103 resultados para satiation


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Satiation amount, satiation time and handling time of Anabas testudineus (Bloch), an air breathing predatory fish was experimentally estimated using guppy (Lebistes reticulatus) as prey. Weight of the fish and satiation time influenced prey handling time. As satiation time is related to the level of hunger, level of hunger was found to influence handling time of prey.

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BACKGROUND: Neural responses to rewarding food cues are significantly different in the fed vs. fasted (>8 h food-deprived) state. However, the effect of eating to satiety after a shorter (more natural) intermeal interval on neural responses to both rewarding and aversive cues has not been examined. OBJECTIVE: With the use of a novel functional magnetic resonance imaging (fMRI) task, we investigated the effect of satiation on neural responses to both rewarding and aversive food tastes and pictures. DESIGN: Sixteen healthy participants (8 men, 8 women) were scanned on 2 separate test days, before and after eating a meal to satiation or after not eating for 4 h (satiated vs. premeal). fMRI blood oxygen level-dependent (BOLD) signals to the sight and/or taste of the stimuli were recorded. RESULTS: A whole-brain cluster-corrected analysis (P < 0.05) showed that satiation attenuated the BOLD response to both stimulus types in the ventromedial prefrontal cortex (vmPFC), orbitofrontal cortex, nucleus accumbens, hypothalamus, and insula but increased BOLD activity in the dorsolateral prefrontal cortex (dlPFC; local maxima corrected to P ≤ 0.001). A psychophysiological interaction analysis showed that the vmPFC was more highly connected to the dlPFC when individuals were exposed to food stimuli when satiated than when not satiated. CONCLUSIONS: These results suggest that natural satiation attenuates activity in reward-related brain regions and increases activity in the dlPFC, which may reflect a "top down" cognitive influence on satiation. This trial was registered at clinicaltrials.gov as NCT02298049.

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Background – Satiation and satiety describe the events which lead to meal termination and the maintenance of hunger induced by physical and metabolic events following food ingestion. Fatty acids, components of dietary fat (triglyceride) may be important, if not essential components of satiation and satiety. Emerging evidence suggests fatty acid now constitutes a sixth taste modality and orally sensed fatty acids mediate unique cephalic and hormonal responses priming the body for fat digestion, and may contribute to sensory specific satiety. Once ingested, fatty acids are sensed in the gastrointestinal tract (GIT) where they cause the release of hormones, stimulate the vagus and enter the blood stream where they act a number of organs (brain, liver) to influence satiety.
Objective – To review the role of fatty acids in sensory and metabolic satiation and satiety.
Design – Literature search and review of papers from the past decade on satiety, satiation, fat taste and fatty acids.
Outcomes – The physiological significance of gustatory fat detection is still unclear, but it may signal the nutritious content of fat similar to the tastes of sweet or umami which signal the presence of carbohydrate or proteins. Like other tastants, fatty acid taste sensitivity is thought to vary in the population and differences in sensitivity may influence dietary choice and fat intake. Fatty acid taste may contribute to sensory specific satiety as foods are eaten. Animal models have observed an inverse relationship between oral fatty acid sensitivity and fat consumption, which leads to obesity. Observations that the obese have heightened preferences for, and consume more fat than lean individuals questions whether such a relationship may also be apparent in humans. At the GIT, fatty acids are sensed by enterocytes and bind to receptors, transporters or ion channels where they initiate gut-brain communication over nutrient status through the vagus and cause the release of satiety hormones which lead to meal termination. Inefficient fatty acid sensing at either or both locations is thought to accompany the aetiology of obesity.
Conclusion – Variations in sensitivity to fatty acids may alter preferences and consumption of fats or hormonal responses to fat ingestion which influence sensory-specific, metabolic and subjective satiety.

