Satiety Ratio Research Articles

Cholecystokinin-8 increases the satiety ratio in diabetic rats more than cholecystokinin-33

Cholecystokinin (CCK) is a satiety peptide and a potential anti-diabetic agent, which exists in different forms (e.g. CCK-8 and CCK-33). In normal rats, CCK-8 and 33 stimulate insulin secretion similarly but their satiety effects vary. In diabetic rats, those effects require testing. Here, we compared size of the first meal (10% sucrose test diet), intermeal interval (IMI, time between first and second meal) and satiety ratio (SR, amount of satiation produced by every unit of food consumed in the first meal) by CCK-8 or 33 (0, 1, 3, 5nmol/kg) intraperitoneally in streptozotocin-injected (diabetic) and citrate buffer-injected (control) rats. We found that both peptides reduce meal size in diabetic and control rats with no difference between groups, CCK-33 (5nmol) prolonged IMI in diabetic rats and CCK-8 and CCK-33 increased satiety ratio in control rats, but only CCK-8 increased it in the diabetic group. Therefore, CCK-8 increases the satiety ratio in diabetic rats more than CCK-33.

Eating Behavior in Rats Subjected to Vagotomy, Sleeve Gastrectomy, and Duodenal Switch

Background/AimFood intake, eating behavior, and metabolic parameters in rats that underwent bilateral truncal vagotomy, sleeve gastrectomy, and duodenal switch procedures were examined. MethodsRats were subjected to bilateral truncal vagotomy plus pyloroplasty (VTPP), pyloroplasty (PP), laparotomy, sleeve gastrectomy (SG), or duodenal switch (DS; with and without SG). ResultsVTPP, but neither PP nor laparotomy, reduced body weight (BW; 10%) transiently (1 week postoperatively). SG reduced BW (10%) for 6 weeks, while DS alone or SG followed by DS led to a continuous BW loss from 15% at 1 week to 50% at 8 weeks postoperatively. Food intake was higher and the satiety ratio was lower during the night than the day for all groups of surgeries. Neither VTPP nor SG had measurable effect on food intake, eating behavior and metabolic parameters. DS reduced daily food intake by more than 50%, which was associated with hypercholecystokinin(CCK)emia, reduced meal size and increased satiety ratio, and increased fecal energy content (measured at 8 weeks). ConclusionsWeight loss after VTPP, SG, or DS differed in terms of degree, duration, and underlying mechanisms. DS without SG was most effective in the long-term, probably due to hyperCCKemia-induced reduction in food intake and long-limb intestinal bypass-induced malabsorption.

Hepatic‐Portal Vein Infusions of Glucagon‐Like Peptide‐1 Reduce Meal Size and Increase c‐Fos Expression in the Nucleus Tractus Solitarii, Area Postrema and Central Nucleus of the Amygdala in Rats

We recently reported that brief, remotely controlled intrameal hepatic-portal vein infusions of glucagon-like peptide-1 (GLP-1) reduced spontaneous meal size in rats. To investigate the neurobehavioural correlates of this effect, we equipped male Sprague-Dawley rats with hepatic-portal vein catheters and assessed (i) the effect on eating of remotely triggered infusions of GLP-1 (1 nmol/kg, 5 min) or vehicle during the first nocturnal meal after 3 h of food deprivation and (ii) the effect of identical infusions performed at dark onset on c-Fos expression in several brain areas involved in the control of eating. GLP-1 reduced (P < 0.05) the size of the first nocturnal meal and increased its satiety ratio. Also, GLP-1 increased (P < 0.05) the number of c-Fos-expressing cells in the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala, but not in the arcuate or paraventricular hypothalamic nuclei. These data suggest that the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala play a role in the eating-inhibitory actions of GLP-1 infused into the hepatic-portal vein; it remains to be established whether activation of these brain nuclei reflect satiation, aversion, or both.

