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At least 19 recordsLinked to original sources
PubMed2000

Leptin deficiency induced by fasting impairs the satiety response to cholecystokinin.

Leptin administration potentiates the satiety response to signals such as cholecystokinin (CCK), that are released from the gut during a meal. To investigate the physiological relevance of this observation, we hypothesized that leptin deficiency, induced by fasting, attenuates the satiety response to CCK. To test this hypothesis, 48-h-fasted or fed rats were injected with i.p. saline or CCK. Fasting blunted the satiety response to 3.0 microg/kg CCK, such that 30-min food intake was suppressed by 65.1% (relative to saline-treated controls) in fasted rats vs. 85.9% in the fed state (P < 0.05). In a subsequent experiment, rats were divided into three groups: 1) vehicle/fed; 2) vehicle/fasted; and 3) leptin-replaced/fasted; and each group received 3.0 microg/kg i.p. CCK. As expected, the satiety response to CCK was attenuated by fasting in vehicle-treated rats (30-min food intake: vehicle/fed, 0.3 +/- 0.1 g; vehicle/fasted, 1.7 +/- 0.4 g; P < 0.01), and this effect was prevented by leptin replacement (0.7 +/- 0.2 g, P < 0.05 vs. vehicle/fasted; P = not significant vs. vehicle/fed). To investigate whether elevated neuropeptide Y (NPY) signaling plays a role in the effect of leptin deficiency to impair the response to CCK, we measured the response to 3.0 microg/kg i.p. CCK after treatment with 7.5 microg intracerebroventricular NPY. We found that both CCK-induced satiety and its ability to increase c-Fos-like-immunoreactivity in key brainstem-feeding centers were attenuated by NPY pretreatment. We conclude that an attenuated response to meal-related satiety signals is triggered by leptin deficiency and may contribute to increased food intake.

Animals↗
PubMed1985

Satiety responses in eating disorders.

Appetite and satiety responses in a test meal paradigm were studied in six anorexia nervosa patients (four had bingeing and purging behaviors) and in nine normal control women. The anorexic patients were distinguished from normal controls by the amounts of food taken and by the pattern of the hunger and fullness responses to the test meal. Possible explanations for these findings are discussed.

Anorexia Nervosa↗
PubMed2005

Palatability and glucose, insulin and satiety responses of chickpea flour and extruded chickpea flour bread eaten as part of a breakfast.

OBJECTIVE: To determine the effect of adding chickpea flour or extruded chickpea flour to white bread on palatability and postprandial glycaemia, insulinaemia and satiety. DESIGN: A randomised, single-blind, cross-over study of four 50 g available carbohydrate breakfasts. SETTING: School of Exercise and Nutrition Sciences, Deakin University. SUBJECTS: In all, 12 healthy subjects were recruited through posted notices. Totally, 11 (nine male, two female) completed the study (mean+/-s.e.m.; age 32+/-2 y; body mass index, 24.7+/-0.8 kg/m(2)). INTERVENTION: After overnight fasting, subjects consumed a control (white) bread (WB) breakfast twice, a chickpea bread (CHB) breakfast once and an extruded chickpea bread (EXB) breakfast once. Palatability and postprandial blood glucose, insulin and satiety responses were determined. Following this, food intakes from an ad libitum buffet and for the remainder of the day were assessed. RESULTS: A trend towards a lower incremental area under the curve (IAUC) of glucose for the CHB breakfast compared to the WB breakfast was observed (P=0.087). The IAUC of insulin and insulinaemic index (II) of the CHB breakfast were higher (P<0.05) than for the WB breakfast. No differences in glycaemic index (GI), satiety response, food intake or palatability were observed. CONCLUSIONS: CHB and EXB demonstrated acceptable palatability. CHB demonstrated some hypoglycaemic effect compared to WB, but neither CHB nor EXB demonstrated effects on satiety or food intake. The hyperinsulinaemic effect of CHB observed in this study requires further investigation.

Adult↗
PubMed1986

Hunger perceptions and satiety responses among normal-weight bulimics and normals to a high-calorie, carbohydrate-rich food.

The hunger perceptions and satiety responses to a high-calorie, carbohydrate-rich food among 10 normal-weight females who met the DSM-III criteria for bulimia were compared with 10 normal-weight females who denied a current or past history of eating or weight disorders. As indicated by self-report responses on the Hunger-Satiety Questionnaire, bulimics did not differ from the normals in their perceptions of hunger sensations. Differences, however, were detected in the responses following eating. Most notably, the bulimics reported feelings of irritability, nervousness, tenseness and depression which persisted 30 minutes later. These findings and directions for future research are discussed.