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Increased energy consumption, especially increased consumption of sweet energy-dense food, is thought to be one of the main contributors to the escalating rates in overweight individuals and obesity globally. The individual's ability to detect or sense sweetness in the oral cavity is thought to be one of many factors influencing food acceptance, and therefore, taste may play an essential role in modulating food acceptance and/or energy intake. Emerging evidence now suggests that the sweet taste signaling mechanisms identified in the oral cavity also operate in the gastrointestinal system and may influence the development of satiety. Understanding the individual differences in detecting sweetness in both the oral and gastrointestinal system towards both caloric sugar and high intensity sweetener and the functional role of the sweet taste system may be important in understanding the reasons for excess energy intake. This review will summarize evidence of possible associations between the sweet taste mechanisms within the oral cavity, gastrointestinal tract and the brain systems towards both caloric sugar and high intensity sweetener and sweet taste function, which may influence satiation, satiety and, perhaps, predisposition to being overweight and obesity.

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We unify and generalize the existence results in Werner (1987), Dana, Le Van and Magnien (1999), Allouch, Le Van and Page (2006) and Allouch and Le Van (2008). We also show that, in terms of weakening the set of assumptions, we cannot go too far.

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Positron emission tomography studies were conducted during genesis of moderate thirst by rapid i.v. infusion of hypertonic saline (0.51 M) and after satiation of thirst by drinking water. The correlation of regional cerebral blood flow with the change in the plasma Na concentration showed a significant group of cerebral activations in the anterior cingulate region and also a site in the middle temporal gyrus and in the periaqueductal gray. Strongest deactivations occurred in the parahippocampal and frontal gyri. The data are consistent with an important role of the anterior cingulate in the genesis of thirst.

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The customary approach to the study of meal size suggests that ‘events’ occurring during a meal lead to its termination. Recent research, however, suggests that a number of decisions are made before eating commences that may affect meal size. The present study sought to address three key research questions around meal size: the extent to which plate cleaning occurs; prevalence of pre-meal planning and its influence on meal size; and the effect of within-meal experiences, notably the development of satiation. To address these, a large-cohort internet-based questionnaire was developed. Results showed that plate cleaning occurred at 91% of meals, and was planned from the outset in 92% of these cases. A significant relationship between plate cleaning and meal planning was observed. Pre meal plans were resistant to modification over the course of the meal: only 18% of participants reported consumption that deviated from expected. By contrast, 28% reported continuing eating beyond satiation, and 57% stated that they could have eaten more at the end of the meal. Logistic regression confirmed pre-meal planning as the most important predictor of consumption. Together, our findings demonstrate the importance of meal planning as a key determinant of meal size and energy intake.

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Evidence that our food environment can affect meal size is often taken to indicate a failure of ‘conscious control’. By contrast, our research suggests that ‘expected satiation’ (fullness that a food is expected to confer) predicts self-selected meal size. However, the role of meal planning as a determinant of actual meal size remains unresolved, as does the extent to which meal planning is commonplace outside the laboratory. Here, we quantified meal planning and its relation to meal size in a large-cohort study. Participants (N= 764; 25.6 yrs, 78% female) completed a questionnaire containing items relating to their last meal. The majority (91%) of meals were consumed in their entirety. Furthermore, in 92% of these cases the participants decided to consume the whole meal, even before it began. A second major objective was to explore the prospect that meal plans are revised based on within-meal experience (e.g., development of satiation). Only 8% of participants reported ‘unexpected’ satiation that caused them to consume less than anticipated. Moreover, at the end of the meal 57% indicated that they were not fully satiated, and 29% continued eating beyond comfortable satiation (often to avoid wasting food). This pattern was neither moderated by BMI nor dieting status, and was observed across meal types. Together, these data indicate that meals are often planned and that planning corresponds closely with amount consumed. By contrast, we find limited evidence for within-meal modification of these plans, suggesting that ‘pre-meal cognition’ is an important determinant of meal size in humans.