Meal parameters and vagal gastrointestinal afferents in mice that experienced early postnatal overnutrition

Early postnatal overnutrition results in a predisposition to develop obesity due in part to hypothalamic and sympathetic dysfunction. Potential involvement of another major regulatory system component — the vagus nerve — has not been examined. Moreover, feeding disturbances have rarely been investigated prior to development of obesity when confounds due to obesity are minimized. To examine these issues, litters were culled on the day of birth to create small litters (SL; overnutrition), or normal size litters (NL; normal nutrition). Body weight, fat pad weight, meal patterns, and vagal sensory duodenal innervation were compared between SL and NL adult mice prior to development of obesity. Meal patterns were studied 18 h/day for 3 weeks using a balanced diet. Then vagal mechanoreceptors were labeled using anterograde transport of wheatgerm agglutinin–horseradish peroxidase injected into the nodose ganglion and their density and morphology were examined. Between postnatal day 1 and weaning, body weight of SL mice was greater than for NL mice. By young adulthood it was similar in both groups, whereas SL fat pad weight was greater in males, suggesting postnatal overnutrition produced a predisposition to obesity. SL mice exhibited increased food intake, decreased satiety ratio, and increased first meal rate (following mild food deprivation) compared to NL mice, suggesting postnatal overnutrition disrupted satiety. The density and structure of intestinal IGLEs appeared similar in SL and NL mice. Thus, although a vagal role cannot be excluded, our meal parameter and anatomical findings provided no evidence for significant postnatal overnutrition effects on vagal gastrointestinal afferents.

Meal patterns, satiety, and food choice in a rat model of Roux-en-Y gastric bypass surgery.

Gastric bypass surgery efficiently and lastingly reduces excess body weight and reverses type 2 diabetes in obese patients. Although increased energy expenditure may also play a role, decreased energy intake is thought to be the main reason for weight loss, but the mechanisms involved are poorly understood. Therefore, the aim of this study was to characterize the changes in ingestive behavior in a rat model of Roux-en-Y gastric bypass surgery (RYGB). Obese (24% body fat compared with 18% in chow-fed controls), male Sprague-Dawley rats maintained for 15 wk before and 4 mo after RYGB or sham-surgery on a two-choice low-fat/high-fat diet, were subjected to a series of tests assessing energy intake, meal patterning, and food choice. Although sham-operated rats gained an additional 100 g body wt during the postoperative period, RYGB rats lost approximately 100 g. Intake of a nutritionally complete and palatable liquid diet (Ensure) was significantly reduced by approximately 50% during the first 2 wk after RYGB compared with sham surgery. Decreased intake was the result of greatly reduced meal size with only partial compensation by meal frequency, and a corresponding increase in the satiety ratio. Similar results were obtained with solid food (regular or high-fat chow) 6 wk after surgery. In 12- to 24-h two-choice liquid or solid diet paradigms with nutritionally complete low- and high-fat diets, RYGB rats preferred the low-fat choice (solid) or showed decreased acceptance for the high-fat choice (liquid), whereas sham-operated rats preferred the high-fat choices. A separate group of rats offered chow only before surgery completely avoided the solid high-fat diet in a choice paradigm. The results confirm anecdotal reports of "nibbling" behavior and fat avoidance in RYGB patients and provide a basis for more mechanistic studies in this rat model.

Microstructural pattern of palatable food intake from weaning to adulthood in male and female OLETF rats.

Ontogenetic trajectories from weaning to adulthood and sex differences in feeding patterns were examined in the Otsuka Long-Evans Tokushima Fatty (OLETF) rat, an animal model of early onset overeating-induced obesity, and a natural cholecystokinin-1 receptor knockout. Overnight patterns of licking a palatable liquid diet (Ensure) were analyzed on Postnatal Days 22, 38, 60, and 90. Because different microstructure profiles may reflect alterations in the influence of positive and negative signals, we examined meal parameters to uncover developing mechanisms underlying eating behavior in this strain. OLETF rats displayed significantly greater caloric intake, larger meals (in number of licks), and more (within-meal) clusters of feeding (which were shorter in duration and contained fewer licks per cluster) than did Long-Evans Tokushima Ohtsuka (LETO) strain controls. OLETF rats also had significantly lower satiety ratios than LETO rats. Moreover, we identified sex differences in the age of emergence of microstructural patterns of obesity-related overeating, suggesting that systems other than cholecystokinin may be disrupted, possibly worsening the OLETF strain's obesity phenotype.

