Regulation Of Feeding Research Articles

Transcriptome Sequencing Analysis Reveals Dynamic Changes in Major Biological Functions during the Early Development of Clearhead Icefish, Protosalanx chinensis

Early development, when many important developmental events occur, is a critical period for fish. However, research on the early development of clearhead icefish is very limited, especially in molecular research. In this study, we aimed to explore the dynamic changes in the biological functions of five key periods in clearhead icefish early development, namely the YL (embryonic), PM (first day after hatching), KK (fourth day after hatching), LC (seventh day after hatching), and SL (tenth day after hatching) stages, through transcriptome sequencing and different analysis strategies. A trend expression analysis and an enrichment analysis revealed that the expression ofgenes encoding G protein-coupled receptors and their ligands, i.e., prss1_2_3, pomc, npy, npb, sst, rln3, crh, gh, and prl that are associated with digestion and feeding regulation gradually increased during early development. In addition, a weighted gene co-expression network analysis (WGCNA) showed that eleven modules were significantly associated with early development, among which nine modules were significantly positively correlated. Through the enrichment analysis and hub gene identification results of these nine modules, it was found that the pathways related to eye, bone, and heart development were significantly enriched in the YL stage, and the ccnd2, seh1l, kdm6a, arf4, and ankrd28 genes that are associated with cell proliferation and differentiation played important roles in these developmental processes; the pak3, dlx3, dgat2, and tas1r1 genes that are associated with jaw and tooth development, TG (triacylglycerol) synthesis, and umami amino acid receptors were identified as hub genes for the PM stage; the pathways associated with aerobic metabolism and unsaturated fatty acid synthesis were significantly enriched in the KK stage, with the foxk, slc13a2_3_5, ndufa5, and lsc2 genes playing important roles; the pathways related to visual perception were significantly enriched in the LC stage; and the bile acid biosynthetic and serine-type peptidase activity pathways were significantly enriched in the SL stage. These results provide a more detailed understanding of the processes of early development of clearhead icefish.

Ghrelin-Ghrelin receptor (GSHR) pathway via endocannabinoid signal affects the expression of NPY to promote the food intake of Siberian sturgeon (Acipenser baerii)

Previous data suggested that activation of endocannabinoid receptor 1 (CB1) was necessary for the orexigenic effect of Ghrelin in rodents, but the information is limited in teleosts. To investigate the feeding regulation pathway of Ghrelin and CB1 in Siberian sturgeon (Acipenser baerii), this study first identified the Ghrelin (345 bp, complete coding sequence) and Ghrelin receptor (GHSR, 500 bp, partial coding sequence) sequences, and then detected their tissue distribution patterns, which showed that Ghrelin is mainly distribution in peripheral tissues, while GSHR is mainly in different brain divisions. Besides, the qPCR before and after feeding showed that the mRNA expressions of Ghrelin and GHSR were inhibited after feeding in telencephalon, diencephalon and mesencephalon. Subsequently, the food intake and appetite factor expressions were measured by i.c.v. co-injection of Ghrelin and GSHR antagonist. The results showed that Ghrelin promoted the food intake of Siberian sturgeon, which was reversed by its receptor antagonist. Besides, i.c.v. injection of Ghrelin decreased telencephalon CART expression while increased NPY expression in the three brain regions. In addition, to further explore the relationship of Ghrelin and CB1 signal regulating feeding, the co-injection of Ghrelin and CB1 antagonists was performed. The results showed that AM6545 (CB1 peripheral restricted antagonist) failed to affect the orexigenic effect of Ghrelin and the expression pattern of NPY mRNA in the telencephalon. While in the diencephalon, the increase of food intake and NPY mRNA expression induced by Ghrelin was completely reversed by Rimonabant (CB1 global antagonist). These results indicate Ghrelin-GSHR pathway promotes the food intake of Siberian sturgeon by inducing the expression of NPY in the diencephalon, and the stimulating effect will be reversed by cannabinoid receptor antagonism. This study provides a foundation for understanding the pathways Ghrelin and CB1 signals in appetite regulation of the teleost.