Arousal↗
PubMed2003

The degree of fat saturation does not alter glycemic, insulinemic or satiety responses to a starchy staple in healthy men.

Inclusion of fat reduces the glycemic response to a carbohydate meal, although the effect of different types of fat on glycemic, insulinemic and satiety responses is unclear. Ten healthy men received 50-g carbohydrate portions of mashed potato with isoenergetic amounts of butter (saturated fatty acid), Sunola oil (monounsaturated fatty acid) or sunflower oil (PUFA) and two 50-g glucose loads on separate days. Capillary blood was collected at regular intervals for 2 h. Satiety ratings were assessed by use of a rating scale. The glycemic index (GI), insulin index (II) and satiety index (SI) scores were calculated. Energy intakes from a meal consumed ad libitum at 2 h and for the remainder of the day were quantified. The GI values ranged from 68 +/- 8 to 74 +/- 10 and the II values ranged from 113 +/- 10 to 122 +/- 17, but there was no effect of fat type. SI scores and subsequent energy intake did not differ among the test meals. Substitution of unsaturated fats for saturated fatty acids had no acute benefits on postprandial glycemia, insulin demand or short-term satiety in young men.

Adult↗
PubMed2006

Sucrose sham feeding on a binge schedule releases accumbens dopamine repeatedly and eliminates the acetylcholine satiety response.

Drinking a sugar solution on an intermittent schedule can promote sugar bingeing and cause signs of dependence while releasing dopamine repeatedly like a drug of abuse. It is hypothesized that sweet taste alone is sufficient for this effect in sucrose bingeing rats. On the theory that acetylcholine in the nucleus accumbens plays a role in satiety, it is further hypothesized that purging the stomach contents will delay acetylcholine release. Rats with gastric fistulas and nucleus accumbens guide shafts for microdialysis were fed 12 h each day. During the first hour, fistulas were open for the sham-feeding group and closed for the real-feeding group, and 10% sucrose was the only food source. For the remaining 11 h, liquid rodent diet was available as well as the 10% sucrose to provide a balanced diet. In microdialysis tests during the first sugar meal on days 1, 2 and 21, extracellular dopamine increased at least 30% each day in both groups. Acetylcholine also increased during the sugar meals for the real-feeding animals, but not during sham feeding. In conclusion, the taste of sugar can increase extracellular dopamine in the nucleus accumbens without fail in animals on a dietary regimen that causes bingeing and sugar dependency. During sham feeding, the acetylcholine satiation signal is eliminated, and the animals drink more. These findings support the hypothesis that dopamine is released repeatedly in response to taste when bingeing on sweet food, and the acetylcholine satiety effect is greatly reduced by purging; this may be relevant to bulimia nervosa in humans.

Acetylcholine↗
PubMed1983

Hyperphagia during lactation: satiety response to CCK and growth of the pancreas.

Cholecystokinin (CCK) secreted from the duodenum during feeding has been shown to elicit satiety and stimulate growth of the pancreas in addition to affecting gastrointestinal function. In previous experiments hyperphagic Zucker obese rats were less sensitive to the effects of CCK on satiety and had a smaller pancreas than normal-weight rats. In the present experiments with hyperphagic lactating Zucker rats, the food intake response to exogenously administered CCK and the size and composition of the pancreas were measured. Food intakes after a 2-h fast were not decreased by 4.0 or 8.0 micrograms/kg CCK-8 during wk 1, 2, or 3 of lactation. However, in the same rats 2 wk after pups were weaned, 4.0 and 8.0 micrograms/kg CCK-8 decreased food intake 32% (2.1 +/- 0.4 vs. 3.1 +/- 0.3 g, paired t = 2.33, P less than 0.03) and 52% (1.5 +/- 0.2 vs. 3.1 +/- 0.5 g, paired t = 3.48, P less than 0.006). On day 18 of lactation, pancreas weight was increased 41% (1.38 +/- 0.05 vs. 0.98 +/- 0.02 g, paired t = 2.68, P less than 0.02) and contents of DNA, RNA, and protein were increased 57, 57, and 73%, respectively. Thus, hyperphagia in lactating female rats was associated with 1) decreased sensitivity to the satiety effect of CCK similar to that in hyperphagic obese rats and 2) hypertrophy of the pancreas in contrast to decreased pancreas size in obese rats.

