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Behavioural Processes Jun 2024Understanding how animal collectives and societies form and function is a fundamental goal in animal biology. To date, research examining fish shoaling behavior has...
Understanding how animal collectives and societies form and function is a fundamental goal in animal biology. To date, research examining fish shoaling behavior has focused mostly on the general principles and ecological relevance of the phenomeon, while the ways in which physiological state (e.g., nutrition) affects collective behavior remain overlooked. Here, we investigated the shoaling behavior of common minnows (Phoxinus phoxinus) with three different nutritional states (control treatment: fasting for 24 h, fasting treatment: fasting for 7 days, and digestion treatment: 1 h after satiation feeding) across two ecological contexts (i.e., without and with food). No effects of either nutritional state or context were found on swimming speed, but the acceleration was greater in the digestion group than in the control group, with that in the fasting group being intermediate. Similar to change tendency in group length and group width of shoals, both interindividual distance and nearest neighbor distance were also greater in the fasting group than in the digestion group, suggesting that fasting and digestion may exert opposite driving forces on group cohesion. However, neither nutritional state nor context influenced the group area, group speed, group percent time moving, or group polarization. Both the foraging efficiency and the percentage of food items consumed by the fish shoals were greater in the fasting and control groups than in the digestion group. Our study suggested that one week of hunger and the energetically demanding stage of food digestion tend to have opposite influences on group shape, while the social foraging context does not influence the individual and group behavior of fish.
PubMed: 38878914
DOI: 10.1016/j.beproc.2024.105059 -
Journal of Agricultural and Food... Jun 2024Understanding the evolutionary genetics of food intake regulation in domesticated animals has relevance to evolutionary biology, animal improvement, and obesity...
Understanding the evolutionary genetics of food intake regulation in domesticated animals has relevance to evolutionary biology, animal improvement, and obesity treatment. Here, we observed that the fatty acid desaturase gene (), which regulates food intake, is suppressed in domesticated silkworms, but expressed in the salivary glands of the wild silkworm . The content of its catalytic product, -vaccenic acid, was related to the expression levels of in the salivary glands of domesticated and wild silkworm strains. These two strains also showed significant differences in food intake. Using orally administering -vaccenic acid and transgenic-mediated overexpression, we verified that -vaccenic acid functions as a satiation signal, regulating food intake and growth in silkworms. Selection analysis showed that experienced selection, especially in the potential promoter, 5'-untranslated, and intron regions. This study highlights the importance of the decrement of satiety in silkworm domestication and provides new insights into the potential involvement of salivary glands in the regulation of satiety in animals, by acting as a supplement to gut-brain nutrient signaling.
Topics: Animals; Bombyx; Salivary Glands; Insect Proteins; Eating; Fatty Acid Desaturases; Domestication
PubMed: 38875711
DOI: 10.1021/acs.jafc.4c02511 -
Advances in Neurobiology 2024This chapter (part one of a trilogy) summarizes the neurobiological foundations of endogenous opioids in the regulation of energy balance and eating behavior,... (Review)
Review
This chapter (part one of a trilogy) summarizes the neurobiological foundations of endogenous opioids in the regulation of energy balance and eating behavior, dysregulation of which translates to maladaptive dietary responses in individuals with obesity and eating disorders, including anorexia, bulimia, and binge eating disorder. Knowledge of these neurobiological foundations is vital to researchers' and clinicians' understanding of pathophysiology as well as the science-based development of multidisciplinary diagnoses and treatments for obesity and eating disorders. We highlight mechanisms of endogenous opioids in both homeostatic and hedonic feeding behavior, review research on the dysregulation of food reward that plays a role in a wide array of obesity and disordered eating, and the clinical implications of neurobiological responses to food for current science-based treatments for obesity and eating disorders.
Topics: Humans; Homeostasis; Hunger; Opioid Peptides; Obesity; Feeding Behavior; Feeding and Eating Disorders; Satiation; Reward; Energy Metabolism; Eating; Animals
PubMed: 38874730
DOI: 10.1007/978-3-031-45493-6_16 -
Trends in Ecology & Evolution Jun 2024Many perennial plants show mast seeding, characterized by synchronous and highly variable reproduction across years. We propose a general model of masting, integrating... (Review)
Review
Many perennial plants show mast seeding, characterized by synchronous and highly variable reproduction across years. We propose a general model of masting, integrating proximate factors (environmental variation, weather cues, and resource budgets) with ultimate drivers (predator satiation and pollination efficiency). This general model shows how the relationships between masting and weather shape the diverse responses of species to climate warming, ranging from no change to lower interannual variation or reproductive failure. The role of environmental prediction as a masting driver is being reassessed; future studies need to estimate prediction accuracy and the benefits acquired. Since reproduction is central to plant adaptation to climate change, understanding how masting adapts to shifting environmental conditions is now a central question.
