Explore the vast range of titles available.

Feeding behavior is influenced primarily by two factors: nutritional needs and food palatability. However, the role of food deprivation and metabolic needs in the selection of appropriate food is poorly understood. Here, we show that the fruit fly, Drosophila melanogaster, selects calorie-rich foods following prolonged food deprivation in the absence of taste-receptor signaling. Flies mutant for the sugar receptors Gr5a and Gr64a cannot detect the taste of sugar, but still consumed sugar over plain agar after 15 h of starvation. Similarly, pox-neuro mutants that are insensitive to the taste of sugar preferentially consumed sugar over plain agar upon starvation. Moreover, when given a choice between metabolizable sugar (sucrose or D-glucose) and nonmetabolizable (zero-calorie) sugar (sucralose or L-glucose), starved Gr5a; Gr64a double mutants preferred metabolizable sugars. These findings suggest the existence of a taste-independent metabolic sensor that functions in food selection. The preference for calorie-rich food correlates with a decrease in the two main hemolymph sugars, trehalose and glucose, and in glycogen stores, indicating that this sensor is triggered when the internal energy sources are depleted. Thus, the need to replenish depleted energy stores during periods of starvation may be met through the activity of a taste-independent metabolic sensing pathway.

1. Individuals of the same species often exhibit consistent differences in metabolic rate, but the effects of such differences on ecologically important behaviours remain largely unknown. In particular, it is unclear whether there is a cause-and-effect relationship between metabolic rate and the tendency to take risks while foraging. Individuals with higher metabolic rates may need to take greater risks while foraging to obtain the additional food required to satisfy their energy requirements. Such a relationship could be exacerbated by food deprivation if a higher metabolic demand also causes greater mass loss and hunger. 2. We investigated relationships among metabolic rate, risk-taking and tolerance of food deprivation in juvenile European sea bass. Individual fish were tested for risk-taking behaviours following a simulated predator attack, both before and after a 7-day period of food deprivation. The results were then related to their routine metabolic rate (RMR), which was measured throughout the period of food deprivation. 3. The amount of risk displayed by individual fish before food deprivation showed no relationship with RMR. After food deprivation, however, the amount of risk among individuals was positively correlated with RMR. In general, most fish showed an increase in risk-taking after food deprivation, and the magnitude of the increase in risk-taking was correlated with the rate of individual mass loss during food deprivation, which was itself strongly correlated with RMR. 4. The observation that RMR was related to risk-taking behaviour after food deprivation, but not before, suggests that although RMR can influence risk-taking, the strength of the relationship is flexible and context dependent. The effects of RMR on risk-taking may be subtle or non-existent in regularly feeding animals, but may lead to variability in risk-taking among individuals when food is scarce or supply is unpredictable. This synergistic relationship between RMR and food deprivation could lead to an increased likelihood of being predated for individuals with a relatively high intrinsic energy demand during times when food is scarce.

