Oleuropein has hypophagic effects in broiler chicks.

Oleuropein, a phenolic compound derived from olives, has known glucoregulatory effects in mammalian models but effects in birds are unknown. We investigated effects of dietary supplementation and exogenous administration of oleuropein on broiler chick feed intake and glucose homeostasis during the first 7 days post-hatch. One hundred and forty-eight day-of-hatch broiler chicks were randomly allocated to one of four dietary treatments with varying oleuropein concentrations (0, 250, 500, or 1,000 mg/kg). Body weight and breast muscle and liver weights were recorded on day 7. In the next experiment, chicks received intraperitoneal (IP) injections of oleuropein at doses of 0 (vehicle), 50, 100, or 200 mg/kg on day 4 post-hatch, with feed intake and blood glucose levels measured thereafter. Lastly, chicks fed a control diet were fasted and administered intracerebroventricular (ICV) injections of oleuropein at doses of 0, 50, 100, or 200 µg, after which feed intake was recorded. Results indicated that IP and ICV injections led to decreased feed intake, primarily at 60 min post-injection, with effects diminishing by 90 min in the IP study. Blood glucose levels decreased 1-h post-IP injection at higher oleuropein doses. These findings suggest that oleuropein acts as a mild appetite suppressant and influences energy metabolism in broiler chickens.

Peripheral and Central Impact of Methionine Source and Level on Growth Performance, Circulating Methionine Levels and Metabolism in Broiler Chickens.

The present study was designed to evaluate the effects of DL-methionine (DL-Met) 2-hydroxy-4-(methylthio) butanoic acid (HMTBa), or S-(5'-Adenosyl)-L-methionine chloride (SAM), using feeding trial and central administration, on live performance, plasma metabolites, and the expression of feeding-related hypothalamic neuropeptides in broilers raised to a market age (35 d). Final average body weight (BW) and feed conversion ratio (FCR) from the feeding trial exceeded the performance measurements published by the primary breeder. At d35, the MTBHa group had better BW and lower feed intake, which resulted in a better FCR than the DL-Met group at 87 TSAA to lysine. At the molecular levels, the expression of hypothalamic neuropeptide (NPY) and monocarboxylate transporter (MCT) 2 did not differ between all treated groups; however, the mRNA abundances of hypothalamic MCT1 and orexin (ORX) were significantly upregulated in DL-Met- treated groups compared to the control. The ICV administration of SAM significantly reduced feed intake at all tested periods (from 30 to 180 min post injection) compared to the aCSF-treated group (control). The central administration of HMTBa increased feed intake, which reached a significant level only 60 min post administration, compared to the control group. ICV administration of DL-Met slightly increased feed intake compared to the control group, but the difference was not statistically discernable. Quantitative real-time PCR analysis showed that the hypothalamic expression of NPY, cocaine- and amphetamine-regulated transcript, MCT1, and MCT2 was significantly upregulated in the ICV-HMTBa group compared to the aCSF birds. The hypothalamic expression of the mechanistic target of rapamycin (mTOR), AMP-activated protein kinase (AMPKα1), D-amino acid oxidase, and hydroxyacid oxidase was significantly upregulated in DL-Met compared to the control group. The mRNA abundances of ORX were significantly increased in the hypothalamus of both DL-Met and HMTBa groups compared to the aCSF birds; however, mTOR gene expression was significantly downregulated in the SAM compared to the control group. Taken together, these data show, for the first time, that DL-Met and HMTBa have a common downstream (ORX) pathway, but also a differential central pathway, typically NPY-MCT for HMTBa and mTOR-AMPK for methionine.

Introducing the Harm Reduction Collaboration Framework for Policy, Systems, and Environmental Change.

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Elucidating the central anorexigenic mechanism of glucagon-like peptide 1 in Japanese quail (Coturnix japonica).

Glucagon-like peptide 1 (GLP-1) elicits a potent reduction in food intake, although the central mechanism mediating this appetite-suppressive effect is not fully understood in all species. To begin to elucidate the molecular mechanisms in quail, we administered GLP-1 via intracerebroventricular (ICV) injection to 7-day-old Japanese quail (Coturnix japonica) and determined effects on food and water intake, behavior, and brain nucleus activation. We observed a reduction in food and water intake, with the lowest effective dose being 0.01 nmol. Quail injected with GLP-1 displayed fewer steps, feeding pecks, exploratory pecks, and jumps, while time spent sitting increased. We quantified c-Fos immunoreactivity at 60 min post-injection in hypothalamic and brainstem nuclei that mediate food intake and determined that the hypothalamic paraventricular nucleus (PVN), and nucleus of the solitary tract and area postrema of the brainstem were activated in response to GLP-1. In conclusion, these results suggest that GLP-1 induces anorexigenic effects that are likely mediated at the level of the PVN and brainstem.

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.

An olive-derived elenolic acid stimulates hormone release from L-cells and exerts potent beneficial metabolic effects in obese diabetic mice.