Gastric Bypass Surgery Causes Body Weight Loss Without Reducing Food Intake in Rats

It is a common dogma that gastric bypass (GB) induces early satiety and consequent reductions in food intake and nutrient absorption. The aim of the present study was to analyze feeding behavioral and metabolic changes in rats after GB. Male Sprague-Dawley rats at the ages of 23 and 42 weeks were placed in metabolic cages connected with a comprehensive laboratory animal monitoring system. At the age of 48 weeks they were subjected to either GB or sham operation, and then placed in metabolic cages at 51 and 62 weeks (or 3 and 14 weeks postoperatively). GB rats lost 20% of the body weight within 2-3 weeks and remained at this lower level until the end of the study at 14 weeks postoperatively. Satiety ratio was higher during daytime than nighttime in both sham-operated and GB rats, but was not significantly different between the two groups. Neither daily accumulated food intake nor food intake per 100 g of body weight was different between sham-operated and GB rats. Apparently, GB rats ate more frequently during daytime and had smaller meal size during nighttime at 3 weeks postoperatively. These changes were not present at 14 weeks postoperatively. Energy density in the feces was the same in GB and sham-operated rats postoperatively. Energy expenditure declined with age, but increased in GB rats compared with age-matched sham-operated rats. GB reduced the body weight without causing early satiety, reducing food intake or inducing malabsorption. It did, however, increase energy expenditure.

Feeding microstructure in diet‐induced obesity susceptible versus resistant rats: central effects of urocortin 2

With one billion people overweight worldwide, the need to identify risk factors and treatments for obesity is urgent. The present study determined whether rats genetically prone to diet-induced obesity (DIO) show preexisting differences in meal microstructure and are sensitive to central anorectic effects of corticotropin-releasing factor type 2 (CRF(2)) receptor stimulation. Male, selectively bred DIO rats and their diet resistant (DR) counterparts (n = 9/genotype) were weaned onto low-fat chow and compared as young adults for spontaneous or intracerebroventricular urocortin 2 administration-induced (0, 0.3, 1, 3 microg) differences in ingestion. DIO rats were hyperphagic selectively at the dark cycle onset, showing shorter latencies to initiate feeding, faster returns to eating following meal completion, and a lower satiety ratio than DR rats. At other times, DIO rats had briefer postmeal intervals, but ate smaller and briefer meals, resulting in normal intake. DIO rats also ate faster than DR rats. Urocortin 2 was less potent in DIO rats, ineffective at the 0.3 microg dose, but produced CRF(2) antagonist-reversible anorexia at higher doses. Though heavier, chow-maintained DIO rats were proportionately as or more lean than DR rats. Thus, DIO rats showed signs of a preexisting, heritable deficit in the maintenance of postmeal satiety and a reduced sensitivity to anorectic CRF(2) agonist stimulation. The meal patterns of DIO rats temporally resemble human 'snacking' behaviour, which predicts adult obesity. Because central CRF(2) stimulation retains full anorectic efficacy at higher doses in the DIO model, manipulating this neuropeptidergic system might yield new therapeutic approaches for diet-induced obesity.

Appetite regulation and functional food claims: Experimental methodology and physiological targets.