Relationships Between IKIGAI Well-Being and Motivation for Autonomous Regulation of Eating and Exercise for Health - Included the Relevance Between Sense of Coherence and Social Support.

Self-regulated motivation is associated with better behavior change, health, and hedonic well-being in the health domain. Meanwhile, there are evidences that eudaemonic well-being contributes to health. As well as reducing lifestyle diseases, the promotion of IKIGAI well-being (encompassing hedonic and eudaemonic well-being) has been targeted in Japan. However, little is known about the impact of IKIGAI well-being on the motivation for health. This study explored the relationships between autonomous motivation for eating and exercise for health, IKIGAI well-being, sense of coherence, and social support. The participants were 622 Japanese (269 males and 353 females, aged 20 to 59years). They completed a questionnaire on motivation for healthy eating (MHE), exercise motivation for health (EMH), sense of coherence, social support, and IKIGAI well-being. IKIGAI well-being was positively associated to the relative autonomy index (RAI)-MHE and RAI-EMH. Social support exerted a positive effect on sense of coherence and IKIGAI well-being; sense of coherence positively affected IKIGAI well-being. The invariances of the model across groups, such as gender, age, and subjective economic status, were verified using multiple-group structural equation models. With IKIGAI well-being as a mediating factor, social support and sense of coherence play important roles in promoting autonomous motivation for healthy eating and exercise.

The Effect of the Central Administration of the Neuropeptide VF on Feed Intake and Its Possible Interactions with Glutamate and Opioid Systems in Broiler Chicken

Arginine-phenylalanine-amide (RFamide)-related peptides known as neuropeptide VF (NPVF) have a crucial role in feeding regulation. The present study purposed to determine the effect of intracerebroventricular (ICV) injection of the NPVF on dietary intake and possible interactions of NPVF with glutamate and opioid systems in broiler chicken. In experiment 1, chickens received ICV administration of the control solution, NPVF (16 nmol), 15 nmol of MK-801 (NMDA glutamate receptors antagonist), and injection of the NPVF with MK-801 together. In experiments, 2–8 chickens were injected intracerebroventricularly with 390 nmol of CNQX (antagonist of AMPA glutamate receptors), 2 nmol of AIDA (an antagonist of mGLUR1 glutamate receptors), 150 nmol of LY341495 (an antagonist of mGLUR2 glutamate receptors), 2 nmol of UBP1112 (an antagonist for mGLUR3 glutamate receptors), 5 µg of β-FNA (an antagonist for mu (µ) receptors), 5 µg of NTI (an antagonist for delta (δ) receptors), nor-BNI (kappa (κ) receptors antagonist; 5 µg) instead of MK-801. Following the injection, at 30, 60, and 120 min, the chick's dietary intake was recorded. As a result, NPVF (16 nmol) reduced feed intake in broilers (P < 0.05). NPVF + MK-801 co-injection reduced the hypophagic action of the NPVF (P < 0.05). Injection of NPVF + CNQX together reduced the anorectic action of NPVF (P < 0.05). Co-injection of NPVF + β-FNA reduced the effects of NPVF injection (P < 0.05). Thus, in newborn broilers, NPVF-induced anorexia is probably mediated by NMDA/ AMPA glutamate and µ opioid receptors.

Hypothalamic TRH mediates anorectic effects of serotonin in rats.

