 4, the chicks were ICV injected with saline, taurine, clorgyline (monoamine oxidase inhibitor: 81 nmol), or taurine with clorgyline. Central taurine lowered rectal temperature at 30 min post-injection and increased norepinephrine in the brainstem and its metabolite 3-methoxy-4-hydroxyphenylglycol in both the diencephalon and brainstem. Similarly, taurine treatment induced increases in serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid in the diencephalon. Fusaric acid completely and PCPA partially, but not clorgyline, attenuated taurine-induced hypothermia. The anorexigenic effect of taurine was partially attenuated by PCPA, but not fusaric acid nor clorgyline. In conclusion, central taurine activates dopamine-ß-hydroxylase and tryptophan hydroxylase to produce norepinephrine and 5-HT, and then induces hypothermia, but 5-HT alone may be linked with taurine-induced anorexia in chicks.

Dietary Flavonoids as Modulators of Lipid Metabolism in Poultry.

Flavonoids, naturally-occurring compounds with multiple phenolic structures, are the most widely distributed phytochemicals in the plant kingdom, and are mainly found in vegetables, fruits, grains, roots, herbs, and tea and red wine products. Flavonoids have health-promoting effects and are indispensable compounds in nutritional and pharmaceutical (i.e., nutraceutical) applications. Among the demonstrated bioactive effects of flavonoids are anti-oxidant, anti-inflammatory, and anti-microbial in a range of research models. Through dietary formulation strategies, numerous flavonoids provide the ability to support bird health while improving the nutritional quality of poultry meat and eggs by changing the profile of fatty acids and reducing cholesterol content. A number of such compounds have been shown to inhibit adipogenesis, and promote lipolysis and apoptosis in adipose tissue cells, and thereby have the potential to affect fat accretion in poultry at various ages and stages of production. Antioxidant and anti-inflammatory properties contribute to animal health by preventing free radical damage in tissues and ameliorating inflammation in adipose tissue, which are concerns in broiler breeders and laying hens. In this review, we summarize the progress in understanding the effects of dietary flavonoids on lipid metabolism and fat deposition in poultry, and discuss the associated physiological mechanisms.

Central Taurine Attenuates Hyperthermia and Isolation Stress Behaviors Augmented by Corticotropin-Releasing Factor with Modifying Brain Amino Acid Metabolism in Neonatal Chicks.

The objective of this study was to determine the effects of centrally administered taurine on rectal temperature, behavioral responses and brain amino acid metabolism under isolation stress and the presence of co-injected corticotropin-releasing factor (CRF). Neonatal chicks were centrally injected with saline, 2.1 pmol of CRF, 2.5 µmol of taurine or both taurine and CRF. The results showed that CRF-induced hyperthermia was attenuated by co-injection with taurine. Taurine, alone or with CRF, significantly decreased the number of distress vocalizations and the time spent in active wakefulness, as well as increased the time spent in the sleeping posture, compared with the saline- and CRF-injected chicks. An amino acid chromatographic analysis revealed that diencephalic leucine, isoleucine, tyrosine, glutamate, asparagine, alanine, ß-alanine, cystathionine and 3-methylhistidine were decreased in response to taurine alone or in combination with CRF. Central taurine, alone and when co-administered with CRF, decreased isoleucine, phenylalanine, tyrosine and cysteine, but increased glycine concentrations in the brainstem, compared with saline and CRF groups. The results collectively indicate that central taurine attenuated CRF-induced hyperthermia and stress behaviors in neonatal chicks, and the mechanism likely involves the repartitioning of amino acids to different metabolic pathways. In particular, brain leucine, isoleucine, cysteine, glutamate and glycine may be mobilized to cope with acute stressors.

The Microbiota-Gut-Brain Axis During Heat Stress in Chickens: A Review.

Heat stress is a global issue for the poultry industries with substantial annual economic losses and threats to bird health and welfare. When chickens are exposed to high ambient temperatures, like other species they undergo multiple physiological alterations, including behavioral changes, such as cessation of feeding, initiation of a stress signaling cascade, and intestinal immune, and inflammatory responses. The brain and gut are connected and participate in bidirectional communication via the nervous and humoral systems, this network collectively known as the gut-brain axis. Moreover, heat stress not only induces hyperthermia and oxidative stress at the gut epithelium, leading to impaired permeability and then susceptibility to infection and inflammation, but also alters the composition and abundance of the microbiome. The gut microflora, primarily via bacterially derived metabolites and hormones and neurotransmitters, also communicate via similar pathways to regulate host metabolic homeostasis, health, and behavior. Thus, it stands to reason that reshaping the composition of the gut microbiota will impact intestinal health and modulate host brain circuits via multiple reinforcing and complementary mechanisms. In this review, we describe the structure and function of the microbiota-gut-brain axis, with an emphasis on physiological changes that occur in heat-stressed poultry.