An Appetite Regulation Task Force and an Expert Group has been established to examine the experimental methodology on appetite control in the light of the regulatory procedures to be implemented regarding satiety claims on foods. What strength of claims can be sustained on the basis of the commonly used scientific designs and experimental procedures? What constitutes a strong or weak design for assessing the effect of a food on satiety? Are diifferent designs required for assessing effects on satiation as opposed to satiety, and how are these related to an effect on body weight regulation? Twenty five years ago it was proposed that it would be advantageous to develop a formula for calculating the energy–satiety ratio of all common foods in order to assess their potential for causing overconsumption and obesity (Heaton, 1981). The Expert Group will examine the feasibility of achieving this. The biological system underlying the control of appetite is becoming better understood and involves close links between peripheral physiology and metabolism, and brain processes. The system embodies mechanisms that are potential targets for foods designed to influence satiety. The Expert Group will establish the strength of evidence regarding food based mechanisms and satiety. Critical processes include the balance between sensory and metabolic satiety, and between homeostatic and hedonic controls over appetite. The relationship between food palatability and satiety is criticial for establishing a valid experimental methodology and for defining relevant biological targets.

NT-4-deficient mice lack sensitivity to meal-associated preabsorptive feedback from lipids

Since mice with a deletion of the neurotrophin-4 (NT-4) gene exhibit a loss of both nodose ganglion neurons and vagal afferent terminals in the small intestines, we hypothesized that the reduced intestinal innervation of the NT-4 knockout (NT-4KO) mouse would lead to a corresponding reduction in the preabsorptive feedback from macronutrients. To explore this prediction, we measured meal patterns in NT-4KOs and controls, while, on different days, intragastric infusions of either lipids (Intralipid; 10%, 20%) or glucose (12.5%, 25%) were yoked to each animal's spontaneous feeding of a pelleted diet (approximately 1 kcal infused/1 kcal ingested). NT-4KO mice were relatively, though not completely, insensitive to the lipid infusions, whereas they were as sensitive as controls to glucose infusions. More specifically, the regulatory deficits of NT-4KOs included 1) attenuated satiation from the lipid infusions, as measured by smaller intrameal reductions of both meal size and meal duration, 2) defects in satiety associated with the fat infusions, as measured by smaller intermeal increases of both satiety ratio and intermeal interval, and (3) losses in daily compensatory responses for lipid calories. These results support the hypothesis that NT-4KO mice have deficits in macronutrient feedback from the gastrointestinal tract, indicate that the defects are specific insofar as they do not include impairments in the feedback of glucose infusions on feeding, and suggest that early feedback about dietary lipids is important in the regulation of satiation, satiety, and longer-term compensation of daily caloric intake.

Melanocortinergic Modulation of Cholecystokinin-Induced Suppression of Feeding through Extracellular Signal-Regulated Kinase Signaling in Rat Solitary Nucleus

Signals from the gut and hypothalamus converge in the caudal brainstem to control ingestive behavior. We have previously shown that phosphorylation of ERK1/2 in the solitary nucleus (NTS) is necessary for food intake suppression by exogenous cholecystokinin (CCK). Here we test whether this intracellular signaling cascade is also involved in the integration of melanocortin-receptor (MCR) mediated inputs to the caudal brainstem. Using fourth ventricular-cannulated rats and Western blotting of NTS tissue, we show that the MC4R agonist melanotan II (MTII) rapidly and dose-dependently increases phosphorylation of both ERK1/2 and cAMP response element-binding protein (CREB). Sequential administration of fourth ventricular MTII and peripheral CCK at doses that alone produced submaximal stimulation of pERK1/2 produced an additive increase. Prior fourth ventricular administration of the MC4R antagonist SHU9119 completely abolished the CCK-induced increases in pERK and pCREB and, in freely feeding rats, SHU9119 significantly increased meal size and satiety ratio. Prior administration of the MAPK kinase inhibitor U0126 abolished the capacity of MTII to suppress 2-h food intake and significantly decreased MTII-induced ERK phosphorylation in the NTS. Furthermore, pretreatment with the cAMP inhibitor, cAMP receptor protein-Rp isomer, significantly attenuated stimulation of pERK induced by either CCK or MTII. The results demonstrate that activation of the ERK pathway is necessary for peripheral CCK and central MTII to suppress food intake. The cAMP-->ERK-->CREB cascade may thus constitute a molecular integrator for converging satiety signals from the gut and adiposity signals from the hypothalamus in the control of meal size and food intake.