Abstract This study evaluated the effects of days-fasting followed by days-refeeding on growth, biochemical, and hepatic parameters in pacu (Piaractus mesopotamicus). One hundred and twenty juveniles P. mesopotamicus with initial average weight and length of 47.7 ± 9.2 g and 13.4 ± 0.9 cm were randomly distributed into six experimental units (20 fish per unit) and subjected to treatments: 30 days-fasting followed by 50 days-refeeding, and control group, fed continuously throughout the period. During the fasting period, samples were collected at 10, 20, and 30 days, while during the refeeding period at 15 and 50 days. Animals in the control group were sampled at the same periods. Weight (g), relative condition factor (Kn), and hepatosomatic index (biometric parameters) were measured. Liver assessments were performed. Additionally, glucose, plasma biochemical parameters levels were measured. After 30 days of fasting, hepatocyte density (73.8 ± 1.09%), liver glycogen (14.9 ± 0.87%) and hepatocyte nuclear volume (27.3 ± 0.30 µm3) were lower compared to the control group (82.0 ± 0.67%, 19.4 ± 0.74% and 43.40 ± 0.48 µm3 respectively). The relative condition factor remained unchanged. Cholesterol values, blood vessels, and sinusoidal density increased significantly during fasting. After refeeding, parameters were restored to the control level. On the 50th day of refeeding, the hepatosomatic index was significantly higher than the control group. The results showed that fasting associated with refeeding did not affect fish growth. The period over 50 days of refeeding may influence the pacu's compensation compared to daily-fed animals. The effects of fasting and its relationship with the pacu's physiological response through nutritional status become useful in contributing to feeding practices in P. mesopotamicus fish farming. Resumo Este estudo avaliou os efeitos de dias de jejum seguidos de dias de realimentação sobre o crescimento, parâmetros bioquímicos e hepáticos em pacu (Piaractus mesopotamicus). Cento e vinte juvenis de P. mesopotamicus com peso e comprimento médios iniciais de 47,7 ± 9,2 g e 13,4 ± 0,9 cm foram distribuídos aleatoriamente em seis unidades experimentais (20 peixes por unidade) e submetidos aos tratamentos: jejum de 30 dias seguido de 50 dias de realimentação e grupo controle, alimentado continuamente durante todo o período. Durante o período de jejum foram coletadas amostras aos 10, 20 e 30 dias, enquanto no período de realimentação aos 15 e 50 dias. Os animais do grupo controle foram amostrados nos mesmos períodos. Peso (g), fator de condição relativo (Kn) e índice hepatossomático (parâmetros biométricos) foram medidos. Avaliações hepáticas foram realizadas. Além disso, foram medidos os níveis bioquímicos do plasma. Após 30 dias de jejum, a densidade dos hepatócitos (73,8 ± 1,09%), o glicogênio hepático (14,9 ± 0,87%) e o volume nuclear dos hepatócitos (27,3 ± 0,30 µm3) foram menores em comparação ao grupo controle (82,0 ± 0,67%, 19,4 ± 0,74%). e 43,40 ± 0,48 µm3 respectivamente). O fator de condição relativo permaneceu inalterado. Os valores de colesterol, vasos sanguíneos e densidade sinusoidal aumentaram significativamente durante o jejum. Após a realimentação, os parâmetros foram restaurados ao nível de controle. No 50º dia de realimentação, o índice hepatossomático foi consideravelmente superior ao do grupo controle. Os resultados mostraram que o jejum associado à realimentação não afetou o crescimento dos peixes. O período superior a 50 dias de realimentação pode influenciar na compensação do pacu em relação aos animais alimentados diariamente. Os efeitos do jejum e sua relação com a resposta fisiológica do pacu por meio do estado nutricional tornam-se úteis para contribuir nas práticas alimentares na piscicultura de P. mesopotamicus.

Milk fatty acid (FA) profile is a dynamic pattern influenced by lactational stage, energy balance and dietary composition. In the first part of this study, effects of the energy balance during the proceeding lactation [weeks 1–21 post partum (pp)] on milk FA profile of 30 dairy cows were evaluated under a constant feeding regimen. In the second part, effects of a negative energy balance (NEB) induced by feed restriction on milk FA profile were studied in 40 multiparous dairy cows (20 feed-restricted and 20 control). Feed restriction (energy balance of −63 MJ NEL/d, restriction of 49 % of energy requirements) lasted 3 weeks starting at around 100 days in milk. Milk FA profile changed markedly from week 1 pp up to week 12 pp and remained unchanged thereafter. The proportion of saturated FA (predominantly 10:0, 12:0, 14:0 and 16:0) increased from week 1 pp up to week 12 pp, whereas monounsaturated FA, predominantly the proportion of 18:1,9c decreased as NEB in early lactation became less severe. During the induced NEB, milk FA profile showed a similarly directed pattern as during the NEB in early lactation, although changes were less marked for most FA. Milk FA composition changed rapidly within one week after initiation of feed restriction and tended to adjust to the initial composition despite maintenance of a high NEB. C18:1,9c was increased significantly during the induced NEB indicating mobilization of a considerable amount of adipose tissue. Besides 18:1,9c, changes in saturated FA, monounsaturated FA, de-novo synthesized and preformed FA (sum of FA >C16) reflected energy status in dairy cows and indicated the NEB in early lactation as well as the induced NEB by feed restriction.