PubMed: 38862358
DOI: 10.1016/j.tree.2024.05.006 -
American Journal of Physiology.... Jun 2024Vagal afferents to the gastrointestinal tract are crucial for regulation of food intake, signaling negative feedback that contributes to satiation and positive feedback... (Review)
Review
Vagal afferents to the gastrointestinal tract are crucial for regulation of food intake, signaling negative feedback that contributes to satiation and positive feedback that produces appetition and reward. Vagal afferents to the small intestinal mucosa contribute to this regulation by sensing luminal stimuli and reporting this information to the brain. These afferents respond to mechanical, chemical, thermal, pH, and osmolar stimuli and to bacterial products and immunogens. Surprisingly little is known about how these stimuli are transduced by vagal mucosal afferents, or how their transduction is organized among these afferents' terminals. Further, the effects of stimulus concentration ranges or physiological stimuli on vagal activity have not been examined for some of these stimuli. And, detection of luminal stimuli has rarely been examined in rodents, which are most frequently employed for studying small intestinal innervation. Here we review what is known about stimulus detection by vagal mucosal afferents and illustrate the complexity of this detection using nutrients as an exemplar. The accepted model proposes nutrients bind to taste receptors on enteroendocrine cells (EECs), which excites them, causing release of hormones that stimulate vagal mucosal afferents. Evidence is reviewed that suggests while this model accounts for many aspects of vagal signaling about nutrients, it cannot account for all aspects. A major goal of this review therefore is to evaluate what is known about nutrient absorption and detection and based on this evaluation to identify candidate mucosal cells and structures that could cooperate with EECs and vagal mucosal afferents in stimulus detection.
PubMed: 38860288
DOI: 10.1152/ajpregu.00252.2023 -
Research Square May 2024Satiation is the physiologic process that regulates meal size and termination, and it is quantified by the calories consumed to reach satiation. Given its role in energy...
Satiation is the physiologic process that regulates meal size and termination, and it is quantified by the calories consumed to reach satiation. Given its role in energy intake, changes in satiation contribute to obesity's pathogenesis. Our study employed a protocolized approach to study the components of food intake regulation including a standardized breakfast, a gastric emptying study, appetite sensation testing, and a satiation measurement by an test. These studies revealed that satiation is highly variable among individuals, and while baseline characteristics, anthropometrics, body composition and hormones, contribute to this variability, these factors do not fully account for it. To address this gap, we explored the role of a germline polygenic risk score, which demonstrated a robust association with satiation. Furthermore, we developed a machine-learning-assisted gene risk score to predict satiation and leveraged this prediction to anticipate responses to anti-obesity medications. Our findings underscore the significance of satiation, its inherent variability, and the potential of a genetic risk score to forecast it, ultimately allowing us to predict responses to different anti-obesity interventions.
PubMed: 38826309
DOI: 10.21203/rs.3.rs-4402499/v1 -
Neuropharmacology Sep 2024Water is critical for survival and thirst is a powerful way of ensuring that fluid levels remain in balance. Overconsumption, however, can have deleterious effects,... (Review)
Review
Water is critical for survival and thirst is a powerful way of ensuring that fluid levels remain in balance. Overconsumption, however, can have deleterious effects, therefore optimization requires a need to balance the drive for water with the satiation of that water drive. This review will highlight our current understanding of how thirst is both generated and quenched, with particular focus on the roles of angiotensin II, glucagon like-peptide 1, and estradiol in turning on and off the thirst drive. Our understanding of the roles these bioregulators play has benefited from modern behavioral analyses, which have improved the time resolution of intake measures, allowing for attention to the details of the patterns within a bout of intake. This has led to behavioral interpretation in ways that are helpful in understanding the many controls of water intake and has expanded our understanding beyond the dichotomy that something which increases water intake is simply a "stimulator" while something that decreases water intake is simply a "satiety" factor. Synthesizing the available information, we describe a framework in which thirst is driven directly by perturbations in fluid intake and indirectly modified by several bioregulators. This allows us to better highlight areas that are in need of additional attention to form a more comprehensive understanding of how the system transitions between states of thirst and satiety.
