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Animals : An Open Access Journal From... Feb 2024The effect of substituting fish meal (FM) by tuna by-product meal (TBM) on growth and feed availability of red sea bream () was investigated. Six experimental diets were...
The effect of substituting fish meal (FM) by tuna by-product meal (TBM) on growth and feed availability of red sea bream () was investigated. Six experimental diets were crested to be isonitrogenous (51.5%) and isolipidic (14.5%). The control (Con) diet contained 55% FM. FM substitution in the Con diet was made in increments of 20 percentage points (20, 40, 60, 80, and 100%), named as the TBM20, TBM40, TBM60, TBM80, and TBM100 diets, respectively. Juvenile red sea bream were stocked into 18, 300 L flow-through tanks (50 fish/tank). Red sea bream were hand-fed with each diet until satiation for 8 weeks. No statistical differences in weight gain, specific growth rate (SGR), and feed consumption were found among red sea bream fed the Con, TBM20, and TBM40 diets. Furthermore, feed utilization of fish fed the TBM20, TBM40, TBM60, and TBM80 diets was comparable to red sea bream fed the Con diet. The biological indices, biochemical composition, and hematological parameters of fish were not statistically altered by dietary FM replacement with TBM. The greatest economic profit index was achieved in the TBM40 diet. In conclusion, the replacement of 40% FM with TBM in red sea bream diet appears to be the most recommendable approach without producing retarded growth and feed availability, but maximizing EPI to farmers.
PubMed: 38473073
DOI: 10.3390/ani14050688 -
Food Science & Nutrition Mar 2024Drinking alcoholic beverages stimulates food intake and contributes to the passive overconsumption of dietary energy. As protein is the most satiating of all the...
Exploring the short-term impact of swapping consumption from standard protein snacks to higher protein snacks on energy intake in social drinkers: Is protein worth a nudge?
Drinking alcoholic beverages stimulates food intake and contributes to the passive overconsumption of dietary energy. As protein is the most satiating of all the macronutrients, increased levels in snacks taken with alcohol have the potential to minimize excess energy consumption. We hypothesized that swapping consumption from retail-available standard protein (SP) snacks to higher protein (HP) snack foods would increase satiety and reduce acute food energy intake in social drinkers. A randomized single-blind crossover trial with 19 healthy participants aged 19-31 years was conducted. Participants attended two separate testing sessions, where they ingested white wine (30 g alcohol) and were offered ad libitum access to either HP snacks with a protein-fortified dip or SP snacks with a dip. There were no significant differences in mean food mass, food energy intake, or subjective appetite ratings between the high and SP snacks (all > .05). Mean protein intake was significantly increased with HP snacks compared with standard snacks ( < .001). Plasma glucose median incremental area under the curve and mean peak were significantly higher with the SP snacks (all < .05) but remained within the reference range. This study demonstrated that consumption of a higher amount of protein after a moderate alcohol dose does not result in a change in food mass and energy intake or promote satiety in healthy young adults. The potential for a simple swap to different snack types is unlikely to bring substantial benefits to social drinkers and reduce passive energy consumption.
PubMed: 38455182
DOI: 10.1002/fsn3.3902 -
Journal of Chemical Neuroanatomy Apr 2024Fluid satiation is an important signal and aspect of body fluid homeostasis. Oxytocin-receptor-expressing neurons (Oxtr) in the dorsolateral subdivision of the lateral...
