Differential energy expenditure is involved in the difference in activity levels between the Djungarian hamster (Phodopus sungorus) and the Roborovskii hamster (P. roborovskii).

The Djungarian hamster (Phodopus sungorus) shows calm behavior, while the Roborovskii hamster (P. roborovskii) exhibits hyperactivity. Even though they belong to the same genus, Phodopus, these two species are quite different. The current study investigated the relationship between energy expenditure and the markedly different levels of activity shown by these hamsters. Roborovskii hamsters showed significantly higher energy expenditure than Djungarian hamsters under both feeding and fasting conditions during darkness. Roborovskii hamsters showed a repeated increase and decrease in energy expenditure under the feeding condition; however, this changed under the fasting condition, during which the repeated increase and decrease in energy expenditure corresponded to the repeated active and sleeping conditions. Djungarian hamsters had a tendency to keep their energy expenditure constant during the fasting condition, while Roborovskii hamsters moved around a lot to find food. The respiratory quotient (RQ) values in Djungarian hamsters were relatively constant. However, Roborovskii hamsters showed a wide variation in RQ. In particular, the RQ value declined immediately before a dark phase commenced, indicating a switchover from the utilization of glucose to that of lipids as a substrate for energy production. In conclusion, Djungarian hamsters and Roborovskii hamsters showed different behavioral patterns that were related to differences in energy metabolism.

Central Interaction Between L-Ornithine and Neuropeptide Y in the Regulation of Feeding Behavior of Neonatal Chicks.

Ornithine has been identified as a potential satiety signal in the brains of neonatal chicks. We hypothesized that brain nutrient signals such as amino acids and appetite-related neuropeptides synergistically regulate food intake. To test this hypothesis, we investigated the interaction between neuropeptide Y (NPY) and ornithine in the control of feeding behavior in chicks and the associated central and peripheral amino acid metabolic processes. Five-day-old chicks were intracerebroventricularly injected with saline, NPY (375 pmol), or NPY plus ornithine (2 or 4 µmol) at 10 µl per chick, and then subjected to ad libitum feeding conditions; food intake was monitored for 30 min after injection. Brain and plasma samples were collected after the experiment to determine free amino acid concentrations. Co-injection of NPY and ornithine significantly attenuated the orexigenic effect induced by NPY in a dose-dependent manner. Central NPY significantly decreased amino adipic acid, asparagine, γ-aminobutyric acid, leucine, phenylalanine, tyrosine, and isoleucine levels, but significantly increased lysine levels in the brain. Co-injection of NPY and ornithine significantly increased ornithine and proline levels in all examined brain regions, but decreased diencephalic tryptophan and glycine levels compared with those of the control and NPY-alone groups. Co-injection of NPY and high-dose ornithine significantly decreased methionine levels in all brain regions. Central NPY significantly suppressed the plasma concentrations of amino acids, including proline, asparagine, methionine, phenylalanine, tyrosine, leucine, isoleucine, glycine, glutamine, alanine, arginine, and valine, and this reduction was greater when NPY was co-injected with ornithine. These results suggest that brain ornithine interacts with NPY to regulate food intake in neonatal chicks. Furthermore, central NPY may induce an anabolic effect that is modified by co-injection with ornithine.

The Greater Impact of Paternal, Compared to Maternal, Hereditary Background on Depressive-Like Behavior in Wistar Kyoto Rats with Different Amino Acid Metabolism in the Pup Brain.

In the pathogenesis of depression, heredity is believed to be a major factor. However, the mechanism by which heredity contributes to the onset of depression is not fully understood. Wistar Kyoto (WKY) rats have been used as an animal model for depression because of their increased depression-like behavior compared to Wistar (WIS) rats. In the present study, pups crossbred from WKY × WIS rats were used to evaluate locomotor activity in an open field test (OFT) and depression-like behavior in a forced swimming test (FST), with a focus on amino acid metabolism. Pups in the WKY♂ × WKY♀ group showed lower locomotor activity in the OFT and higher depression-like behavior in the FST than those in the WIS♂ × WIS♀ group. In addition, multiple regression analysis showed that the paternal strain had a greater effect than the maternal strain on locomotor activity and depression-like behavior in OFT and FST, respectively. Several amino acids in the brainstem, hippocampus, and striatum were significantly decreased through the influence of the WKY paternal strain, but not the WKY maternal strain. Based on these data from comparing WKY and WIS rats, we hypothesize that the hereditary effects of the WKY paternal strain on behavioral tests are partially caused by dysregulation of the amino acid metabolism in the brain.

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.