A new way of looking at eating

the analysis of meals, especially of spontaneous meals, has long had a problematic place in the behavioral neuroscience of eating. Only a small minority of eating researchers now, or ever, have concerned themselves with meal patterns. On first glance this seems paradoxical. After all, eating occurs

A mechanism underlying mature-onset obesity: evidence from the hyperphagic phenotype of brain-derived neurotrophic factor mutants

Mice deficient in brain-derived neurotrophic factor (BDNF) develop mature-onset obesity, primarily due to overeating. To gain insight into the mechanism of this hyperphagia, we characterized food intake, body weight, meal pattern, and meal microstructure in young and mature mice fed balanced or high-fat diets. Hyperphagia and obesity occurred in mature but not young BDNF mutants fed a balanced diet. This hyperphagia was mediated by increased meal number, which was associated with normal meal size, meal duration, and satiety ratio. In contrast, the high-fat diet induced premature development of hyperphagia and obesity in young BDNF mutants and a similar magnitude hyperphagia in mature mutants. This hyperphagia was supported by increased meal size and was accompanied by a reduced satiety ratio. Thus the mechanism underlying hyperphagia was present before significant weight gain, but whether it occurred, and whether meal frequency or meal size was altered to support it, was modulated by a process associated with aging and by diet properties. Meal pattern changes associated with the balanced diet suggested meal initiation, and the oropharyngeal positive feedback that drives feeding, were enhanced and might have contributed to overeating in BDNF mutants, whereas negative feedback was normal. Consistent with this hypothesis, meal microstructure revealed that all hyperphagic mutant groups exhibited increased intake rates at meal onset. Therefore, the central nervous system targets of BDNF actions may include orosensory brain stem neurons that process and transmit positive feedback or forebrain neurons that modulate its strength.

The Time of Day of Food Intake Influences Overall Intake in Humans

Circadian and diurnal rhythms affect food intake, and earlier research has suggested that meal sizes increase, whereas the after-meal intervals and satiety ratios decrease over the day. We hypothesized that the time of day of food intake would be related to total intake such that intake early in the day would tend to reduce overall intake, whereas intake later in the day would tend to increase intake over the entire day. The intakes of 375 male and 492 female free-living individuals, previously obtained via 7-d diet diaries, were reanalyzed. The total and meal intakes of food energy, the amounts of the macronutrients ingested and the density of intake occurring during five 4-h periods (0600-0959, 1000-1359, 1400-1759, 1800-2159 and 2200-0159 h) were identified and related to overall and meal intakes during the entire day. The proportion of intake in the morning was negatively correlated with overall intake (r=-0.13, P<0.01), whereas the proportion ingested late in the evening was positively correlated with overall intake (r=0.14, P<0.01). The energy densities of intake during all periods of the day were positively related to overall intake (range, r=0.13-0.23, P<0.01). The results suggest that low energy density intake during any portion of the day can reduce overall intake, that intake in the morning is particularly satiating and can reduce the total amount ingested for the day, and that intake in the late night lacks satiating value and can result in greater overall daily intake.

Meal pattern analysis of diet-induced obesity in susceptible and resistant rats.