Animals↗
PubMed2006

Influence of bread volume on glycaemic response and satiety.

The role of carbohydrates in health and disease has received a high profile in recent years, in particular the glycaemic index (GI) as a physiological classification of carbohydrate foods. A common carbohydrate source in the UK is white bread, which is considered to have a high GI value and low satiety value. In the present study, the possibility of favourably altering the GI of white bread by manipulating bread structure (loaf form) was investigated. In a randomised repeated-measures design, ten subjects were tested for glycaemic and satiety responses to four loaves of varying volume, but of consistent macronutrient content. Peak plasma glucose levels and GI values were shown to be significantly reduced by lowering loaf volume (P=0.007, P<0.001 respectively). In addition, a greater satiety index (SI) was seen with decreased loaf volume (P<0.001). In conclusion, the present study demonstrates that reducing the volume of white bread, which is generally considered to be high-GI and low-SI, can favourably alter metabolic and appetite responses. Relatively small differences in the GI of regularly consumed starch foods have been shown to have beneficial effects on health.

Blood Glucose↗
PubMed1991

Characterization of the enhanced responsiveness to postingestive satiety signals in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated Han/Wistar rats.

Previous studies have shown that under free-feeding conditions, TCDD-treated Han/Wistar (H/W) rats consume less sucrose solution but ingest more saccharin solution than their controls thus implying hyperresponsiveness to postingestive satiety signals. In this study, nutrient preloads were employed to further elucidate this phenomenon. Male H/W rats were given a single high but usually non-lethal intraperitoneal dose (1000 micrograms/kg) of TCDD. Feed intake was stimulated by 24 hr feed deprivation at various time points after TCDD exposure. When TCDD-dosed rats were allowed to drink either a 20% sucrose or a 0.25% saccharin solution and then given access to feed, those that had had sucrose ate only about 50% of the amount consumed by the saccharin group. Although the preloads were similar in control rats, no such difference in subsequent feeding occurred. The sucrose solution also produced a longer-lasting suppression of feed intake in TCDD-treated compared with control rats when infused directly into the stomach. By contrast, TCDD-treated H/W rats failed to exhibit an augmented satiety response to parenterally applied glucose independent of testing time. Oral corn oil reduced feed intake in both control and TCDD-exposed rats, but the inhibition was slightly larger in TCDD-treated animals. TCDD did not markedly affect the responsiveness of H/W rats to the suppression of feeding by CCK-8 or bombesin. It is concluded that gastrointestinal factors appear critical to the exaggerated response of TCDD-treated H/W rats to nutrient energy.

Administration, Oral↗
PubMed2005

Leptin action in the forebrain regulates the hindbrain response to satiety signals.

The capacity to adjust energy intake in response to changing energy requirements is a defining feature of energy homeostasis. Despite the identification of leptin as a key mediator of this process, the mechanism whereby changes of body adiposity are coupled to adaptive, short-term adjustments of energy intake remains poorly understood. To investigate the physiological role of leptin in the control of meal size and the response to satiety signals, and to identify brain areas mediating this effect, we studied Koletsky (fa(k)/fa(k)) rats, which develop severe obesity due to the genetic absence of leptin receptors. Our finding of markedly increased meal size and reduced satiety in response to the gut peptide cholecystokinin (CCK) in these leptin receptor-deficient animals suggests a critical role for leptin signaling in the response to endogenous signals that promote meal termination. To determine if the hypothalamic arcuate nucleus (ARC) (a key forebrain site of leptin action) mediates this leptin effect, we used adenoviral gene therapy to express either functional leptin receptors or a reporter gene in the area of the ARC of fa(k)/fa(k) rats. Restoration of leptin signaling to this brain area normalized the effect of CCK on the activation of neurons in the nucleus of the solitary tract and area postrema, key hindbrain areas for processing satiety-related inputs. This intervention also reduced meal size and enhanced CCK-induced satiety in fa(k)/fa(k) rats. These findings demonstrate that forebrain signaling by leptin, a long-term regulator of body adiposity, limits food intake on a meal-to-meal basis by regulating the hindbrain response to short-acting satiety signals.

Animals↗
PubMed1992

Dietary restraint and responsiveness to sensory-based food cues as measured by cephalic phase salivation and sensory specific satiety.