Heat Stress Responses in Birds: A Review of the Neural Components.

Heat stress is one of the major environmental conditions causing significant losses in the poultry industry and having negative impacts on the world's food economy. Heat exposure causes several physiological impairments in birds, including oxidative stress, weight loss, immunosuppression, and dysregulated metabolism. Collectively, these lead not only to decreased production in the meat industry, but also decreases in the number of eggs laid by 20%, and overall loss due to mortality during housing and transit. Mitigation techniques have been discussed in depth, and include changes in air flow and dietary composition, improved building insulation, use of air cooling in livestock buildings (fogging systems, evaporation panels), and genetic alterations. Most commonly observed during heat exposure are reduced food intake and an increase in the stress response. However, very little has been explored regarding heat exposure, food intake and stress, and how the neural circuitry responsible for sensing temperatures mediate these responses. That thermoregulation, food intake, and the stress response are primarily mediated by the hypothalamus make it reasonable to assume that it is the central hub at which these systems interact and coordinately regulate downstream changes in metabolism. Thus, this review discusses the neural circuitry in birds associated with thermoregulation, food intake, and stress response at the level of the hypothalamus, with a focus on how these systems might interact in the presence of heat exposure.

DNA methylation-modifiers reduced food intake in juvenile chickens (Gallus gallus) and Japanese quail (Coturnix japonica).

S-Adenosylmethionine (SAM) is the major endogenous methyl donor for methyltransferase reactions, while 5-Azacytidine (AZA) is a synthetic drug inhibiting DNA methyltransferase activity. Both molecules can thus influence DNA methylation patterns in an organism and thereby affect gene expression and ultimately behavior in the long-term. Whether or not effects on behavior are exerted on a shorter time scale is unclear. The goal of this study was to explore the direct effects of SAM and AZA on appetite regulation, using broiler chicken and Japanese quail as the animal models. Fed or 180 min-fasted broilers (at day 4 post-hatch) or 360 min-fasted quail (at day 7 post-hatch) were intracerebroventricularly injected with SAM or AZA and food intake was measured for 360 min. For broilers, there was no effect of AZA, at any dose, on food intake in either fed or fasted chicks at any time point. In contrast, 1 and 10 µg doses of SAM reduced food intake in fed chicks at 60 min post-injection. In fasted chicks, although there were no differences for the first 30 min post-injection, SAM suppressed food intake during the second 30-min period. For quail, however, AZA (25 µg dose) decreased food intake at 60 and 150-360 min post-injection in fasted birds. A reduction in food intake was also observed at 120- and 360-min post-injection in fed quail in response to 5 and 25 µg doses of AZA, respectively. SAM had no effect when quail were fasted, whereas 1 µg dose of SAM suppressed food consumption in fed quail during the third 30-min period. Thus, when administered directly into the central nervous system, SAM may act as a transient appetite suppressant in both broilers and quail, whereas the direct inhibitory effect of AZA on food consumption depends on species and nutritional states.

Dietary Supplementation of Baicalein Affects Gene Expression in Broiler Adipose Tissue During the First Week Post-hatch.

Dietary supplementation of baicalein, a flavonoid, has anti-obesity effects in mammals and broiler chickens. The aim of this study was to determine the effect of dietary baicalein supplementation on broiler growth and adipose tissue and breast muscle deposition. Fifty Hubbard × Cobb-500 day-of-hatch broiler chicks were assigned to a control starter diet or control diet supplemented with 125, 250, or 500 mg/kg baicalein and diets were fed for the first 6 days post-hatch. Body weight, average daily body weight gain, and average daily food intake were all reduced by 500 mg/kg baicalein. Breast muscle and subcutaneous and abdominal fat weights were also reduced in chicks that consumed the baicalein-supplemented diets. mRNAs for genes encoding factors involved in adipogenesis and fat storage, 1-acylglycerol-3-phosphate-O-acyltransferase 2, CCAAT/enhancer-binding protein ß, perilipin-1, and sterol regulatory element-binding transcription factor 1, were more highly expressed in the adipose tissue of broilers supplemented with baicalein than the controls, independent of depot. Diacylglycerol acyltransferase and peroxisome proliferator-activated receptor gamma mRNAs, involved in triacylglycerol synthesis and adipogenesis, respectively, were greater in subcutaneous than abdominal fat, which may contribute to differences in expansion rates of these depots. Results demonstrate effects of dietary supplementation of baicalein on growth performance in broilers during the early post-hatch stage and molecular effects in major adipose tissue depots. The mild reduction in food intake coupled to slowed rate of breast muscle and adipose tissue accumulation may serve as a strategy to modulate broiler growth and body composition to prevent metabolic and skeletal disorders later in life.