To characterize the meal patterns of free feeding Sprague-Dawley rats that become obese or resist obesity when chronically fed a high-fat diet. Male Sprague-Dawley rats (N = 120) were weaned onto a high-fat diet, and body weight was monitored for 19 weeks. Rats from the upper [diet-induced obese (DIO)] and lower [diet-resistant (DR)] deciles for body-weight gain were selected for study. A cohort of chow-fed (CF) rats weight-matched to the DR group was also studied. Food intake was continuously monitored for 7 consecutive days using a BioDAQ food intake monitoring system. DIO rats were obese, hyperphagic, hyperleptinemic, hyperinsulinemic, hyperglycemic, and hypertriglyceridemic relative to the DR and CF rats. The hyperphagia of DIOs was caused by an increase in meal size, not number. CF rats ate more calories than DR rats; however, this was because of an increase in meal number, not size. When expressed as a function of lean mass, CF and DR rats consumed the same amount of calories. The intermeal intervals of DIO and DR rats were similar; both were longer than CF rats. The nocturnal satiety ratio of DIO rats was significantly lower than DR and CF rats. The proportion of calories eaten during the nocturnal period did not differ among groups. The hyperphagia of a Sprague-Dawley rat model of chronic diet-induced obesity is caused by an increase in meal size, not number. These results are an important step toward understanding the mechanisms underlying differences in feeding behavior of DIO and DR rats.

Contribution of snacks and meals in the diet of French adults: a diet-diary study

To investigate the relative contributions of meals and snacks in the daily intake of free-living humans, 54 French adults maintained food intake diaries for four 7-day periods. They recorded all food and fluid intakes mentioning whether, in their opinion, each intake event was a snack or a meal. The weekly food diaries also contained information on the circumstances of each event such as time and place, number of persons present, and affective states (hunger, satiety, etc.) before and after intake. On average, 2.7 meals and 1.3 snacks were consumed each day. Very few days included no snacking. Total daily energy and nutrient intake were not different between days with and days without snacks. Snacks differed from meals in several dimensions. Meals were about twice as large as snacks in energy and weight. Nutrient intake, in absolute values, was higher in meals. In proportions, however, snacks contained more CHO and less fat and proteins. Most foods were consumed in larger amounts in the context of meals but a few (sweets, cereal bars, biscuits, and sodas) were mostly consumed as snacks. Hunger was more intense before but less intense after meals than snacks. The satiety ratio was higher for snacks than meals. Time of day affected many intake parameters. For example, afternoon snacks exhibited a high satiety ratio for a modest intake. The present study describes the status of several potential determining factors at the time of snacks in humans, demonstrating a specific role for snacks, as opposed to meals, in the daily eating pattern of healthy adults.

Central melanocortin receptor agonist reduces spontaneous and scheduled meal size but does not augment duodenal preload-induced feeding inhibition

Central melanocortin (MC) receptor agonists inhibit food intake and may be downstream mediators of the effects of central leptin, which (1) reduces food intake by selectively decreasing meal size and (2) augments the feeding-inhibitory effects of gastrointestinal food stimuli. Central administration of the MC-3/4 receptor (MC-3/4R) agonist, MTII, inhibits feeding in rats, but its effects on meal pattern and potential interactions with gastrointestinal controls of food intake remain unclear. We examined meal patterns and intake in male Sprague–Dawley rats following central intracerebroventricular administration of MTII (0.01–1.0 nmol) in two situations: (1) during daytime 60-min scheduled access to liquid glucose (12.5%) in combination with a duodenal preload of 12.5% glucose or physiological saline (4.4 ml/10 min), and (2) during subsequent overnight access to 45 mg of solid chow pellets. Both duodenal glucose preloads and MTII reduced subsequent glucose intake. However, no dose of MTII augmented the reductions in food intake produced by duodenal glucose alone. During overnight access to pelleted chow, the 0.1- and 1.0-nmol doses of MTII reduced food intake, meal size, meal duration, and body weight, and increased the satiety ratio (duration of intermeal interval/preceding meal size) but did not change meal frequency. The present data (1) demonstrate that MTII, like leptin, reduces food intake by a selective reduction in meal size and not meal frequency, and (2) suggest that MTII increases the feeding-inhibitory potency of negative feedback signals critical to the control of meal size during spontaneous chow access, but not scheduled access to palatable liquid nutrient solutions.