It generally is assumed that a common neural substrate mediates both the palatability and the reward value of nutritive events. However, recent evidence suggests this assumption may not be true. Whereas opioid circuitry in both the nucleus accumbens and ventral pallidum has been reported to mediate taste-reactivity responses to palatable events, the assignment of reward or inventive value to goal-directed actions has been found to involve the basolateral amygdala. Here we found that, in rats, the neural processes mediating palatability and incentive value are indeed dissociable. Naloxone infused into either the ventral pallidum or nucleus accumbens shell blocked the increase in sucrose palatability induced by an increase in food deprivation without affecting the performance of sucrose-related actions. Conversely, naloxone infused into the basolateral amygdala blocked food deprivation-induced changes in sucrose-related actions without affecting sucrose palatability. This double dissociation of opioid-mediated changes in palatability and incentive value suggests that the role of endogenous opioids in reward processing does not depend on a single neural circuit. Rather, changes in palatability and in the incentive value assigned to rewarding events seem to be mediated by distinct neural processes.

Food restriction is a robust nongenic, nonsurgical and nonpharmacologic intervention known to improve health and extend lifespan in various species. Food is considered the most essential and frequently consumed natural reward, and current observations have demonstrated homeostatic responses and neuroadaptations to sustained intermittent or chronic deprivation. Results obtained to date indicate that food deprivation affects glutamatergic synapses, favoring the insertion of GluA2-lacking α-Ammino-3-idrossi-5-Metil-4-idrossazol-Propionic Acid receptors (AMPARs) in postsynaptic membranes. Despite an increasing number of studies pointing towards specific changes in response to dietary restrictions in brain regions, such as the nucleus accumbens and hippocampus, none have investigated the long-term effects of such practice in the dorsal striatum. This basal ganglia nucleus is involved in habit formation and in eating behavior, especially that based on dopaminergic control of motivation for food in both humans and animals. Here, we explored whether we could retrieve long-term signs of changes in AMPARs subunit composition in dorsal striatal neurons of mice acutely deprived for 12 hours/day for two consecutive days by analyzing glutamatergic neurotransmission and the principal forms of dopamine and glutamate-dependent synaptic plasticity. Overall, our data show that a moderate food deprivation in experimental animals is a salient event mirrored by a series of neuroadaptations and suggest that dietary restriction may be determinant in shaping striatal synaptic plasticity in the physiological state.

Many birds use regulated drops in night-time body temperature (Tb) to conserve energy critical to winter survival. However, a significant degree of hypothermia may limit a bird's ability to respond to predatory attack. Despite this likely energy–predation trade-off, the behavioural costs of avian hypothermia have yet to be examined. We thus monitored the nocturnal hypothermia of mourning doves (Zenaida macroura) in a laboratory setting in response to food deprivation. Nocturnal flight tests were used to quantify the flight ability of hypothermic doves. Many hypothermic doves (39% of tests) could not fly while carrying a small weight, but could do so after quickly warming up to typical daytime Tb. Doves that were unable to fly during their first test were more hypothermic than those that could fly, with average Tb reductions of 5.3°C and 3.3°C, respectively, but there was no overall indication of a threshold Tb reduction beyond which doves were consistently incapable of flight. These results suggest that energy-saving hypothermia interferes with avian antipredator behaviour via a reduction in flight ability, likely leading to a trade-off between energy-saving hypothermia and the risk of predation.