Ferulic acid, a phytochemical with transient anorexigenic effects in birds.

Ferulic acid (FA) is a phenolic acid found within the plant cell wall that has physiological benefits as an antioxidant. Although metabolic benefits of FA supplementation are described, lacking are reports of effects on appetite regulation. Thus, our objective was to determine if FA affects food or water intake, using chicks as a model. At 4 days post-hatch, broiler chicks were intraperitoneally injected with 0 (vehicle), 12.5, 25, or 50 mg/kg of FA. Chicks treated with 50 mg/kg of FA consumed 70% less food than controls at 30 min post-injection, and the effect dissipated thereafter. Water intake was not affected at any time. In a behavior analysis, FA-treated chicks defecated fewer times than vehicle-injected chicks, while other behaviors were not affected. There was an increase in c-Fos immunoreactivity within the hypothalamic arcuate nucleus (ARC) of FA-treated chicks, and no differences were detected in other nuclei. mRNA abundance was measured in the whole hypothalamus and the ARC. There was decreased hypothalamic galanin, ghrelin, melanocortin receptor 3, and pro-opiomelanocortin (POMC) mRNA in FA-treated chicks. Within the ARC, there was an increase in c-Fos mRNA and a decrease in POMC mRNA in response to FA. It is likely that the mechanism responsible for mediating FA's transient effects on food intake originates within the ARC, possibly involving POMC. A greater understanding of the short-term, mild appetite-suppressive effects of FA may have applications to treating eating disorders and modulating food intake in animal models of obesity.

Prostaglandin E2-induced anorexia involves hypothalamic brain-derived neurotrophic factor and ghrelin in chicks.

Central administration of prostaglandin E2 (PGE2) is associated with potent anorexia in rodents and chicks, although hypothalamic mechanisms are not fully understood. The objective of the present study was to identify hypothalamic nuclei and appetite-related factors that are involved in this anorexigenic effect, using chickens as a model. Intracerebroventricular injection of 2.5, 5, and 10 nmol of PGE2 suppressed food and water intake in broiler chicks in a dose-dependent manner. c-Fos immunoreactivity was increased in the paraventricular nucleus (PVN) at 60 min post injection of 5 nmol of PGE2. Under the same treatment condition, hypothalamic expression of melanocortin receptor 3 and ghrelin mRNAs increased, whereas neuropeptide Y receptor sub-type 5 and tropomyosin receptor kinase B (TrkB) mRNAs decreased in PGE2-treated chicks. In the PVN, chicks injected with PGE2 had more brain-derived neurotrophic factor (BDNF), ghrelin, and c-Fos mRNA but less corticotrophin-releasing factor receptor 1 (CRFR1), CRFR2, and TrkB mRNA expression. In conclusion, PGE2 injection resulted in decreased food and water intake that likely involves BDNF and ghrelin originating in the PVN. Because the anorexigenic effect is so potent and hypothalamic mechanisms are similar in chickens and rodents, a greater understanding of the role of PGE2 in acute appetite regulation may have implications for treating eating and metabolic disorders in humans.

Central GABAA receptor mediates taurine-induced hypothermia and possibly reduces food intake in thermo-neutral chicks and regulates plasma metabolites in heat-exposed chicks.

The aim of this study was to examine the central action of taurine on body temperature and food intake in neonatal chicks under control thermoneutral temperature (CT) and high ambient temperature (HT). Intracerebroventricular injection of taurine caused dose-dependent hypothermia and reduced food intake under CT. The mRNA expression of the GABAA receptors, GABAAR-α1 and GABAAR-γ, but not that of GABABR, significantly decreased in the diencephalon after central injection of taurine. Subsequently, we found that picrotoxin, a GABAAR antagonist, attenuated taurine-induced hypothermia. Central taurine significantly decreased the brain concentrations of 3-methoxy-4-hydroxyphenylglycol, a major metabolite of norepinephrine; however, the concentrations of serotonin, dopamine, and the epinephrine metabolites, 3,4-hydroxyindoleacetic acid and homovanillic acid, were unchanged. Although hypothermia was not observed under HT after central injection of taurine, plasma glucose and uric acid levels were higher, and plasma sodium and calcium levels were lower, than those in chicks under CT. In conclusion, brain taurine may play a role in regulating body temperature and food intake in chicks through GABAAR. The changes in plasma metabolites under heat stress suggest that brain taurine may play an important role in maintaining homeostasis in chicks.