Responsiveness to sensory-based food cues was examined in restrained and unrestrained, normal-weight subjects identified with the Three-Factor Eating Questionnaire. Salivary flow rate was measured with no food present and while subjects viewed hot pizza. In the presence of food, restrained eaters had a mean salivary flow rate (0.388 g/min) greater than twice that of the unrestrained eaters (0.186 g/min). During sensory specific satiety testing, subjects tasted and rated the pleasantness of 9 foods, then received a meal of either cheese and crackers or cookies. Changes in pleasantness for the tasted foods were evaluated at 2, 20, and 40 min following the meal. Both restrained and unrestrained subjects displayed similar patterns of sensory specific satiety, i.e., the pleasantness foods which were eaten decreased relative to foods tasted but not eaten. These patterns were unaffected by the type of food consumed in the test meal. These data demonstrate that restrained eaters show moderately enhanced salivary responses but no changes in sensory-specific satiety to food stimuli, suggesting that heightened responsiveness to the sensory properties of foods may not be a generalized phenomenon in restrained eaters.

Adult↗
PubMed1998

Rats maintained on high-fat diets exhibit reduced satiety in response to CCK and bombesin.

Rats maintained on high-fat diets often exhibit increased food intake and weight gain. We hypothesized that high-fat diets might result in reduced sensitivity to hormonal signals responsible for terminating food intake--satiety signals. The intestinal hormone cholecystokinin (CCK) and the gastrointestinal neuropeptide, bombesin (BBS) both have been proposed as satiety signals. To determine whether maintenance on high-fat diets alters sensitivity to satiating effects of CCK and bombesin (BBS), rats were maintained on a low fat diet (LF), a high-fat diet that was isocaloric with the low-fat diet (HF), or one of two hypercaloric high-fat diets (HF-1, HF-2) that differed from HF and LF in fat, fiber, and total caloric content. CCK and bombesin reduced food intake significantly less in rats maintained on high-fat diets, compared to those on the low fat diet. Neither high caloric intake, which was associated with increased body weight gain on the two hypercaloric diets, nor fiber content of the diet accounted for the reduced response of HF rats to CCK. Rather, reduced sensitivity to CCK was related only to the high proportion of calories taken as fat. We also determined whether reduced CCK sensitivity was due to the maintenance on a particular diet or to the diet eaten during a CCK test. After CCK, rats maintained on LF reduced food intake more (49%) than rats maintained on HF (22%), regardless of whether they ate HF or LF during the CCK test itself. These findings indicate that maintenance of rats on high-fat diets reduces sensitivity to some peptide satiety signals. Reduced sensitivity to satiety signals might contribute to overeating and obesity often observed when rats are maintained on high-fat diets.

Animals↗
PubMed2026

Determinants of Meal Satisfaction and Their Association With Childhood Obesity: A Systematic Review.

Meal satisfaction is considered a multidimensional concept that includes sensory enjoyment, cognitive, emotional, and physiological components and relates to contentment with the meal experience as a whole. However, its relevance to eating behavior and body weight remains unclear, especially in children. The present review investigated the potential relationship between meal satisfaction-related constructs and childhood obesity, and whether this relation is shaped by individual factors and the external environment. Seventeen eligible studies from 350 records published between 2008 and 2024 were included. No study directly assessed meal satisfaction; instead, proxy measures were used. Food enjoyment emerged as the proxy most consistently associated with BMI, often clustering with higher food responsiveness, lower satiety responsiveness, and emotional overeating. Parental feeding practices, especially pressure to eat, significantly contributed to variation in children's eating behavior and were associated with lower food enjoyment. Overall, meal satisfaction could be a key aspect to consider in childhood obesity prevention programs. However, to date, the available evidence is heterogeneous and predominantly observational. Future longitudinal and intervention studies are needed, alongside child-appropriate instruments to objectively quantify food satisfaction in children. Research that helps understand the role of contextual eating factors on children's meal satisfaction and eating behavior is also warranted.

Humans↗
PubMed1996

The effect of satiety on responses of gustatory neurons in the amygdala of alert cynomolgus macaques.

An alert cynomolgus macaque was fed a sweet solution to satiety as the activity of a gustatory neuron in the amygdala was recorded to that solution and to four other taste stimuli. This experiment was conducted a total of 14 times in two monkeys. The responses of individual neurons to the satiety stimuli were suppressed by as little as 1%, and as much as 100% by the induction of satiety (mean suppression = 58%). Nine of the 14 cells responded to the satiety solution with excitation, and their responses were suppressed by a mean of 62% by satiety. Five neurons responded with inhibition, and their responses were suppressed by a mean of 50%. Responses to other taste stimuli, not associated with satiety, were affected to a lesser extent. The amygdala is a taste relay between the primary gustatory cortex, where satiety has no influence on responses to taste stimuli, and the lateral hypothalamic area where the effect of satiety is total. The data presented here indicate that the amygdala is a functional as well as anatomical intermediary between these two areas, and serves as a stage in the process through which sensory stimuli are imbued with motivational significance.