Insulin resistance and progressive decline in functional ß-cell mass are two key factors for developing type 2 diabetes (T2D), which is largely driven by overweight and obesity, a significant obstacle for effective metabolic control in many patients with T2D. Thus, agents that simultaneously ameliorate obesity and act on multiple pathophysiological components could be more effective for treating T2D. Here, we report that elenolic acid (EA), a phytochemical, is such a dual-action agent. we show that EA dose-dependently stimulates GLP-1 secretion in mouse clonal L-cells and isolated mouse ileum crypts. In addition, EA induces L-cells to secrete peptide YY (PYY). EA induces a rapid increase in intracellular [Ca2+]i and the production of inositol trisphosphate in L-cells, indicating that EA activates phospholipase C (PLC)-mediated signaling. Consistently, inhibition of (PLC) or Gαq ablates EA-stimulated increase of [Ca2+]i and GLP-1 secretion. In vivo, a single dose of EA acutely stimulates GLP-1 and PYY secretion in mice, accompanied with an improved glucose tolerance and insulin levels. Oral administration of EA at a dose of 50 mg/kg/day for 2 weeks normalized the fasting blood glucose and restored glucose tolerance in high-fat diet-induced obese (DIO) mice to levels that were comparable to chow-fed mice. In addition, EA suppresses appetite, reduces food intake, promotes weight loss, and reverses perturbated metabolic variables in obese mice. These results suggest that EA could be a dual-action agent as an alternative or adjuvant treatment for both T2D and obesity.

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.

Deletion of GPR30 Drives the Activation of Mitochondrial Uncoupling Respiration to Induce Adipose Thermogenesis in Female Mice.

Thermogenic adipocytes possess a promising approach to combat obesity with its capability promoting energy metabolism. We previously discovered that deletion of GPR30 (GPRKO), a presumably membrane-associated estrogen receptor, protected female mice from developing obesity, glucose intolerance, and insulin resistance when challenged with a high-fat diet (HFD). In vivo, the metabolic phenotype of wild type (WT) and GPRKO female mice were measured weekly. Acute cold tolerance test was performed. Ex vivo, mitochondrial respiration of brown adipose tissue (BAT) was analyzed from diet-induced obese female mice of both genotypes. In vitro, stromal vascular fractions (SVF) were isolated for beige adipocyte differentiation to investigate the role of GPR30 in thermogenic adipocyte. Deletion of GPR30 protects female mice from hypothermia and the mitochondria in BAT are highly energetic in GPRKO animals while the WT mitochondria remain in a relatively quiescent stage. Consistently, GPR30 deficiency enhances beige adipocyte differentiation in white adipose tissue (WAT) and activates the thermogenic browning of subcutaneous WAT due to up-regulation of UCP-1, which thereby protects female mice from HFD-induced obesity. GPR30 is a negative regulator of thermogenesis, which at least partially contributes to the reduced adiposity in the GPRKO female mice. Our findings provide insight into the mechanism by which GPR30 regulates fat metabolism and adiposity in female mice exposed to excess calories, which may be instrumental in the development of new therapeutic strategies for obesity.

Synchronous and metachronous bilateral breast cancer among women with a history of lobular carcinoma in situ.

PURPOSE: Lobular carcinoma in situ (LCIS) confers increased cancer risk in either breast, but it remains unclear if this population is at increased risk for bilateral breast cancer (BC) development. Here we report bilateral BC incidence among women with a history of LCIS. METHODS: Women with classic-type LCIS diagnosed from 1980 to 2017 who developed unilateral BC (UBC) or bilateral BC were identified. Bilateral BC was categorized as synchronous (bilateral BC diagnosed < 6 months apart; SBBC) or metachronous (bilateral BC diagnosed ≥ 6 months apart; MBBC). Five-year incidence rates of bilateral BC among this population were evaluated. Comparisons were made to identify factors associated with bilateral BC. RESULTS: At 7 years' median follow-up, 249/1651 (15%) women with LCIS developed BC; 34 with bilateral BC (2%). There were no clinicopathologic feature differences between those with UBC and bilateral BC. SBBC occurred in 18 without significant differences versus UBC. Among 211 with UBC and a contralateral breast at risk, 16 developed MBBC at a median follow-up of 3 years. MBBC patients were less likely to receive endocrine therapy and more likely to receive chemotherapy versus UBC. Tumor histology was not associated with MBBC. Estimated 5-year MBBC risk was 6.4%. Index estrogen/progesterone receptor positivity and endocrine therapy were the only factors associated with MBBC risk. CONCLUSION: Bilateral BC occurred in 2% of women with LCIS history at median follow-up of 7 years. Similar to the general BC population, a decrease in MBBC is seen among women with a history of LCIS who develop hormone receptor-positive disease and those who receive endocrine therapy, highlighting the protective effects of this treatment.

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.

COVID-19-associated psychosis: A systematic review of case reports.

OBJECTIVES: To describe the comorbidities, presentations, and outcomes of adults with incident psychosis and a history of COVID-19. METHODS: We completed a descriptive systematic review of case reports according to PRISMA guidelines, including cases of adult patients with incident psychosis and antecedent or concurrent COVID-19. We extracted patient demographics, comorbidities, clinical course, and outcomes, and assessed cases for quality using a standardized tool. RESULTS: Of 2396 articles, we included 40 reports from 17 countries, comprising 48 patients. The mean age of patients was 43.9 years and 29 (60%) were males. A total of 7 (15%) had a documented psychiatric history, 6 (13%) had a substance use history and 11 (23%) had a comorbid medical condition. Delusions were the most common (44 [92%]) psychiatric sign and psychosis lasted between 2 and 90 days. A total of 33 (69%) patients required hospitalization to a medical service and 16 (33%) required inpatient psychiatric admission. The majority (26 [54%]) of cases did not assess for delirium and 15 (31%) cases were judged to be of high risk of bias. CONCLUSIONS: Despite the growing awareness of COVID-19's association with incident psychosis at a population level, cases of COVID-19-associated psychosis often lacked clinically relevant details and delirium was frequently not excluded. PROSPERO registration number: CRD42021256746.

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.