Fluid satiation is an important signal and aspect of body fluid homeostasis. Oxytocin-receptor-expressing neurons (Oxtr) in the dorsolateral subdivision of the lateral parabrachial nucleus (dl LPBN) are key neurons which regulate fluid satiation. In the present study, we investigated brain regions activated by stimulation of Oxtr neurons in order to better characterise the fluid satiation neurocircuitry in mice. Chemogenetic activation of Oxtr neurons increased Fos expression (a proxy marker for neuronal activation) in known fluid-regulating brain nuclei, as well as other regions that have unclear links to fluid regulation and which are likely involved in regulating other functions such as arousal and stress relief. In addition, we analysed and compared Fos expression patterns between chemogenetically-activated fluid satiation and physiological-induced fluid satiation. Both models of fluid satiation activated similar brain regions, suggesting that the chemogenetic model of stimulating Oxtr neurons is a relevant model of physiological fluid satiation. A deeper understanding of this neural circuit may lead to novel molecular targets and creation of therapeutic agents to treat fluid-related disorders.
Topics: Animals; Parabrachial Nucleus; Mice; Receptors, Oxytocin; Neurons; Satiation; Male; Mice, Inbred C57BL; Brain
PubMed: 38452468
DOI: 10.1016/j.jchemneu.2024.102403 -
Diabetes, Obesity & Metabolism Apr 2024Hypothalamic obesity (HO) is a rare and complex disorder that confers substantial morbidity and excess mortality. HO is a unique subtype of obesity characterized by...
Hypothalamic obesity (HO) is a rare and complex disorder that confers substantial morbidity and excess mortality. HO is a unique subtype of obesity characterized by impairment in the key brain pathways that regulate energy intake and expenditure, autonomic nervous system function, and peripheral hormonal signalling. HO often occurs in the context of hypothalamic syndrome, a constellation of symptoms that follow from disruption of hypothalamic functions, for example, temperature regulation, sleep-wake circadian control, and energy balance. Genetic forms of HO, including the monogenic obesity syndromes, often impact central leptin-melanocortin pathways. Acquired forms of HO occur as a result of tumours impacting the hypothalamus, such as craniopharyngioma, surgery or radiation to treat those tumours, or other forms of hypothalamic damage, such as brain injury impacting the region. Risk for severe obesity following hypothalamic injury is increased with larger extent of hypothalamic damage or lesions that contain the medial and posterior hypothalamic nuclei that support melanocortin signalling pathways. Structural damage in these hypothalamic nuclei often leads to hyperphagia, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue, the collective effect of which is rapid weight gain. Individuals with hyperphagia are perpetually hungry. They do not experience fullness at the end of a meal, nor do they feel satiated after meals, leading them to consume larger and more frequent meals. To date, most efforts to treat HO have been disappointing and met with limited, if any, long-term success. However, new treatments based on the distinct pathophysiology of disturbed energy homeostasis in acquired HO may hold promise for the future.
Topics: Humans; Leptin; Hypothalamic Diseases; Obesity; Hypothalamus; Craniopharyngioma; Hyperphagia; Pituitary Neoplasms; Melanocortins; Energy Metabolism
PubMed: 38450938
DOI: 10.1111/dom.15530 -
Journal of Diabetes Investigation Jul 2024Diet directly affects glucose metabolism, and eating behavior is influenced by various daily life stressors. This study was conducted to investigate the relationship...
AIMS/INTRODUCTION
Diet directly affects glucose metabolism, and eating behavior is influenced by various daily life stressors. This study was conducted to investigate the relationship between common psychosomatic stressors on endocrine hormones and eating behavior in patients with type 2 diabetes.
MATERIALS AND METHODS
This cross-sectional study was performed in 40 patients with type 2 diabetes. Resting hormone blood sampling and four self-reported questionnaires were employed.
RESULTS
Patients who scored higher on the 'anger/hostility' (AH) subcategory of the profile of mood state (POMS) questionnaire had significantly higher serum cortisol (β = 0.40, P = 0.01 by least squares adjusted for age and sex). In the eating behavior questionnaire, the subcategories of 'feeling of hunger/satiation' (β = 0.49, P < 0.01) and 'eating as diversion' (β = 0.39, P = 0.03) were associated with higher serum cortisol. Resting morning cortisol levels were higher in participants who rated high on the POMS-AH and in those who reported 'irritated when hungry' and 'tend to eat when irritated or anxious'. Sleep quality showed no association with eating behavior.