Intrameal hepatic-portal infusion of glucose reduces spontaneous meal size in rats

To test whether glucose (GLC) or insulin (INS) acutely reduces spontaneous meal size, we tested the effects of remotely controlled, intrameal hepatic-portal vein infusions of GLC or INS on rats' spontaneous feeding patterns. Experiment 1 included four blocks of three test infusions and one control infusion. The test infusions in each block were 0.25, 0.5, 1.0 or 1.5 mmol GLC; 2, 4, 6, or 8 mU INS; or the four combinations with dose ratios of 1 mmol GLC/8 mU INS, respectively. Control infusions and the INS vehicle were saline infusions that were equiosmotic to the GLC infusion used in that block. Infusions (0.1 ml×5 min) were done during the first spontaneous dark-phase meal. None of the test infusions affected meal size, meal duration or the duration of the subsequent intermeal interval. In Experiment 2, a similar design was used to test infusions of 1 mmol GLC, 2 mU INS and GLC/INS. Both GLC alone and GLC/INS reduced the size and duration of the first spontaneous dark-phase meal. The subsequent intermeal interval was unaffected, but GLC alone also increased the satiety ratio (min/g) of the meal. The size and duration of the second dark-phase meal were unaffected. INS alone did not affect any meal parameters. In Experiment 3, infusions of 1 mmol GLC and 2 mU INS were repeated during each of the first three meals of the dark phase. These infusions reduced the size and duration of each meal, as well as 6-h cumulative food intake, but did not affect any other meal parameter. These experiments demonstrate for the first time that intrameal hepatic-portal infusions of GLC or of GLC and INS is sufficient to acutely and selectively reduce spontaneous meal size in the rat. The findings are consistent with the idea that meal-contingent changes in hepatic-portal GLC concentration contribute to satiation.

Prandial lactate infusion inhibits spontaneous feeding in rats.

To investigate the acute effects of lactate on spontaneous feeding, we infused lactate in the hepatic portal vein (0.5, 1.0, and 1.5 mmol lactate/meal) or in the vena cava (1.0 and 1.5 mmol lactate/meal) of ad libitum-fed rats during their first spontaneous nocturnal meal. Infusions (5 min, 0.1 ml/min) were remotely controlled, and a computerized feeding system recorded meal patterns. In separate crossover tests, meal size decreased independent of the infusion route after 1.0 and 1.5 mmol but not after 0.5 mmol lactate. The subsequent intermeal interval (IMI) tended to decrease only after vena cava infusion of 1.0 mmol lactate. The size of the second nocturnal meal increased after the 1.0 mmol lactate infusion. Hepatic portal infusion of 1.5 mmol lactate increased the satiety ratio [subsequent IMI (min)/meal size (g)] by 175%, which was higher than the insignificant 43% increase after vena cava infusion. Hepatic portal infusion of 1.5 mmol lactate also increased systemic plasma lactate but not glucose concentration at 1 min after the end of infusion. The results are consistent with the idea that meal-induced increases in circulating lactate play a role in the control of meal size (satiation). Moreover, the results suggest that lactate also contributes to postprandial satiety and that the liver is involved in this effect. The exact mechanisms of lactate's inhibitory effects on feeding and the site(s) where lactate acts to terminate meals remain to be identified.

Palatability and intake relationships in free-living humans: measurement and characterization in the French

To investigate palatability influences on the ad lib eating behavior of free-living humans, 54 French participants were paid to maintain food intake diaries for four 7-day periods. They recorded their intake along with palatability ratings, on a seven-point scale, of each individual item eaten and also a global rating of the palatability of the entire meal. Higher levels of palatability were found to be related to larger meal sizes, durations, and deprivation ratios, smaller satiety ratios, greater hunger, and lower depression and anxiety. The global palatability rating was found to be superior to individual item palatability ratings as a measure of the palatability of the meal. Although palatability was found to have fairly large effects on intake, it accounted for less than 2% of the variance. It was concluded that, in the natural environment, there are a large number of other powerful variables present that add variance. In addition, people tend to self-select only a restricted range of highly palatable foods. As a result, in the natural environment, the influence of palatability on intake is limited.