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Previously, expected satiety (ES) has been measured using software and two-dimensional pictures presented on a computer screen. In this context, ES is an excellent predictor of self-selected portions, when quantified using similar images and similar software. In the present study we sought to establish the veracity of ES as a predictor of behaviours associated with real foods. Participants (N = 30) used computer software to assess their ES and ideal portion of three familiar foods. A real bowl of one food (pasta and sauce) was then presented and participants self-selected an ideal portion size. They then consumed the portion ad libitum. Additional measures of appetite, expected and actual liking, novelty, and reward, were also taken. Importantly, our screen-based measures of expected satiety and ideal portion size were both significantly related to intake (p < .05). By contrast, measures of liking were relatively poor predictors (p > .05). In addition, consistent with previous studies, the majority (90%) of participants engaged in plate cleaning. Of these, 29.6% consumed more when prompted by the experimenter. Together, these findings further validate the use of screen-based measures to explore determinants of portion-size selection and energy intake in humans.

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Why do some people remain lean while others are susceptible to obesity, and why do obese individuals vary in their successes in losing weight? Despite physiological processes that promote satiety and satiation, some individuals are more susceptible to overeating. While the phenomena of susceptibility to weight gain, resistance to treatment or weight loss, and individual variability are not novel, they have yet to be exploited and systematically examined to better understand how to characterise phenotypes of obesity. The identification and characterisation of distinct phenotypes not only highlight the heterogeneous nature of obesity but may also help to inform the development of more tailored strategies for the treatment and prevention of obesity. This review examines the evidence for different susceptible phenotypes of obesity that are characterised by risk factors associated with the hedonic and homeostatic systems of appetite control.

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Increased frequency of eating in the absence of homeostatic need, notably through snacking, is an important contributor to overconsumption and may be facilitated by increased availability of palatable food in the obesogenic environment. Opportunistic initiation of snacking is likely to be subject to individual differences, although these are infrequently studied in laboratory-based research paradigms. This study examined psychological factors associated with opportunistic initiation of snacking, and predictors of intake in the absence of homeostatic need. Fifty adults (mean age 34.5 years, mean BMI 23.9 kg/m2, 56% female) participated in a snack taste test in which they ate a chocolate snack to satiation, after which they were offered an unanticipated opportunity to initiate a second eating episode. Trait and behavioural measures of self control, sensitivity to reward, dietary restraint and disinhibited eating were taken. Results showed that, contrary to expectations, those who initiated snacking were better at inhibitory control compared with those who did not initiate. However, amongst participants who initiated snacking, intake (kcal) was predicted by higher food reward sensitivity, impulsivity and BMI. These findings suggest that snacking initiation in the absence of hunger is an important contributor to overconsumption. Consideration of the individual differences promoting initiation of eating may aid in reducing elevated eating frequency in at-risk individuals.

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Gastric motility disorders, including delayed gastric emptying (gastroparesis), impaired postprandial fundic relaxation, and gastric myoelectrical disorders, can occur in type 1 diabetes, chronic renal failure, and functional dyspepsia (FD). Symptoms like upper abdominal pain, early satiation, bloating, nausea and vomiting may be related to gastroparesis. Diabetic gastroparesis is related to autonomic neuropathy. Scintigraphy is the gold standard in measuring gastric emptying, but it is expensive, requires specific equipment, and exposes patients to radiation. It also gives information about the intragastric distribution of the test meal. The 13C-octanoic acid breath test (OBT) is an alternative, indirect method of measuring gastric emptying with a stable isotope. Electrogastrography (EGG) registers the slow wave originating in the pacemaker area of the stomach and regulating the peristaltic contractions of the antrum. This study compares these three methods of measuring gastric motility in patients with type 1 diabetes, functional dyspepsia, and chronic renal failure. Currently no effective drugs for treating gastric motility disorders are available. We studied the effect of nizatidine on gastric emptying, because in preliminary studies this drug has proven to have a prokinetic effect due to its cholinergic properties. Of the type 1 patients, 26% had delayed gastric emptying of solids as measured by scintigraphy. Abnormal intragastric distribution of the test meal occurred in 37% of the patients, indicating impaired fundic relaxation. The autonomic neuropathy score correlated positively with the gastric emptying rate of solids (P = 0.006), but HbA1C, plasma glucose levels, or abdominal symptoms were unrelated to gastric emptying or intragastric distribution of the test meal. Gastric emptying of both solids and liquids was normal in all FD patients but abnormal intragastric distribution occurred in 38% of the patients. Nizatidine improved symptom scores and quality of life in FD patients, but not significantly. Instead of enhancing, nizatidine slowed gastric emptying in FD patients (P < 0.05). No significant difference appeared in the frequency of the gastric slow waves measured by EGG in the patients and controls. The correlation between gastric half-emptying times of solids measured by scintigraphy and OBT was poor both in type 1 diabetes and FD patients. According to this study, dynamic dual-tracer scintigraphy is more accurate than OBT or EGG in measuring gastric emptying of solids. Additionally it provides information about gastric emptying of liquids and the intragastric distribution of the ingested test meal.