CONCLUSIONS
Mood state is associated with eating behavior. Anger increases cortisol levels and may lead to compulsive eating. Various forms of hostility are important factors in appetite control and increased cortisol secretion, and can be an impediment to successful dietary self-management in patients with type 2 diabetes. Thus, assessment of mood state and control of negative mood are important therapeutic targets in diabetes management.
Topics: Humans; Male; Female; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Middle Aged; Japan; Feeding and Eating Disorders; Feeding Behavior; Self-Management; Aged; Hydrocortisone; Surveys and Questionnaires; Adult
PubMed: 38426367
DOI: 10.1111/jdi.14176 -
International Journal of Obesity (2005) Jun 2024Obesity originates from an imbalance between energy intake and expenditure. Changes in energy intake components (satiation, postprandial satiety, emotional eating) and...
BACKGROUND
Obesity originates from an imbalance between energy intake and expenditure. Changes in energy intake components (satiation, postprandial satiety, emotional eating) and energy expenditure have been linked to obesity and are referred to as obesity phenotypes. We aim to study if these obesity phenotypes have a cumulative effect on body weight and body mass index (BMI).
SUBJECT/METHODS
This is a cross-sectional study of adult patients with obesity (BMI > 30 kg/m) who completed the validated tests to measure the obesity phenotypes. A total of 464 were included in this study.
INTERVENTIONS/METHODS
We defined higher calories to fullness during an ad libitum meal as abnormal satiation, accelerated time to half gastric emptying with scintigraphy as abnormal postprandial satiety, higher anxiety score on the Hospital Anxiety and Depression Scale as hedonic eating behavior, and decreased percentage of measured resting energy expenditure as abnormal energy expenditure. The primary analysis was done on the number of phenotypes ( ≤ 1 and ≥ 2) with body weight and BMI using an independent t-test.
RESULTS
Our cohort included 464 patients (mean [SD] age 42.0 [10.9] years, 79% females, weight 111.2 [22.9] kg, BMI 38.9 [7.0] kg/m). There were 294 patients who had ≤ 1 phenotype, and 170 patients with ≥ 2 phenotypes with no baseline demographical differences (i.e., age and sex). Having ≥ 2 phenotypes was associated with higher body weight (115 [25] kg vs. 109 [21] kg; p = 0.004), BMI (40 [8] kg/m vs. 38 [7] kg/m; p = 0.02) and waist (118 [15] cm vs. 115 [13] cm; p = 0.04) and hip (129 [14] cm vs. 125 [13] cm; p = 0.01) circumferences compared to ≤ 1 phenotype.
CONCLUSION
Obesity phenotypes are associated with an additive effect on the body weight and BMI. Patients who have multiple obesity phenotypes may require a more aggressive approach to enhance weight loss.
Topics: Humans; Female; Male; Body Mass Index; Obesity; Cross-Sectional Studies; Adult; Phenotype; Body Weight; Middle Aged; Energy Metabolism; Satiation; Energy Intake
PubMed: 38418919
DOI: 10.1038/s41366-024-01492-9 -
Current Biology : CB Feb 2024Satiety-promoting neurons of the hindbrain have long been known for their role in meal termination. An innovative new study now reveals how different hindbrain cell...
Satiety-promoting neurons of the hindbrain have long been known for their role in meal termination. An innovative new study now reveals how different hindbrain cell types mediate appetite on distinct timescales.
Topics: Eating; Appetite; Satiation; Rhombencephalon; Neurons
PubMed: 38412828
DOI: 10.1016/j.cub.2024.01.033 -
Current Biology : CB Feb 2024Seed masting, a reproductive strategy characterized by variable and synchronous investment in reproduction among years, has attracted much attention. Masting trees incur...