Amygdala↗
PubMed1994

Dose-response effects of boiled carrots and effects of carrots in lactic acid in mixed meals on glycaemic response and satiety.

OBJECTIVE: To evaluate the effect of dosage on the metabolic response to vegetables added to a mixed lunch meal, and to relate the amounts to the tripartite plate model. Carrots were chosen as an example, and the carrots were blanched, frozen and boiled to include possible effects of processing and cooking. The effects of carrots steeped in lactic acid, as produced at fermentation, were also studied. DESIGN: The test meals with carrots, and the control meal without vegetables, were balanced regarding energy (2000 kJ) and digestible carbohydrates (60 g) and similar in fat (17 g) and protein (16-19 g) content. The carrot portions of 100, 200 and 300 g contained 2.9, 5.8 and 8.7 g dietary fibre respectively. The meals were served in the morning after an overnight fast and in random order. Blood samples for the analysis of blood glucose, plasma insulin and C-peptide were collected and satiety was graded until 210 min postprandially. SETTING: The study was performed at the research laboratory, Dalby Health Sciences Centre (primary care). SUBJECTS: The 10 healthy, male volunteers, around 40 years of age, were recruited at random from the district's population list. None dropped out. RESULTS: The larger the carrot portion the lower were the glucose and insulin/C-peptide responses and the higher the satiety scores. The minimum amount causing significant effects was 200 g. According to the plate model, 200 g of boiled carrots was the most that could be included on half the plate. Addition of lactic acid to 200 g carrots augmented the effects on satiety scores and hormonal response. CONCLUSIONS: The addition of generous amounts of vegetables to a mixed meal improves the metabolic response.

Adult↗
PubMed2001

Development of the Children's Eating Behaviour Questionnaire.

Individual differences in several aspects of eating style have been implicated in the development of weight problems in children and adults, but there are presently no reliable and valid scales that assess a range of dimensions of eating style. This paper describes the development and preliminary validation of a parent-rated instrument to assess eight dimensions of eating style in children; the Children's Eating Behaviour Questionnaire (CEBQ). Constructs for inclusion were derived both from the existing literature on eating behaviour in children and adults, and from interviews with parents. They included responsiveness to food, enjoyment of food, satiety responsiveness, slowness in eating. fussiness, emotional overeating, emotional undereating. and desire for drinks. A large pool of items covering each of these constructs was developed. The number of items was then successively culled through analysis of responses from three samples of families of young children (N = 131; N = 187; N = 218), to produce a 35-item instrument with eight scales which were internally valid and had good test-retest reliability. Investigation of variations by gender and age revealed only minimal gender differences in any aspect of eating style. Satiety responsiveness and slowness in eating diminished from age 3 to 8. Enjoyment of food and food responsiveness increased over this age range. The CEBQ should provide a useful measure of eating style for research into the early precursors of obesity or eating disorders. This is especially important in relation to the growing evidence for the heritability of obesity, where good measurement of the associated behavioural phenotype will be crucial in investigating the contribution of inherited variations in eating behaviour to the process of weight gain.

Body Constitution↗
PubMed1998

Role of small intestine in caloric compensations to oil premeals in rats.

We postulated that dose-responsive satiety after oil premeals varies with the number of gut sensors stimulated by lipolytic products along intestine. These experiments in fasted rats on satiety after oil premeals were performed to 1) determine whether satiety was induced by lipolytic products but not triglycerides; 2) confirm that oil empties from the stomach at rates that vary with oil loads; 3) ascertain that increasing rates of oil entry into duodenum extend the length of gut contacted by lipolytic products; and 4) judge whether length of gut contacted correlated with dose-responsive satieties to dietary oils. 5) Using specific antagonists, we attempted to define how satiety was signalled by gut sensors. Timing and degrees of satiety did not correlate with timing and extent of gastric distensions but, rather, with the timing and extent of spread of lipolytic products along small bowel. Satiety after the highest premeal load of oil was blocked by Pluronic L-81, an inhibitor of intestinal secretion of apolipoprotein A-IV, but was unaffected by MK-329 (a specific antagonist of cholecystokinin) or by capsaicin blockade of chemosensory nerves.

Analysis of Variance↗