Supplementation of L-Ornithine Could Increase Sleep-like Behavior in the Mouse Pups.

Along the maternal-fetal-neonatal axis, one of the problems relating to the maternal-neonatal axis is infant sleep problems including nighttime crying. One possible solution could be to provide the newborn with sleep-promoting ingredients through breast milk or formula. So far, it has been reported that L-ornithine has a sleep-related effect. Therefore, we investigated the effect of dietary L-ornithine on maternal mouse plasma and milk L-ornithine levels in Experiment 1. In Experiment 2, a single dose of L-ornithine was applied to know the time-course changes in plasma, mammary gland and milk L-ornithine levels. Experiment 3 was conducted to confirm sleep behavior as well as changes in polyamine levels in milk. L-Ornithine levels in maternal plasma significantly increased by both dietary regimen and single oral administration in Experiments 1 and 2. Both L-ornithine treatments also increased its levels in milk, although not to a concentration as high as in plasma. In Experiment 3, the level of polyamines, which are metabolized from L-ornithine, did not significantly differ after L-ornithine administration. In sleep-like behavior observations, the average concentration of L-ornithine in milk did not increase the sleep-like behavior of mouse pups. However, more concentrated L-ornithine solutions can significantly increase sleep-like behavior. These results revealed that even if mothers ingested L-ornithine to increase L-ornithine levels in breast milk, it is difficult to promote sleep in newborns. Because it is difficult to raise L-ornithine in breast milk to sleep-inducing levels, L-ornithine added formula may partially improve infant sleep and has the potential for preventing infant sleep problems such as nighttime crying.

Thermal manipulation modifies embryonic growth, hepatic free amino acid concentrations, and hatching performance in layer-type chicks.

Thermal manipulation (TM) of incubation temperature has been demonstrated to alter metabolism and post-hatch thermotolerance in broiler strains (meat-type chickens). Fewer reports were focused on layer-type chickens and there was no report on amino acid metabolism during TM in layer-type embryos. In this study, we investigated the effects of TM on embryonic development, hepatic amino acid metabolism, and hatching performance in layer-type chickens. Fertilized eggs were incubated under control thermoneutral temperature (CT, 37.6°C) and TM with high temperature (TMH, 39°C, 8 h/day) or low temperature (TML, 20°C, 1 h/day) from embryonic day (ED) 8 to ED 15. The embryonic weight and relative embryonic weight (yolk-free embryonic weight to the initial egg weight) significantly declined in the TML group at ED 13 (P < 0.01) and ED 16 (P < 0.0001), and were significantly increased (P < 0.001) in the TMH group at ED 16, in comparison with the embryos in the CT group. The concentrations of all hepatic free amino acids were significantly increased (P < 0.01) with embryonic development. Interestingly, TMH and TML caused similar effects on hepatic amino acid metabolism, in which most of the essential and non-essential amino acids were significantly declined (P < 0.05) under TM treatments at ED 13 but not affected at ED 16. Until hatching, TML, but not TMH, caused a significant (P < 0.05) delay (31-38 min/day from ED 8) in incubation duration. The hatchability in the TML group was lower than the other two groups, which indicated that 20°C as cold stimulation was not suitable for layer embryos. The body weight, yolk weight, yolk-free body mass, and chick quality were not affected by TM treatments. However, the relative weight of the liver, but not the heart, was significantly reduced (P < 0.05) at hatching by TML treatment. In conclusion, TML, but not TMH, caused to delay in embryogenesis and affected the internal organ of chicks at hatch. Similar changes in amino acid metabolism under TMH and TML indicated that thermal stress induced by both high and low extreme ambient temperatures influences embryonic amino acid metabolism in a similar fashion in layer-type embryos.

A new and efficient method for producing food ingredients high in l-ornithine using unused parts of white cabbage (Brassica oleracea var. capitata).

A surplus of unused parts of vegetables (e.g., white cabbage [cabbage] cores and outer leaves) is generated daily by factories of fresh-cut vegetables. These parts are difficult to effectively utilize and are often discarded as biodegradable industrial waste. This study aimed to develop an efficient method for producing l-ornithine from cabbage residues. First, we added protease (Sumizyme FP) to the cores and outer leaves of sterile cabbages. After 8 days, the amount of l-arginine released was approximately fivefold the amount in the initial content. As l-arginine is a precursor of l-ornithine, the addition of protease combined with Pediococcus pentosaceus produced l-ornithine. However, the rapid lactic acid fermentation suppressed the metabolism of l-arginine to l-ornithine, which we overcame by adjusting the pH by adding eggshell. The anaerobic fermentation of the cores and outer leaves of sterile cabbages with 5% eggshell for 8 days produced 184 ± 2 µmol of l-ornithine/100 g cabbage. PRACTICAL APPLICATIONS: This level of l-ornithine production is higher than that observed in freshwater clams (81-116 µmol/100 g), which are considered to be high in l-ornithine. This method can be applied to the production of inexpensive and safe l-ornithine-containing food materials derived from vegetables. Furthermore, ingestions of vegetables fermented by this method would provide a variety of health benefits of l-ornithine. The widespread adoption of this method will not only reduce the amount of waste generated daily from fresh-cut vegetable factories, but will also enable upcycling as a higher value-added food material.