Among the modulatory functions of thyrotropin-releasing hormone (TRH), an anorectic behavior in rodents is observed when centrally injected. Hypothalamic PVN neurons receive serotonergic inputs from dorsal raphe nucleus and express serotonin (5HT) receptors such as 5HT1A, 5HT2A/2C, 5HT6, which are involved in 5HT-induced feeding regulation. Rats subjected to dehydration-induced anorexia (DIA) model show increased PVN TRH mRNA expression, associated with their decreased food intake. We analyzed whether 5HT input is implicated in the enhanced PVN TRH transcription that anorectic rats exhibit, given that 5HT increases TRH expression and release when studied in vitro By using mHypoA-2/30 hypothalamic cell cultures, we found that 5HT stimulated TRH mRNA, pCREB and pERK1/2 levels. By inhibiting basal PKA or PKC activities or those induced by 5HT, pCREB or pERK1/2 content did not increase suggesting involvement of both kinases in their phosphorylation. 5HT effect on TRH mRNA was not affected by PKA inhibition, but it diminished in the presence of PKCi suggesting involvement of PKC in 5HT-induced TRH increased transcription. This likely involves 5HT2A/2C and the activation of alternative transduction pathways than those studied here. In agreement with the in vitro data, we found that injecting 5HT2A/2C antagonists into the PVN of DIA rats reversed the increased TRH expression of anorectic animals, as well as their decreased food intake; also, the agonist reduced food intake of hungry restricted animals along with elevated PVN TRH mRNA levels. Our results support that the anorectic effects of serotonin are mediated by PVN TRH in this model.Significance statementInteraction between brain peptides and neurotransmitters' pathways regulates feeding behavior, but when altered it could lead to the development of eating disorders, such as anorexia. An abnormal increased TRH expression in hypothalamic PVN results in dehydration-induced anorectic rats, associated to their low food intake. The role of neurotransmitters in that alteration is unknown, and since serotonin inhibits feeding and has receptors in PVN, we analyzed its participation in increasing TRH expression and reducing feeding in anorectic rats. By antagonizing PVN serotonin receptors in anorectic rats, we identify decreased TRH expression and increased feeding, suggesting that the anorectic effects of serotonin are mediated by PVN TRH. Elucidating brain networks involved in feeding regulation would help to design therapies for eating disorders.

The orphan receptor GPR68 is expressed in the hypothalamus and is involved in the regulation of feeding

Currently, up to 35% off all drugs approved for the treatment of human diseases belong to the G-protein-coupled receptor (GPCR) family. Out of the almost 800 existing GPCRs, 25% have no known endogenous ligands and are regarded as orphan receptors; many of these are currently under investigation as potential pharmacological targets. Here, we hypothesised that orphan GPCRs expressed in the hypothalamus could be targets for the treatment of obesity and other metabolic diseases. Using bioinformatic tools, we identified 78 class A orphan GPCRs that are expressed in the hypothalamus of mice. Initially, we selected two candidates and determined their responsivities to nutritional interventions: GPR162, the GPCR with highest expression in the hypothalamus, and GPR68, a GPCR with intermediate expression in the hypothalamus and that has never been explored for its potential involvement in metabolic regulation. GPR162 expression was not modified by fasting/feeding or by the consumption of a high-fat diet, and was therefore not subsequently evaluated. Conversely, GPR68 expression increased in response to the consumption of a high-fat diet and reduced under fasting conditions. Using immunofluorescence, GPR68 was identified in both proopiomelanocortin-expressing and agouti-related peptide–expressing neurons in the hypothalamic arcuate nucleus. Acute inhibition of GPR68 with an allosteric modulator promoted an increase in the expression of the orexigenic agouti-related peptide and neuropeptide Y, whereas 4- and 12-h inhibition of GPR68 resulted in increased caloric intake. Thus, GPR68 has emerged as an orphan GPCR that is expressed in the hypothalamus and is involved in the regulation of feeding.

The Actions of Centrally Administered Nesfatin-1 on Emesis, Feeding, and Locomotor Activity in Suncus murinus (House Musk Shrew).