Seed masting, a reproductive strategy characterized by variable and synchronous investment in reproduction among years, has attracted much attention. Masting trees incur a cost in delayed reproduction, and thus masting requires an ecological or evolutionary explanation. The two broad causal mechanisms to explain seed masting are resource availability and economies of scale (EOS); the former assumes reproductive investment simply covaries with environment, the latter suggests an adaptive advantage. Two of the most commonly proposed EOS for masting are predator satiation and pollination efficiency. Here we suggest an additional EOS: pathogen escape. We borrow from the disease ecology literature to describe alternative models of pathogen-mediated masting. By comparing and contrasting their ecological dynamics, we show how predator satiation and pathogen escape may favour masting through similar mechanisms of mass-action interactions and temporal delays. However, pathogen- and predator-mediated dynamics may also diverge as a result of host epidemiological structure and the spatial scale of the interaction. We propose that pathogen escape should be considered among the list of putative mechanisms to help explain the many diverse observations of masting across space and phylogeny.
Topics: Seeds; Reproduction; Pollination; Trees; Biological Evolution
PubMed: 38412815
DOI: 10.1016/j.cub.2023.12.027 -
Neuroscience and Biobehavioral Reviews Apr 2024Addiction poses significant social, health, and criminal issues. Its moderate heritability and early-life impact, affecting reproductive success, poses an evolutionary... (Review)
Review
Addiction poses significant social, health, and criminal issues. Its moderate heritability and early-life impact, affecting reproductive success, poses an evolutionary paradox: why are humans predisposed to addictive behaviours? This paper reviews biological and psychological mechanisms of substance and behavioural addictions, exploring evolutionary explanations for the origin and function of relevant systems. Ancestrally, addiction-related systems promoted fitness through reward-seeking, and possibly self-medication. Today, psychoactive substances disrupt these systems, leading individuals to neglect essential life goals for immediate satisfaction. Behavioural addictions (e.g. video games, social media) often emulate ancestrally beneficial behaviours, making them appealing yet often irrelevant to contemporary success. Evolutionary insights have implications for how addiction is criminalised and stigmatised, propose novel avenues for interventions, anticipate new sources of addiction from emerging technologies such as AI. The emerging potential of glucagon-like peptide 1 (GLP-1) agonists targeting obesity suggest the satiation system may be a natural counter to overactivation of the reward system.
Topics: Humans; Substance-Related Disorders; Gambling; Behavior, Addictive; Video Games; Satiation
PubMed: 38402919
DOI: 10.1016/j.neubiorev.2024.105603 -
Foods (Basel, Switzerland) Feb 2024In today's fast-paced world, people increasingly rely on a variety of processed foods due to their busy lifestyles. The enhanced flavors, vibrant colors, and ease of... (Review)
Review
In today's fast-paced world, people increasingly rely on a variety of processed foods due to their busy lifestyles. The enhanced flavors, vibrant colors, and ease of accessibility at reasonable prices have made ready-to-eat foods the easiest and simplest choice to satiate hunger, especially those that undergo thermal processing. However, these foods often contain an unsaturated amide called 'Acrylamide', known by its chemical name 2-propenamide, which is a contaminant formed when a carbohydrate- or protein-rich food product is thermally processed at more than 120 °C through methods like frying, baking, or roasting. Consuming foods with elevated levels of acrylamide can induce harmful toxicity such as neurotoxicity, hepatoxicity, cardiovascular toxicity, reproductive toxicity, and prenatal and postnatal toxicity. This review delves into the major pathways and factors influencing acrylamide formation in food, discusses its adverse effects on human health, and explores recent techniques for the detection and mitigation of acrylamide in food. This review could be of interest to a wide audience in the food industry that manufactures processed foods. A multi-faceted strategy is necessary to identify and resolve the factors responsible for the browning of food, ensure safety standards, and preserve essential food quality traits.
PubMed: 38397533
DOI: 10.3390/foods13040556