Temporal patterns of increased growth hormone secretion in mice after oral administration of L-ornithine: possible involvement of ghrelin receptors.

l-Ornithine is known to stimulate growth hormone (GH) release in mammals. Here, we demonstrated that increases in plasma GH levels after oral administration of l-ornithine were first observed 150 min after administration, and the elevated levels were sustained for more than 90 min in mice. The increase was significantly delayed compared with the reported timing of plasma and tissue levels of l-ornithine after administration. The l-ornithine-induced increase in GH release was completely blocked by [D-Lys3]-GHRP-6, a ghrelin receptor antagonist, but not by cyclosomatostatin or JV-1-38, antagonists of somatostatin and GH-releasing hormone, respectively. These results suggest the involvement of ghrelin receptor-mediated pathways in l-ornithine-induced increases in GH release.

Central administration of neuropeptide Y reduces the cellular heat stress response and may enhance spleen antioxidative functions in heat-exposed chicks.

Previously it was found that mRNA expression of neuropeptide Y (NPY) was increased in the chicken brain under heat stress. NPY has also been reported as an anti-stress factor to regulate brain functions in heat-exposed chicks. However, to the best of our knowledge, there is no report on the action of central NPY in the immune organs under heat stress. The aim of this study was to examine whether central injection of NPY can regulate heat stress response in the spleen and liver. After intracerebroventricular (ICV) injection of NPY, chicks were exposed to control thermoneutral temperature (CT: 30 ± 1 °C) or high ambient temperature (HT: 35 ± 1 °C) chambers for 60 min. Central injection of NPY caused lowering in rectal temperature under CT, but not under HT. Moreover, ICV injection of NPY caused a significant lower mRNA expression of heat-shock protein-70 and higher expression of glutathione synthase in the spleen, but not liver. Furthermore, plasma uric acid concentrations were significantly increased by the ICV injection of NPY in chicks under HT. These results indicate that brain NPY may contribute to attenuate the intracellular heat stress response and enhance antioxidative status in the immune organ, spleen 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.

Repeated restraint stress modifies fatty acid and amino acid metabolism in the mouse skin.

In modern society, stress caused by relationships and emotions is one of the greatest social problems. Similar to humans, domestic and captive animals live under various stresses. Several stresses have been associated with skin disorders, such as atopic dermatitis, but there is a lack of reliable and objective indicators for the characterization of this association. This study aimed to define the changes in fatty acid composition and amino acid concentration in the skin following repeated restraint stress in ICR mice. Mice subjected to 30 min of daily restraint stress for 8 days showed changes in the composition of saturated fatty acids, such as an increase in palmitic acid content, which are the substrates of Δ-9 desaturase. Conversely, unsaturated fatty acids decreased with stress treatment, which appeared to be a result of these fatty acids being the substrate of Δ-6 desaturase. Changes in fatty acid composition after stress treatment may be one of the factors that cause skin inflammation. The water-retention capacity may have been lowered by stress treatment because histidine and leucine, which are natural moisturizing factors, were significantly decreased. The collagen content in the skin gradually decreased after repeated stress treatment. Our results indicate that repeated restraint stress may impact skin health through changes in both the fatty acid composition and amino acid concentration in mice.

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.

Effect of regular and irregular stimulation cycles of dexamethasone on circadian clock in NIH3T3 cells.

Animal studies have shown that irregular light-dark cycles cause circadian desynchronization, while few studies have addressed the effect of regular/irregular stimulation cycles of signaling hormones on the cellular clock in vitro. Here, we examined how cellular clocks respond to regular and irregular stimulation cycles of dexamethasone, using NIH3T3 cells transfected with the Bmal1 promoter-driven luciferase (Bmal1-Luc) reporter gene. Cyclic stimulation with dexamethasone at different time intervals (18-28 h, 3 times regularly) revealed that Bmal1-Luc bioluminescence rhythms can be entrained to 22 and 24 h cycles during the stimulation period, but not to other cycles. The rhythm entrained for 24 h cycles persisted for at least one day after the last stimulation. Irregular dexamethasone treatment (16, 24, and 16 h, sequentially; short-term jet lag protocol) resulted in an overall upregulation and phase shifts of the temporal expression of several clock genes and cell cycle genes, including c-Myc and p53. Regular dexamethasone stimulation three times with 24 h cycles also caused upregulation of Per1 and Per2 expression, but not c-Myc and p53 expression. In conclusion, our study identified the entrainable range of the circadian clock in NIH3T3 cells to the dexamethasone stimulation cycle and demonstrated that irregular dexamethasone treatment could disturb the expression of cell cycle genes.