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Guanylyl cyclase C (GC-C) is a multidomain, membrane-associated receptor guanylyl cyclase. GC-C is primarily expressed in the gastrointestinal tract, where it mediates fluid-ion homeostasis, intestinal inflammation, and cell proliferation in a cGMP-dependent manner, following activation by its ligands guanylin, uroguanylin, or the heat-stable enterotoxin peptide (ST). GC-C is also expressed in neurons, where it plays a role in satiation and attention deficiency/hyperactive behavior. GC-C is glycosylated in the extracellular domain, and differentially glycosylated forms that are resident in the endoplasmic reticulum (130 kDa) and the plasma membrane (145 kDa) bind the ST peptide with equal affinity. When glycosylation of human GC-C was prevented, either by pharmacological intervention or by mutation of all of the 10 predicted glycosylation sites, ST binding and surface localization was abolished. Systematic mutagenesis of each of the 10 sites of glycosylation in GC-C, either singly or in combination, identified two sites that were critical for ligand binding and two that regulated ST-mediated activation. We also show that GC-C is the first identified receptor client of the lectin chaperone vesicular integral membrane protein, VIP36. Interaction with VIP36 is dependent on glycosylation at the same sites that allow GC-C to fold and bind ligand. Because glycosylation of proteins is altered in many diseases and in a tissue-dependent manner, the activity and/or glycan-mediated interactions of GC-C may have a crucial role to play in its functions in different cell types.