Topics: Thirst; Humans; Animals; Drinking; Glucagon-Like Peptide 1; Angiotensin II; Estradiol; Satiation
PubMed: 38823577
DOI: 10.1016/j.neuropharm.2024.110009 -
Appetite May 2024Terminating a meal after achieving satiation is a critical step in maintaining a healthy energy balance. Despite the extensive collection of information over the last... (Review)
Review
Terminating a meal after achieving satiation is a critical step in maintaining a healthy energy balance. Despite the extensive collection of information over the last few decades regarding the neural mechanisms controlling overall eating, the mechanism underlying different temporal phases of eating behaviors, especially satiation, remains incompletely understood and is typically embedded in studies that measure the total amount of food intake. In this review, we summarize the neural circuits that detect and integrate satiation signals to suppress appetite, from interoceptive sensory inputs to the final motor outputs. Due to the well-established role of cholecystokinin (CCK) in regulating the satiation, we focus on the neural circuits that are involved in regulating the satiation effect caused by CCK. We also discuss several general principles of how these neural circuits control satiation, as well as the limitations of our current understanding of the circuits function. With the application of new techniques involving sophisticated cell-type-specific manipulation and mapping, as well as real-time recordings, it is now possible to gain a better understanding of the mechanisms specifically underlying satiation.
PubMed: 38801994
DOI: 10.1016/j.appet.2024.107512 -
Appetite May 2024Glycomacropeptide (GMP) has a unique amino acid profile which may make less satiating than other dietary proteins. This study assessed the feasibility and likely...
Glycomacropeptide (GMP) has a unique amino acid profile which may make less satiating than other dietary proteins. This study assessed the feasibility and likely acceptability of a leucine-enriched GMP drink and determined appetite response in older adults (OA). Thirteen OA (11f; 70 ± 4 years) were recruited for sensory assessments of a leucine-enriched GMP drink when mixed with water and with fruit smoothie, compared with whey protein isolate (WHEY). Participants also partook in a single focus group exploring acceptability to protein and supplementation. Separately, a counterbalanced, double-blind study with twelve OA (8f; 69 ± 3 years) was conducted to determine appetite and gut hormone responses. Fasting subjective appetite was recorded using visual analogue scales and a fasted venous blood sample was collected (to measures acyl-ghrelin, PYY, GLP-1, and CCK) before participants consumed either: GMP protein (27g + 3g leucine, 350 mL water), WHEY (30g, 350 mL water), or water. Participants rested for 240 min, with appetite measures and blood sampling throughout. An ad libitum pasta-based meal was then consumed. Sensory testing revealed low pleasantness rating for GMP in water vs. WHEY (16 ± 14 vs 31 ± 24, p = 0.016). GMP addition to smoothie reduced pleasantness (26 ± 21 vs. 61 ± 29, p = 0.009) and worsened the aroma (46 ± 15 vs. 69 ± 28, p = 0.014). The focus group revealed uncertainty of protein needs and a scepticism of supplements, with preference for food. Gut hormone response did not differ between GMP and WHEY (nAUC for all gut hormones p > 0.05). There was no difference between conditions for lunch ad libitum intake (549 ± 171 kcal, 512 ± 238 kcal, 460 ± 199 kcal for GMP, WHEY, and water, p = 0.175), or for subjective appetite response. Leucine-enriched GMP was not less satiating than WHEY, and low palatability and scepticism of supplements question the likely acceptability of GMP supplementation. Providing trusted nutritional advice and food enrichment/fortification may be preferred strategies for increasing protein intake in OA.
PubMed: 38795943
DOI: 10.1016/j.appet.2024.107509 -
Neuron May 2024Hungry animals need compensatory mechanisms to maintain flexible brain function, while modulation reconfigures circuits to prioritize resource seeking. In Drosophila,...
Hungry animals need compensatory mechanisms to maintain flexible brain function, while modulation reconfigures circuits to prioritize resource seeking. In Drosophila, hunger inhibits aversively reinforcing dopaminergic neurons (DANs) to permit the expression of food-seeking memories. Multitasking the reinforcement system for motivation potentially undermines aversive learning. We find that chronic hunger mildly enhances aversive learning and that satiated-baseline and hunger-enhanced learning require endocrine adipokinetic hormone (AKH) signaling. Circulating AKH influences aversive learning via its receptor in four neurons in the ventral brain, two of which are octopaminergic. Connectomics revealed AKH receptor-expressing neurons to be upstream of several classes of ascending neurons, many of which are presynaptic to aversively reinforcing DANs. Octopaminergic modulation of and output from at least one of these ascending pathways is required for shock- and bitter-taste-reinforced aversive learning. We propose that coordinated enhancement of input compensates for hunger-directed inhibition of aversive DANs to preserve reinforcement when required.
PubMed: 38795709
DOI: 10.1016/j.neuron.2024.04.035