Hypothalamic-pituitary-adrenal axis regulation and organization in urban and rural song sparrows.

Urban habitats present animals with persistent disturbances and acute stressors not present in rural habitats or present at significantly lower levels. Differences in the glucocorticoid stress response could underlie colonization of these novel habitats. Despite urban habitats characterization as more stressful, previous comparisons of urban and rural birds have failed to find consistent differences in baseline and stress induced glucocorticoid levels. Another aspect of glucocorticoid regulation that could underlie an animal's ability to inhabit novel habitats, but has yet to be well examined, is more efficient termination of the glucocorticoid stress response which would allow birds in urban habitats to recover more quickly after a disturbance. The glucocorticoid stress response is terminated by negative feedback achieved primarily through their binding of receptors in the hippocampus and hypothalamus and subsequent decreased synthesis and release from the adrenals. We investigated if male song sparrows (Melospiza melodia) in urban habitats show more efficient termination of the glucocorticoid stress response than their rural counterparts using two approaches. First, we measured glucocorticoid receptor, mineralocorticoid receptor and 11ß-HSD2 (an enzyme that inactivates corticosterone) mRNA expression in negative feedback targets of the brain (the hippocampus and hypothalamus) as a proxy measure of sensitivity to negative feedback. Second, we measured plasma corticosterone levels after standardized restraint and again following a challenge with the synthetic glucocorticoid, dexamethasone, as a means of assessing how quickly birds decreased glucocorticoid synthesis and release. Though there were no differences in the hypothalamus of urban and rural song sparrows, urban birds had lower glucocorticoid receptor and 11ß-HSD2 mRNA expression in the hippocampus. Further, urban and rural birds had similar reductions in corticosterone following the dexamethasone challenge, suggesting that they do not differ in how quickly they decrease glucocorticoid synthesis and release. Thus, urban and rural song sparrows display similar termination of the glucocorticoid stress response even though urban birds have decreased hippocampal glucocorticoid receptor and 11ß-HSD2 abundance.

The anorexigenic effect of neuropeptide AF in Japanese quail, Coturnix japonica, is associated with activation of the melanocortin system.

Neuropeptide AF (NPAF) decreases food and water intake in birds and food intake in mammals. In this study, the objective was to determine the effects of centrally administered NPAF on food and water intake, hypothalamic c-Fos immunoreactivity and hypothalamic mRNA abundance of appetite-regulating factors in Japanese quail (Coturnix japonica). Seven days post hatch, 6 h fasted quail were intracerebroventricularly (ICV) injected with 0 (vehicle), 4, 8, or 16 nmol of NPAF and food and water intake were measured at 30 min intervals for 180 min. In Experiment 1, chicks which received 4, 8, and 16 nmol ICV NPAF had reduced food intake for 120, 60 and 180 min following injection, respectively, and reduced water intake during the entire 180 min observation. In Experiment 2, there was increased c-Fos immunoreactivity in the paraventricular nucleus, the ventromedial nucleus of the hypothalamus, and the dorsomedial hypothalamic nucleus in NPAF-injected quail. In Experiment 3, ICV NPAF was associated with decreased corticotropin-releasing factor mRNA, and an increase in hypothalamic proopiomelanocortin and melanocortin receptor 4 mRNA. These results demonstrate that central NPAF suppresses food and water intake in quail, effects that are likely mediated via the melanocortin system in the hypothalamus.

Migratory state and patterns of steroid hormone regulation in the pectoralis muscle of a nomadic migrant, the pine siskin (Spinus pinus).