Spermidine resets circadian clock phase in NIH3T3 cells.

Irregular light-dark cycles desynchronize the circadian clock via hormonal and neuronal pathways and increase the risk of various diseases. This study demonstrated that a single pulse of spermidine-a polyamine-strongly induced circadian phase advances in the presence or absence of dexamethasone (a synthetic glucocorticoid) in NIH3T3 cells transfected with the Bmal1 promotor-driven luciferase reporter gene. The spermidine-induced phase advances were 2-3 fold greater than were the dexamethasone-induced shifts. The phase resetting effect of spermidine occurred in a dose- and time-dependent manner and was not blocked by RU486, an antagonist of glucocorticoid receptors. Spermidine treatment modulated the expression of clock genes within 60 min, which was sooner than changes in the expression of autophagy-related genes. These findings suggested that spermidine is a potent modulator of the circadian phase, acting through glucocorticoid receptor-independent pathways, and may be useful for treating diseases related to circadian desynchrony.

L-Leucine In Ovo Administration Causes Growth Retardation and Modifies Specific Amino Acid Metabolism in Broiler Embryos.

L-Leucine (L-Leu) in ovo administration was demonstrated to afford thermotolerance and modified amino acids metabolism in post-hatched broiler chicks under heat stress. This study aimed to investigate the changes in embryonic growth and amino acid metabolism after in ovo injection of L-Leu. Fertilized broiler eggs were subjected to in ovo injection of sterile water or L-Leu on embryonic day (ED) 7. The weight of embryos and yolk sacs were measured on ED 12, 14, 16, and 18. Plasma and livers were collected on ED 14 and 18 for free amino acid analysis. The weight and relative weight of embryos were significantly lowered by in ovo administration of L-Leu, but those of yolk sacs were not altered. Moreover, L-Leu in ovo injection significantly reduced the plasma proline concentration during embryogenesis and increased the plasma concentrations of tyrosine (Tyr) and lysine (Lys) in ED 18. Hepatic Lys concentration was also significantly increased by L-Leu in ovo injection. Interestingly, Leu concentrations in the plasma and liver were not affected by L-Leu administration. These results indicated that in ovo administered L-Leu was metabolized before ED 14 and affected embryonic growth and amino acid metabolism during embryogenesis.

Produced ß-hydroxybutyrate after ß-hydroxy-ß-methylbutyrate (HMB) administration may contribute HMB function in mice.

ß-Hydroxy-ß-methylbutyrate (HMB) is an intermediate in the metabolism of the branched-chain amino acid leucine. HMB has several demonstrated effects on skeletal muscle function, some of which are contradictory. In addition, the effect of exogenous HMB intake on the levels of intermediate metabolites is not known. Therefore, we investigated changes in HMB metabolites after oral HMB administration in mice. First, ICR mice were treated with either distilled water or HMB (0.215 g/10 mL/kg). Sampling was performed at 0, 1, 6, 12, and 24 h after administration. Next, ICR mice were given distilled water or HMB (0.215 g/10 mL/kg/d) for 10 d. Mice given HMB shown a significant increase in liver ß-methylcrotonyl-CoA and increased ß-hydroxybutyrate in plasma and the gastrocnemius muscle 1 h after HMB administration. Mice administered HMB for 10 d showed significantly decreased food intake and body weight; however, the relative weight of the gastrocnemius muscle was significantly increased. These results may be attributed to an increase in ß-hydroxybutyrate resulting from exogenous HMB, since ß-hydroxybutyrate inhibits food intake and suppresses skeletal muscle catabolism. In conclusion, ß-hydroxybutyrate, a metabolite of HMB, was found to play an important role in the function of HMB.

Neuropeptide Y modifies a part of diencephalic catecholamine but not indolamine metabolism in chicks depending on feeding status.