Nesfatin-1 is an anorectic peptide expressed in both peripheral tissues and brain areas involved in the regulation of feeding, emotion and emesis. The aim of the present study is to characterize the distribution of NUCB2/nesfatin-1 in Suncus murinus and to investigate the actions of nesfatin-1 to affect gastrointestinal contractility, emesis, food and water intake, and locomotor activity. The deduced amino acid sequence of S. murinus nesfatin-1 using in silico cloning showed high homology with humans and rodents. NUCB2 mRNA was detected throughout the entire brain and in the gastrointestinal tract, including the stomach and gut. Western blot analysis and immunohistochemistry confirmed the expression of nesfatin-1 protein in these regions. The NUCB2 mRNA levels in the hypothalamus, hippocampus and brainstem were significantly decreased, whereas that in the striatum were increased after 24 h starvation compared to ad libitum-fed animals (p < 0.05). In in vitro studies, nesfatin-1 (0.3–1,000 pM) failed to contract or relax the isolated gastric antrum and intestinal segments. In conscious, freely moving animals, intracerebroventricular administration of nesfatin-1 (1–50 pmol) induced emesis (p < 0.05) and suppressed 6-h cumulative food intake (p < 0.05), without affecting the latency to feeding. Nesfatin-1 (25 pmol, i.c.v.) decreased 24-h cumulative food and water intake by 28.3 and 35.4%, respectively (p < 0.01). No significant differences in locomotor activity were observed. In conclusion, NUCB2/nesfatin-1 might be a potent regulator of feeding and emesis in S. murinus. Further studies are required to elucidate the mechanism of actions of this peptide as a mediator linking the brainstem NUCB2/nesfatin-1 to forebrain system.

Oxytocin Receptor-Expressing Neurons in the Paraventricular Thalamus Regulate Feeding Motivation through Excitatory Projections to the Nucleus Accumbens Core.

Oxytocin receptors (OTR) have been found in the paraventricular thalamus (PVT) for the regulation of feeding and maternal behaviors. However, the functional projections of OTR-expressing PVT neurons remain largely unknown. Here, we used chemogenetic and optogenetic tools to test the role of OTR-expressing PVT neurons and their projections in the regulation of food intake in both male and female OTR-Cre mice. We found chemogenetic activation of OTR-expressing PVT neurons promoted food seeking under trials with a progressive ratio schedule of reinforcement. Using Feeding Experimentation Devices for real-time meal measurements, we found chemogenetic activation of OTR-expressing PVT neurons increased meal frequency but not cumulative food intake because of a compensatory decrease in meal sizes. In combination with anterograde neural tracing and slice patch-clamp recordings, we found optogenetic stimulation of PVT OTR terminals excited neurons in the posterior basolateral amygdala (pBLA) and nucleus accumbens core (NAcC) as well as local PVT neurons through monosynaptic glutamatergic transmissions. Photostimulation of OTR-expressing PVT-NAcC projections promoted food-seeking, whereas selective activation of PVT-pBLA projections produced little effect on feeding. In contrast to selective activation of OTR terminals, photostimulation of a broader population of glutamatergic PVT terminals exerted direct excitation followed by indirect lateral inhibition on neurons in both NAcC and anterior basolateral amygdala. Together, these results suggest that OTR-expressing PVT neurons are a distinct population of PVT glutamate neurons that regulate feeding motivation through projections to NAcC.SIGNIFICANCE STATEMENT The paraventricular thalamus plays an important role in the regulation of feeding motivation. However, because of the diversity of paraventricular thalamic neurons, the specific neuron types promoting food motivation remain elusive. In this study, we provide evidence that oxytocin receptor-expressing neurons are a specific group of glutamate neurons that primarily project to the nucleus accumbens core and posterior amygdala. We found that activation of these neurons promotes the motivation for food reward and increases meal frequency through projections to the nucleus accumbens core but not the posterior amygdala. As a result, we postulate that oxytocin receptor-expressing neurons in the paraventricular thalamus and their projections to the nucleus accumbens core mainly regulate feeding motivation but not food consumption.

Leptin Receptor Deficiency Results in Hyperphagia and Increased Fatty Acid Mobilization during Fasting in Rainbow Trout (Oncorhynchus mykiss).