The endocrine system is known to mediate responses to environmental change and transitions between different life stages (e.g., a non-breeding to a breeding life stage). Previous works from the field of environmental endocrinology have primarily focused on changes in circulating hormones, but a comprehensive understanding of endocrine signaling pathways requires studying changes in additional endocrine components (e.g., receptor densities) in a diversity of contexts and life stages. Migratory birds, for instance, can exhibit dramatic changes in their physiology and behavior, and both sex steroids as well as glucocorticoids are proposed mediators of the transition into a migratory state. However, the role of changes in endocrine signaling components within integral target tissues, such as flight muscles, in modulating the transition into a migratory state remains poorly understood. Here, we examined changes in gene expression levels of and correlational patterns (i.e., integration) between 8 endocrine signaling components associated with either glucocorticoids or sex steroid signaling in the pectoralis muscles of a nomadic migratory bird, the pine siskin (Spinus pinus). The pectoralis muscle is essential to migratory flight and undergoes conspicuous changes in preparation for migration, including hypertrophy. We focus on endocrine receptors and enzymes (e.g., 5α-reductase) that modulate the signaling capacity of circulating hormones within target tissues and may influence either catabolic or anabolic functioning within the pectoralis. Endocrine signaling components were compared between captive birds sampled prior to the expression of vernal migratory preparation and during the expression of a vernal migratory state. While birds exhibited differences in the size and color of the flight muscle and behavioral shifts indicative of a migratory state (i.e., zugunruhe), none of the measured endocrine components differed before and after the transition into the migratory state. Patterns of integration amongst all genes did, however, differ between the two life stages, suggesting the contrasting demands of different life stages may shape entire endocrine signaling networks within target tissues rather than individual components. Our work aligns with previous endocrine studies on pine siskins and, viewed together, suggest additional studies are needed to understand the endocrine system's role in mediating the development and progression of the vernal migratory state in this species. Further, the patterns observed in pine siskins, a nomadic migrant, differ from previous studies on obligate migrants and suggest that different mechanisms or interactions between endocrine signaling components may mediate the migratory transition in nomadic migrants.

Chronic stress, epigenetics, and adipose tissue metabolism in the obese state.

In obesity, endocrine and metabolic perturbations, including those induced by chronic activation of the hypothalamus-pituitary-adrenal axis, are associated with the accumulation of adipose tissue and inflammation. Such changes are attributable to a combination of genetic and epigenetic factors that are influenced by the environment and exacerbated by chronic activation of the hypothalamus-pituitary-adrenal axis. Stress exposure at different life stages can alter adipose tissue metabolism directly through epigenetic modification or indirectly through the manipulation of hypothalamic appetite regulation, and thereby contribute to endocrine changes that further disrupt whole-body energy balance. This review synthesizes current knowledge, with an emphasis on human clinical trials, to describe metabolic changes in adipose tissue and associated endocrine, genetic and epigenetic changes in the obese state. In particular, we discuss epigenetic changes induced by stress exposure and their contribution to appetite and adipocyte dysfunction, which collectively promote the pathogenesis of obesity. Such knowledge is critical for providing future directions of metabolism research and targets for treating metabolic disorders.

Chronic stress and adipose tissue in the anorexic state: endocrine and epigenetic mechanisms.

Although adipose tissue metabolism in obesity has been widely studied, there is limited research on the anorexic state, where the endocrine system is disrupted by reduced adipose tissue mass and there are depot-specific changes in adipocyte type and function. Stress exposure at different stages of life can alter the balance between energy intake and expenditure and thereby contribute to the pathogenesis of anorexia nervosa. This review integrates information from human clinical trials to describe endocrine, genetic and epigenetic aspects of adipose tissue physiology in the anorexic condition. Changes in the hypothalamus-pituitary-thyroid, -adrenal, and -gonadal axes and their relationships to appetite regulation and adipocyte function are discussed. Because of the role of stress in triggering or magnifying anorexia, and the dynamic but also persistent nature of environmentally-induced epigenetic modifications, epigenetics is likely the link between stress and long-term changes in the endocrine system that disrupt homoeostatic food intake and adipose tissue metabolism. Herein, we focus on the adipocyte and changes in its function, including alterations reinforced by endocrine disturbance and dysfunctional adipokine regulation. This information is critical because of the poor understanding of anorexic pathophysiology, due to the lack of suitable research models, and the complexity of genetic and environmental interactions.

Reduced food intake during exposure to high ambient temperatures is associated with molecular changes in the nucleus of the hippocampal commissure and the paraventricular and arcuate hypothalamic nuclei.