The role of the monoaminergic system in the feeding behavior of neonatal chicks has been reported, but the functional relationship between the metabolism of monoamines and appetite-related neuropeptides is still unclear. This study aimed to investigate the changes in catecholamine and indolamine metabolism in response to the central action of neuropeptide Y (NPY) in different feeding statuses and the underlying mechanisms. In Experiment 1, the diencephalic concentrations of amino acids and monoamines following the intracerebroventricular (ICV) injection of NPY (375 pmol/10 µl/chick), saline solution under ad libitum, and fasting conditions for 30 min were determined. Central NPY significantly decreased L-tyrosine concentration, the precursor of catecholamines under feeding condition, but not under fasting condition. Central NPY significantly increased dopamine metabolites, including 3,4-dihydroxyphenylacetic acid and homovanillic acid (HVA). The concentration of 3-methoxy-4-hydroxyphenylglycol was significantly reduced under feeding condition, but did not change under fasting condition by NPY. However, no effects of NPY on indolamine metabolism were found in either feeding status. Therefore, the mechanism of action of catecholamines with central NPY under feeding condition was elucidated in Experiment 2. Central NPY significantly attenuated diencephalic gene expression of catecholaminergic synthetic enzymes, such as tyrosine hydroxylase, L-aromatic amino acid decarboxylase, and GTP cyclohydrolase I after 30 min of feeding. In Experiment 3, co-injection of α-methyl-L-tyrosine, an inhibitor of tyrosine hydroxylase with NPY, moderately attenuated the orexigenic effect of NPY, accompanied by a significant positive correlation between food intake and HVA levels. In Experiment 4, there was a significant interaction between NPY and clorgyline, an inhibitor of monoamine oxidase A with ICV co-injection which implies that co-existence of NPY and clorgyline enhances the orexigenic effect of NPY. In conclusion, central NPY modifies a part of catecholamine metabolism, which is illustrated by the involvement of dopamine transmission and metabolism under feeding but not fasting conditions.

Dysregulated metabolism and behaviors by disrupting gut microbiota in prenatal and neonatal mice.

The live microbiota ecosystem in the intestine plays a critical role in maintaining the normal physiological and psychological functions in both animals and human beings. However, the chronic effect of microbiota disturbances during prenatal and neonatal developing periods on animal's health remains less studied. In the current study, pregnant ICR mice were fed with an antibiotic diet (7-g nebacitin [bacitracin-neomycin sulphate 2:1]/kg standard diet) from day 14 of conception, and their offspring were provided with the same diet till the termination of the experiments. Dams treated with antibiotics showed increased body weight along with enlarged gut. Antibiotic-treated offspring revealed decreased bodyweight, increased food, water, and sucrose intake. Administration of antibiotics affected corticosterone responsivity to acute 20 min restraint challenge in male pups. In behavior tests, female pups showed decreased movement in open field while male pups revealed decreased latency to open arms in elevated plus maze test and immobility time in tail suspension test. Together, these results suggested that early antibiotic exposure may impact on the food intake, body weight gain, and emotional behavior regulation in mice.

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.

Photoperiodic changes in hippocampal neurogenesis and plasma metabolomic profiles in relation to depression-like behavior in mice.

Photoperiod alters affective behaviors and brain neuroplasticity in several mammalian species. We addressed whether neurogenesis and signaling pathways of insulin-like growth factor-I (IGF-I), a key modulator of neuroplasticity, are regulated by photoperiod in C57BL/6 J mice, a putative model of seasonal affective disorder. We also examined the effects of photoperiod on plasma metabolomic profiles in relation to depression-like behavior to understand a possible linkage between peripheral metabolism and behavior. Mice that were maintained under long-day conditions (LD) exhibited a higher number of 5-bromo-2'-deoxyuridine-positive cells and higher levels of astrocyte marker in the dentate gyrus of the hippocampus compared to that of mice under short-day conditions (SD). Plasma IGF-I levels and levels/expression of IGF-I signaling molecules in the hippocampus (Brn-4, NeuroD1, and phospho-Akt) involved in neuronal proliferation and differentiation were higher in the mice under LD. Metabolome analysis using plasma of the mice under LD and SD identified several metabolites that were highly correlated with immobility in the forced swim test, a depression-like behavior. Negative correlations with behavior occurred in the levels of 23 metabolites, including metabolites related to neurogenesis and antidepressant-like effects of exercise, metabolites in the biosynthesis of arginine, and the occurrence of branched chain amino acids. Three metabolites had positive correlations with the behavior, including guanidinosuccinic acid, a neurotoxin. Taken together, photoperiodic responses of neurogenesis and neuro-glial organization in the hippocampus may be involved in photoperiodic alteration of depression-like behavior, mediated through multiple pathways, including IGF-I and peripheral metabolites.