Leptin is a pleiotropic hormone known for regulating appetite and metabolism. To characterize the role of leptin signaling in rainbow trout, we used CRISPR/Cas9 genome editing to disrupt the leptin receptor (LepR) genes, lepra1 and lepra2. We compared wildtype (WT) and mutant fish that were either fed to satiation or feed deprived for six weeks. The LepR mutants exhibited a hyperphagic phenotype, which led to heavier body weight, faster specific growth rate, increased viscero- and hepatosomatic indices, and greater condition factor. Muscle glycogen, plasma leptin, and leptin transcripts (lepa1) were also elevated in fed LepR mutant fish. Expression levels of several hypothalamic genes involved in feed regulation were analyzed (agrp, npy, orexin, cart-1, cart-2, pomc-a1, pomc-b). No differences were detected between fed WT and mutants except for pomc-b (proopiomelanocortin-b), where levels were 7.5-fold higher in LepR fed mutants, suggesting that pomc-b expression is regulated by leptin signaling. Fatty acid (FA) content did not statistically differ in muscle of fed mutant fish compared to WT. However, fasted mutants exhibited significantly lower muscle FA concentrations, suggesting that LepR mutants exhibit increased FA mobilization during fasting. These data demonstrate a key role for leptin signaling in lipid and energy mobilization in a teleost fish.

Dysmetabolism and Neurodegeneration: Trick or Treat?

Accumulating evidence suggests the existence of a strong link between metabolic syndrome and neurodegeneration. Indeed, epidemiologic studies have described solid associations between metabolic syndrome and neurodegeneration, whereas animal models contributed for the clarification of the mechanistic underlying the complex relationships between these conditions, having the development of an insulin resistance state a pivotal role in this relationship. Herein, we review in a concise manner the association between metabolic syndrome and neurodegeneration. We start by providing concepts regarding the role of insulin and insulin signaling pathways as well as the pathophysiological mechanisms that are in the genesis of metabolic diseases. Then, we focus on the role of insulin in the brain, with special attention to its function in the regulation of brain glucose metabolism, feeding, and cognition. Moreover, we extensively report on the association between neurodegeneration and metabolic diseases, with a particular emphasis on the evidence observed in animal models of dysmetabolism induced by hypercaloric diets. We also debate on strategies to prevent and/or delay neurodegeneration through the normalization of whole-body glucose homeostasis, particularly via the modulation of the carotid bodies, organs known to be key in connecting the periphery with the brain.

Role of Lateral Hypothalamus Area in the Central Regulation of Feeding

Role of Lateral Hypothalamus Area in the Central Regulation of Feeding

Role of the thyrotropin-releasing hormone of the limbic system in mood and eating regulation.

Thyrotropin-releasing hormone (TRH) and its receptors are expressed in the hypothalamus and limbic regions. Brain thyrotropin-releasing hormone actions are exerted directly through its receptors and indirectly by modulating the effects of neurotransmitters such as glutamate, gamma-aminobutyric acid, acetylcholine, and dopamine. The thyrotropin-releasing hormone has been implicated in eating and mood regulation. We integrate studies that analyze the role of limbic thyrotropin-releasing hormone on displaying depressive- and anxiety-like behaviors and anorexia or hyperphagia. Since the decade of 1970s, different efforts have been made to identify some of the thyrotropin-releasing hormone effects and its analogs in feeding regulation or to ameliorate symptoms in patients diagnosed with mood disorders, and to correlate anxious or depressive parameters with thyrotropin-releasing hormone levels in the cerebrospinal fluid or its expression in postmortem brain areas of affected patients. Pharmacological studies where the thyrotropin-releasing hormone is administered to animals by different routes and to distinct brain areas have elucidated its actions in behavioral changes of mood and feeding parameters. In addition, a variety of animal models of depression, anxiety, or anorexia and hyperphagia has suggested the association between the hypothalamic and limbic TRHergic system and the regulation of mood and feeding alterations. Different approaches employ the administration of anti-depressant, anxiolytic or anorectic agents to animals and describe changes in thyrotropin-releasing hormone content or expression in hypothalamic or limbic regions. The different effects on mood that result from modulating thyrotropin-releasing hormone expression may be beneficial to treat patients diagnosed with eating disorders.

Structural and molecular characterization of paraventricular thalamic glucokinase-expressing neuronal circuits in the mouse.