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生物多样性的维持、监测、保育与恢复是生物多样性科学的核心研究内容( DIVERSITAS)。作为世界上典型的植被类型,常绿阔叶林以其丰富的生物多样性而倍受世人关注。我国的常绿阔叶林是全球分布面积最大,发育最为典型的常绿阔叶林,其分布区多为农业区,与长江流域的生态安全密切相关:伴随着人们的生产活动,生境的岛屿化与破碎化问题越来越突出,常绿阔叶林的合理保育问题和生态恢复问题已成为大家关注的焦点。本研究“常绿阔叶林恢复生态学研究初报”正是在这种背景下开展的,主要实验研究工作与结果如下: 1.系统综述了生态系统退化程度的诊断指标体系、途径与方法,绘制了生态系 统退化程度的概念模型,为恢复生态学研究和生态恢复实践提供参考。 2.固定样地的建立:为深入开展生物多样性与恢复生态学研究,本研究建立了一系列固定样地(常绿阔叶林固定样地、常绿落叶阔叶林固定样地、退化生态系统恢复与重建实验样地等),这些样地的建立为进一步深化研究奠定了坚实基础。 3.种群大小级结构特征:对栲树Castanopsis fargesii和油茶Camellia oleifera种 群大小级结构特征研究表明,栲树种群大小级结构(高度级和胸围级)呈弱双峰型分布,油茶种群大小级结构呈倒“J”型分布。对树木大小级划分标 准的比较研究表明划分标准的选择应基于研究目的和物种性质。作者认为应深入研究干扰特别是生境的岛屿化与破碎化对常绿阔叶林稳定性的影响。 4.种子扩散与种群维持:种子扩散是种群维持的一个关键阶段,而建群种的维持机制可在一定程度上反映群落的维持机理。对都江堰常绿阔叶林固定样地的主要建群种栲树种子扩散的研究表明,种子雨密度、种子在地上保留密度以及种子丢失状况是个动态过程,种子雨在2001年持续了约3个月的时间,种子年产量达到每平方米73.37个正常种子;研究发现栲树种子下落后能在地上保留一段相当长的时间(捕食者饱和现象“predator satiation"),这为种子萌发提供了更多的时间和机会,从而使得栲树种群能通过大年(the mast year)的高种子产量与捕食者饱和现象顺利完成自然更新;捕食者饱和现象有助于解释栲树的优势种群地位和稳定机制,以及对整个生态系统稳定性的贡献;作者提出了一个描述栲树种子扩散命运的概念模型,该模型表明种子雨与种子丢失的不同阶段是在不同程度上以不同方式贡献于栲树的自然更新。总之,栲树自然更新伴随着一个复杂的种子扩散过程。 5.光因子调控与生态恢复:光是影响植物生长的一个重要生态因子。研究了三种不同遮荫处理(100% PAR、40% PAR和22% PAR)对青冈Cyclobalanopsis glauca幼苗在亚热带弃耕地上的影响作用,两年的研究结果显示:青冈幼苗 可以在弃耕地上正常生长:两种遮荫处理(40% PAR和22% PAR)对青冈的萌芽和幼苗生长有正效应,并且22% PAR遮荫处理有明显的促进作用;本研究也说明了植物在不同的遮荫处理作用下有不同的生长策略。关于在生态恢复中如何利用光因素对植物生长的影响以及遮荫的复合效应问题值得深入研究。 6.种间关系与生态恢复:杂草竞争是植被恢复中的一个重要问题。对两种常绿阔叶树种(青冈和石栎Lithocarpus glaber)在不同坡位(坡上位、中位、下位)和有无地上杂草竞争的情况下的对比研究表明:不同物种在不同坡位,其幼苗生长对杂草竞争的反应是不同的;在坡上位和下位,除草处理能显著地提高青冈幼苗的田间保存率、苗高、基径和冠幅的生长,而在中位,除草处理的效果不显著;但是对于石栎来说,除草处理仅能显著地提高坡中位幼苗基径的生长量;研究说明了(地上)杂草竞争对植物生长的影响(程度)因物种而异,因而除草处理并不是对所有常绿阔叶树种的幼苗生长有促进作用,杂草竞争也不是一切常绿阔叶树种在弃耕地上建立与定居的障碍因子。作者建议在生态恢复实践中应根据具体情况选择除草与否,关于杂草竞争/除草在植被恢复中的作用值得进一步研究。

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Three different stocking rates in a semi-intensive pilot shrimp project was adopted in duplicates of three treatments designated as T1, T2 and T3 having initial per meter square stocking density of shrimp of 40, 44 and 51 respectively of 0.025g size post larva. The study was conducted for 84 days. Commercial pelleted diets designated as starter - 1, 2, 3 and grower were fed at a satiation level during the study period with a feeding frequency of 4 to 5 times per day. Feed rationing was based on the survivability, body weight and tray checking. 5-25% of the pond water was exchanged daily. Sampling was done for growth after every 2nd week. Monthly sampling was done for mortality in the ponds. Mean weight gain of the shrimp in treatments T1, T2 and T3 were 16.96 ± 1.14, 16.04 ± 1.38 and 14.08 ± 1.17g respectively and T1 with a low stocking density showed a significantly best growth among the treatments. Total mortality in treatments T1, T2 and T3 were as 30.00, 39.77 and 31.37% respectively. Significantly higher feed conversion ratio (FCR) of 1.87 was obtained with shrimp in treatment T3 followed by shrimp in T1 and T2 with FCR values of 1.70 and 1.41 respectively. A positive correlation of growth and salinity was observed during the study. Total production per unit area was the highest in the treatment T3 (4928 kg/ha) and followed by T1 (4747 kg/ha) and T2 (4251 kg/ha). The result show significantly negative correlation between individual growth and density.