Exposure to high ambient temperatures (HAT) is associated with increased mortality, weight loss, immunosuppression, and metabolic malfunction in birds, all of which are likely downstream effects of reduced food intake. While the mechanisms mediating the physiological responses to HAT are documented, the neural mechanisms mediating behavioral responses are poorly understood. The aim of the present study was thus to investigate the hypothalamic mechanisms mediating heat-induced anorexia in four-day old broiler chicks. In Experiment 1, chicks exposed to HAT reduced food intake for the duration of exposure compared to controls in a thermoneutral environment (TN). In Experiment 2, HAT chicks that were administered an intracerebroventricular (ICV) injection of neuropeptide Y (NPY) increased food intake for 60 min post-injection, while TN chicks that received NPY increased food intake for 180 min post-injection. In Experiment 3, chicks in both the TN and HAT groups that received ICV injections of corticotropin-releasing factor (CRF) reduced food intake for up to 180 min post-injection. In Experiment 4, chicks that were exposed to HAT and received an ICV injection of astressin ate the same as controls in the TN group. In Experiment 5, chicks exposed to HAT that received an ICV injection of α-melanocyte stimulating hormone reduced food intake at both a high and low dose, with the low dose not reducing food intake in TN chicks. In Experiment 6, there was increased c-Fos expression in the hypothalamic paraventricular nucleus (PVN), lateral hypothalamic area (LHA), and the nucleus of the hippocampal commissure (NHpC). In Experiment 7, exposure to HAT was associated with decreased CRF mRNA in the NHpC, increased CRF mRNA in the PVN, and decreased NPY mRNA in the arcuate nucleus (ARC). In sum, these results demonstrate that exposure to HAT causes a reduction in food intake that is likely mediated via downregulation of NPY via the CRF system.

The anorexigenic effect of beta-melanocyte-stimulating hormone involves corticotrophin-releasing factor and mesotocin in birds.

Beta-melanocyte-stimulating hormone (ß-MSH), when centrally injected, induces anorexigenic effects in rodents and chickens but its mechanism remains unclear. Thus, the primary goal of this research was to elucidate the hypothalamic mechanism using chickens. Intracerebroventricular injection of 0.3, 1.0 and 3.0 nmol of ß-MSH decreased food intake for 540 min. Expression of hypothalamic mRNAs were affected by ß-MSH injection, including corticotrophin-releasing factor (CRF) and its receptor subtype 1 (CRFR1), mesotocin (MT) and its receptor (MTR), pro-opiomelanocortin, cocaine- and amphetamine-regulated transcript (CART), growth hormone secretagogue receptor (GHSR) and neuropeptide Y (NPY) receptor subtype 5 (NPYR5). Within the arcuate nucleus, expressions of NPY, agouti-related peptide, MT and MTR were increased by ß-MSH injection. ß-MSH-treated chicks had more CRF, CRFR1, CRF receptor subtype 2, GHSR, NPY receptor subtype 1 (NPYR1) and NPYR5 mRNA but lower levels of CART and ghrelin, in the paraventricular nucleus. Greater amounts of mRNA for MTR, GHSR, NPYR1 and NPYR5 and less CRF expression were observed in the ventromedial hypothalamus. In conclusion, central injection of ß-MSH potently reduced food intake and was associated with changes in mRNA expression of some anorexigenic factors in a hypothalamic nucleus-specific manner.

The hypothalamic mechanism of neuropeptide S-induced satiety in Japanese quail (Coturnix japonica) involves the paraventricular nucleus and corticotropin-releasing factor.

Neuropeptide S (NPS), a 20-amino acid neuropeptide, is produced in the brain and is associated with appetite suppression.Our group was the first to report this anorexigenic effect in birds using chicken as a model, although a hypothalamic molecular mechanism remains to be elucidated. Thus, we designed the present study using Japanese quail(Coturnix japonica).In Experiment 1, quail intracerebroventricularly injected with NPS reduced both food and water intake. In Experiment 2, food-restricted quail injected with NPS displayed a reduction in water intake.In Experiment 3, NPS-injected quail reduced their feeding and exploratory pecks.In Experiment 4, we quantified the number of cells expressing the early intermediate gene product c-Fos (as a marker of neuronal activation) in appetite associated hypothalamic nuclei and found that immunoreactivity was increased in the paraventricular nucleus (PVN). In Experiment 5, we utilized real-time PCR to screen for neuropeptide changes within the PVN of NPS-injected quail. Mesotocin and corticotropin-releasing factor (CRF) mRNAs increased in response to NPS injection. In Experiment 6, co-injection of astressin, a CRF receptor antagonist, was sufficient to block the food intake-suppressive effects of NPS, but in Experiment 7, co-injection of an oxytocin receptor antagonist was not sufficient to block the food intake-suppressive effects of NPS. Collectively, results support that NPS induces an anorexigenic response in Japanese quail that is mediated within the PVN and is associated with CRF.