The thalamic paraventricular nucleus (PVT) is a structure highly interconnected with several nuclei ranging from forebrain to hypothalamus and brainstem. Numerous rodent studies have examined afferent and efferent connections of the PVT and their contribution to behavior, revealing its important role in the integration of arousal cues. However, the majority of these studies used a region‐oriented approach, without considering the neuronal subtype diversity of the nucleus. In the present study, we provide the anatomical and transcriptomic characterization of a subpopulation of PVT neurons molecularly defined by the expression of glucokinase (Gck). Combining a genetically modified mouse model with viral tracing approaches, we mapped both the anterograde and the retrograde projections of Gck‐positive neurons of the anterior PVT (GckaPVT). Our results demonstrated that GckaPVT neurons innervate several nuclei throughout the brain axis. The strongest connections are with forebrain areas associated with reward and stress and with hypothalamic structures involved in energy balance and feeding regulation. Furthermore, transcriptomic analysis of the Gck‐expressing neurons revealed that they are enriched in receptors for hypothalamic‐derived neuropeptides, adhesion molecules, and obesity and diabetes susceptibility transcription factors. Using retrograde labeling combined with immunohistochemistry and in situ hybridization, we identify that GckaPVT neurons receive direct inputs from well‐defined hypothalamic populations, including arginine‐vasopressin‐, melanin‐concentrating hormone‐, orexin‐, and proopiomelanocortin‐expressing neurons. This detailed anatomical and transcriptomic characterization of GckaPVT neurons provides a basis for functional studies of the integration of homeostatic and hedonic aspects of energy homeostasis, and for deciphering the potential role of these neurons in obesity and diabetes development.

Possible role of transcription factors (BSX, NKX2.1, IRX3 and SIRT1) in the regulation of appetite in goldfish (Carassius auratus).

The homeobox genes play important roles in the embryonic development of animals. Recent evidence suggests they might also regulate feeding and act as transcription factors of appetite regulators. Examples of these genes are a brain-specific homeobox transcription factor (BSX), NK2 homeobox 1 (NKX2.1) and the Iroquois homeobox 3 (IRX3). Sirtuin1 (SIRT1) acts as a transcription factor for nutrient (e.g. lipid, glucose) homeostasis and responds to stress and nutrient availability, and has been shown to interact with appetite regulators. Very little is known about the role of these genes in the regulation of feeding and nutrient homeostasis in fish. In this study, we assessed the roles of BSX, NKX2.1, IRX3 and SIRT1 in the central regulation of feeding in goldfish by examining their mRNA brain distribution, assessing the effects of fasting on their brain expression and assessing the effects of peripheral injections of cholecystokinin (CCK, a brain-gut peptide), on their brain expression. All genes showed a widespread distribution in the brain, with high levels in the hypothalamus. In both hypothalamus and telencephalon, fasting induced increases in BSX, IRX3 and NKX2.1 expressions but had no effect on SIRT1 expression levels. CCK injections increased hypothalamic expression levels of IRX3 and SIRT1, and telencephalic expression levels of NKX2.1 and SIRT1, with no effect on either hypothalamic BSX or NKX2.1 expression levels or telencephalon BSX or IRX3 expression levels. Our results suggest that, in goldfish as in mammals, central BSX, NKX2.1, IRX3 and SIRT1 are present in regions of the brain regulating feeding, are sensitive to nutrient status and interact with appetite-regulating peptides.

Endogenous Androgens Diminish Food Intake and Activation of Orexin A Neurons in Response to Reduced Glucose Availability in Male Rats.

Sex steroids modify feeding behavior and body weight regulation, and androgen reportedly augments food intake and body weight gain. To elucidate the role of endogenous androgens in the feeding regulation induced by reduced glucose availability, we examined the effect of gonadectomy (orchiectomy) on food intake and orexin A neuron’s activity in the lateral hypothalamic/perifornical area (LH/PFA) in response to reduced glucose availability (glucoprivation) induced by 2-deoxy-d-glucose (2DG) administration in male rats. Rats (7W) were bilaterally orchiectomized (ORX group) or sham operated (Sham group). Seventeen days after the surgery, food intake response to 2DG (400 mg/kg, i.v.) was measured for 4 h after the infusion. The same experiment was performed for the immunohistochemical examination of c-Fos-expressing orexin A neurons in the LH/PFA and c-Fos expression in the arcuate nucleus (Arc). Food intake induced by glucoprivation was greater in the ORX group than the Sham group, and the glucoprivation-induced food intake was inversely correlated with plasma testosterone concentration. Glucoprivation stimulated c-Fos expression of the orexin A neurons at the LH/PFA and c-Fos expression in the dorsomedial Arc. The number and percentage of c-Fos-expressing orexin A neurons in the LH/PFA and c-Fos expression in the dorsomedial Arc were significantly higher in the ORX group than the Sham group. This indicates that endogenous androgen, possibly testosterone, diminishes the food intake induced by reduced glucose availability, possibly via the attenuated activity of orexin A neuron in the LH/PFA and neurons in the dorsomedial Arc.