Purpose Amphetamine (AMPH) increases locomotor activities in animals, and the locomotor response to AMPH is further modulated by caloric deficits such as food deprivation and restriction. The increment in locomotor activity regulated by AMPH‐caloric deficit concomitance can be further modulated by varying feeding schedules (e.g., acute and chronic food deprivation and acute feeding after chronic food deprivation). However, the effects of different feeding schedules on AMPH‐induced locomotor activity are yet to be explicated. Here, we have explored the stimulatory responses of acutely administered D‐amphetamine in locomotion under systematically varying feeding states (fed/sated and food deprivation) and schedules (chronic and acute) in zebrafish larvae. Method We exposed wild‐type and transgenic [Tg(mnx1:GCaMP5)] zebrafish larvae to 0.7 µM concentration of AMPH and measured swimming activity and spinal motor neuron activity in vivo in real time. The analysis involved time‐elapsed and cumulative manner pre‐ and post‐AMPH treatment in four different caloric states including acute and chronic schedules of feeding and hunger. Both locomotor and motor neuron activities were compared in all four states in both fish lines. Findings Our results show that locomotion and motor neuron activity increased in both chronic and acute food deprivation post‐AMPH treatment cumulatively. A steady increase in locomotion was observed in acute food deprivation compared to an immediate abrupt increase in chronic food‐deprivation state. The ad libitum‐fed larvae exhibited a moderate increase both in locomotion and motor neuron activity. Conversely to all other caloric states, food‐sated (acute feeding after chronic food deprivation) larvae moved moderately less and exhibited a mild decrease in motor neuron activity after AMPH treatment. Conclusion These results reveal the importance of cohesive effects of feeding schedule and AMPH treatment by revealing the changes in stimulatory characteristics of AMPH on locomotion and motor neuron activity in acute and chronic feeding states. This preclinical explores the concomitant effect of different feeding states and amphetamine on behavior and brain using larval zebrafish as an animal model. Here, the zebrafish larvae were kept in satiated and food‐deprived state acutely and chronically followed by an acute amphetamine treatment. The findings show that food deprivation significantly potentiated the stimulatory effects of amphetamine compared to fed states by increasing their locomotion and spinal motor neuron activity.

The purpose of present study was to ascertain whether the response of gastrointestinal (gut) melatonin to altered feeding conditions was related to the levels of different antioxidants and digestive enzymes in the same gut tissues of a sub-tropical carp (Catla catla). Accordingly, the fish were subjected to food deprivation for 4 or 8 days and separately to re-feeding for 4 or 8 or 12 days after deprivation of food for 8 days, and their gut tissue homogenates were used to measure the levels of melatonin, both enzymatic [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST)] and non-enzymatic [reduced glutathione (GSH)] antioxidants, as well as different digestive enzymes (α-amylase, cellulase, protease, and lipase). Notably, the gut levels of melatonin, SOD, CAT, GPx, and GST underwent gradual increase with the progress of food deprivation, but a sudden fall after restoration of food supply for 4 days and a rise thereafter. Conversely, the activity of all the digestive enzymes significantly decreased after deprivation of food, but started increasing when food supply was reinforced. Gut melatonin concentrations by showing a positive correlation with the titers of different antioxidants (in both food-deprived and re-fed fish groups) and a negative (in food-deprived fish) or a positive (in re-fed fish) correlation with the activity of each digestive enzyme underlined possible physiological interplay between them. Collectively, our findings lend support to the hypothesis that gut melatonin response to altered feeding conditions in carp might be associated with the oxidative status as well as the digestive functions of the gastrointestinal tissues itself.

The fetal genome regulates maternal physiology and behavior via its placenta, which produces hormones that act on the maternal hypothalamus. At the same time, the fetus itself develops a hypothalamus. In this study we show that many of the genes that regulate placental development also regulate the developing hypothalamus, and in mouse the coexpression of these genes is particularly high on embryonic days 12 and 13 (days E12–13). Such synchronized expression is regulated, in part, by the maternally imprinted gene, paternally expressed gene 3 (Peg3), which also is developmentally coexpressed in the hypothalamus and placenta at days E12–13. We further show that challenging this genomic linkage of hypothalamus and placenta with 24-h food deprivation results in disruption to coexpressed genes, primarily by affecting placental gene expression. Food deprivation also produces a significant decrease in Peg3 gene expression in the placenta, with consequences similar to many of the placental gene changes induced by Peg3 mutation. Such genomic dysregulation does not occur in the hypothalamus, where Peg3 expression increases with food deprivation. Thus, changes in gene expression brought about by food deprivation are consistent with the fetal genome's maintaining hypothalamic development at a cost to its placenta. This biased change to gene dysregulation in the placenta is linked to autophagy and ribosomal turnover, which sustain, in the short term, nutrient supply for the developing hypothalamus. Thus, the fetus controls its own destiny in times of acute starvation by short-term sacrifice of the placenta to preserve brain development.