REV-ERBα Agonist SR9009 Promotes a Negative Energy Balance in Goldfish.

REV-ERBα (nr1d1, nuclear receptor subfamily 1 group D member 1) is a transcriptional repressor that in mammals regulates nutrient metabolism, and has effects on energy homeostasis, although its role in teleosts is poorly understood. To determine REV-ERBα’s involvement in fish energy balance and metabolism, we studied the effects of acute and 7-day administration of its agonist SR9009 on food intake, weight and length gain, locomotor activity, feeding regulators, plasma and hepatic metabolites, and liver enzymatic activity. SR9009 inhibited feeding, lowering body weight and length gain. In addition, the abundance of ghrelin mRNA decreased in the intestine, and abundance of leptin-aI mRNA increased in the liver. Hypocretin, neuropeptide y (npy), and proopiomelanocortin (pomc) mRNA abundance was not modified after acute or subchronic SR9009 administration, while hypothalamic cocaine- and amphetamine-regulated transcript (cartpt-I) was induced in the subchronic treatment, being a possible mediator of the anorectic effects. Moreover, SR9009 decreased plasma glucose, coinciding with increased glycolysis and a decreased gluconeogenesis in the liver. Decreased triglyceride levels and activity of lipogenic enzymes suggest a lipogenesis reduction by SR9009. Energy expenditure by locomotor activity was not significantly affected by SR9009. Overall, this study shows for the first time in fish the effects of REV-ERBα activation via SR9009, promoting a negative energy balance by reducing energetic inputs and regulating lipid and glucose metabolism.

Motivated to eat green or your greens? Comparing the role of motivation towards the environment and for eating regulation on ecological eating behaviours – A Self-Determination Theory perspective

Agriculture being responsible for 35% of gas emission worldwide (Foley, 2011), it is now relevant more than ever before to adopt more sustainable eating behaviours. Given its nature, ecological eating is considered both an eating and an environmental behaviour. The literature, however, has yet to identify whether ecological eating is primarily associated with motivation towards the environment or the regulation of eating. Using Self-Determination Theory framework, the present research aimed to identify the principal motivational predictors of ecological eating by using a path model combining and comparing the predicting value of eating and environmental motivation on ecological eating behaviours. Results suggest that ecological eating predominately belongs to the environmental domain, is mainly related to self-determined motivation towards the environment, and to a lesser extent, self-determined motivation towards eating. Understanding the motivational processes underlying ecological eating is critical to designing efficient intervention and directing future research.

Opioids in the medial nucleus of the solitary tract are not involved in feeding disorder in activity-based anorexia in rats

<h2>Summary</h2><h3>Background & aims</h3> Activity-based anorexia (ABA) is an abnormal behavior caused by mealtime restriction and excessive running. A previous study revealed that running causes the secretion of opioids in rats, and excessive opioids are known to decrease food intake. Thus, we hypothesized that the suppression of food intake in ABA rats that experienced mealtime restriction and excessive wheel running was due to an increase in opioids caused by running. Our previous study showed that ABA rats consumed more food than the control group after an intraperitoneal injection of naloxone. This result indicates that opioids are involved in the regulation of food intake in ABA rats. Here, we queried the involvement of the medial nucleus of the solitary tract (mNST) of the brain that mediates satiety information from the internal organs in rats' ABA and also examined whether opioids in the mNST were involved in feeding regulation in them. <h3>Methods</h3> Each ABA rat was given a running wheel and received feeding time restriction, followed by microinjection of naloxone or saline into the mNST. Each control rat was subjected to only feeding time restriction and then microinjection of naloxone or saline into the mNST. <h3>Results</h3> The results showed that food intake of the ABA group was not increased by naloxone injection into the mNST. <h3>Conclusions</h3> Our results suggest that the mNST is not involved in the regulation of food intake by opioids. Regulation of food intake by opioids may occur in other parts of the brain, such as the parabrachial nucleus and/or hypothalamus.

Cloning and expression of kiss genes and regulation of feeding in Siberian sturgeon (Acipenser baerii).

In 1996, kiss was reported to regulate feeding in mammals, but studies are limited in fish. Our study aimed to explore the possible role of kiss in the regulation of feeding in Siberian sturgeon (Acipenser baerii). kiss1 and kiss2 were cloned, and the expression patterns were analyzed in Siberian sturgeon. The complete coding regions of kiss1 and kiss2 genes were 393 and 471bp. Both kiss1 and kiss2 showed the highest expression level in the hypothalamus. During the periprandial and fasting experiments, the expression of kiss1 and kiss2 highly significantly increased in the hypothalamus after feeding (P < 0.01). Compared with the feeding group, in hypothalamus, kiss1 expression in the fasting group highly significantly decreased (P < 0.01). In contrast, kiss2 expression had no significant difference on days 1 and 7 (P > 0.05) but highly significantly increased on day 14 (P < 0.01). Subsequently, the feeding function was verified by intraperitoneal (i.p.) injection of Kp1(10) and Kp1(10) into fish. The resultsshowed that i.p. injection of 1µg/g BW Kp1(10) or 0.01µg/g BW Kp2(10) could significantly reduce 0-1h food intake (P < 0.05) and affected the expression levels of apelin, ghrelin, leptin, nmu, etc. in the hypothalamus. Theseresultssuggested that kiss1 plays an anorexic role in both short- and long-term feeding regulation, while kiss2 plays a short-term anorexic and long-term orexigenic role. This study described kiss as a novel regulator of appetite in fish and laid the groundwork for further studies focused on physiological function. HIGHLIGHTS: • The kiss1 and kiss2 of Siberian sturgeon were cloned. • The expression levels of kiss1 and kiss2 mRNA were the highest in the hypothalamus. • Postprandial hypothalamic kiss1 and kiss2 expression levels increased in the periprandial experiment. • In the fasting test, the expression of hypothalamic kiss1 decreased after fasting, while the expression of kiss2 increased after fasting on the 14th day. • Siberian sturgeon food intake was reduced, and appetite factors expression levels in the hypothalamus were altered after intraperitoneal injection of Kp1(10) and Kp2(10).

Developing anemone aquaculture for the marine aquarium trade: A case study using the bubble‐tip anemone Entacmaea quadricolor

Anemones are important aquaculture targets for the marine aquarium trade. We explore survival and growth of whole (W) and half (H) bubble-tip anemones (Entacmaea quadricolor) under: no food (−F−N), directed feeding (+F−N) and/or providing dissolved nutrients (−F+N, +F+N). Treatment effects were assessed using multiple endpoints including: survivorship, weight loss, behaviour and symbiotic-community responses. Survival analysis confirms highly significant differences among treatments. All treatments resulted in weight loss, but only +F−N resulted in significantly lower weight loss than -F+N. All anemones were highly mobile; however, no significant differences for days active, upside down and detached were recorded and the vast majority of anemones did not expel zooxanthellae. Zooxanthellae and chlorophyll pigment concentrations varied over time indicating host-symbiont plasticity. Cutting does not affect zooxanthellae number or pigment concentrations, but dissolved nutrient delivery significantly reduces zooxanthellae numbers and the chlorophyll C concentration per zooxanthellae cell compared with controls. Cutting is a simple culture method that should be routinely used, but more precise regulation of nutrient delivery and feeding is required before they can be incorporated. Finally, for hobbyists to make informed decisions about choosing an anemone, we recommend a review of E. quadricolor's and other species’ suitability for long-term aquarium captivity.