Response Satiation Research Articles

Gut microbiota depletion affects caecal satiety hormones expression and satiation in response to western diet

Gut microbiota depletion affects caecal satiety hormones expression and satiation in response to western diet

Intact vagal gut-brain signalling prevents hyperphagia and excessive weight gain in response to high-fat high-sugar diet.

AimThe tools that have been used to assess the function of the vagus nerve lack specificity. This could explain discrepancies about the role of vagal gut‐brain signalling in long‐term control of energy balance. Here we use a validated approach to selectively ablate sensory vagal neurones that innervate the gut to determine the role of vagal gut‐brain signalling in the control of food intake, energy expenditure and glucose homoeostasis in response to different diets.MethodsRat nodose ganglia were injected bilaterally with either the neurotoxin saporin conjugated to the gastrointestinal hormone cholecystokinin (CCK), or unconjugated saporin as a control. Food intake, body weight, glucose tolerance and energy expenditure were measured in both groups in response to chow or high‐fat high‐sugar (HFHS) diet. Willingness to work for fat or sugar was assessed by progressive ratio for orally administered solutions, while post‐ingestive feedback was tested by measuring food intake after an isocaloric lipid or sucrose pre‐load.ResultsVagal deafferentation of the gut increases meal number in lean chow‐fed rats. Switching to a HFHS diet exacerbates overeating and body weight gain. The breakpoint for sugar or fat solution did not differ between groups, suggesting that increased palatability may not drive HFHS‐induced hyperphagia. Instead, decreased satiation in response to intra‐gastric infusion of fat, but not sugar, promotes hyperphagia in CCK‐Saporin‐treated rats fed with HFHS diet.ConclusionsWe conclude that intact sensory vagal neurones prevent hyperphagia and exacerbation of weight gain in response to a HFHS diet by promoting lipid‐mediated satiation.

Impact of physical activity level and dietary fat content on passive overconsumption of energy in non-obese adults

BackgroundPassive overconsumption is the increase in energy intake driven by the high-fat energy-dense food environment. This can be explained in part because dietary fat has a weaker effect on satiation (i.e. process that terminates feeding). Habitually active individuals show improved satiety (i.e. process involved in post-meal suppression of hunger) but any improvement in satiation is unknown. Here we examined whether habitual physical activity mitigates passive overconsumption through enhanced satiation in response to a high-fat meal.MethodsTwenty-one non-obese individuals with high levels of physical activity (HiPA) and 19 individuals with low levels of physical activity (LoPA) matched for body mass index (mean = 22.8 kg/m2) were recruited. Passive overconsumption was assessed by comparing ad libitum energy intake from covertly manipulated high-fat (HFAT; 50% fat) or high-carbohydrate (HCHO; 70% carbohydrate) meals in a randomized crossover design. Habitual physical activity was assessed using SenseWear accelerometers (SWA). Body composition, resting metabolic rate, eating behaviour traits, fasting appetite-related peptides and hedonic food reward were also measured.ResultsIn the whole sample, passive overconsumption was observed with greater energy intake at HFAT compared to HCHO (p < 0.01), without any differences between activity groups (p > 0.05). SWA confirmed that HiPA were more active than LoPA (p < 0.01). HiPA had lower body fat and greater fat-free mass than LoPA (p < 0.05 for both) but did not differ in resting metabolic rate, eating behaviour traits, appetite-related peptides or food reward (p > 0.05 for all).ConclusionsNon-obese individuals with high or low physical activity levels but matched for BMI showed similar susceptibility to passive overconsumption when consuming an ad libitum high-fat compared to a high-carbohydrate meal. This occurred despite increased total daily energy expenditure and improved body composition in HiPA. Greater differences in body composition and/or physical activity levels may be required to impact on satiation.

Su2072 The Bitter Taste Receptor Agonist Denatonium Benzoate Alters Intragastric Pressure Profiles During Nutrient Drink Test in Healthy Volunteers

Background: Bitter taste receptors are expressed in the stomach and the duodenum but their function is unclear. We assessed the effects of a potent bitter tastant on intragastric pressure (IGP, a measure of gastric accommodation) and satiation in response to a liquid meal. Methods: We conducted a single-blind crossover trial of 16 healthy volunteers (8 female; mean age 30±2 yrs; mean BMI 23.8±0.9) given 1 μmol/kg (0.1mL/kg) of a 10mM denatonium benzoate (DB) solution or placebo in random order on separate occasions at least 1 week apart. First, both a standard high-resolution manometry (HRM) catheter and a 4mm feeding catheter were positioned intra-gastrically via the nose with location confirmed by detection of the lower esophageal sphincter (LES) and/or fluoroscopy. After an adjustment period, DB or placebo was administered through the feeding catheter. After 30 min, nutrient drink (ND; 30% fat, 42% carbohydrate, 28% protein) was infused into the stomach at 60mL/ min until maximum satiation, at which point it was stopped. Satiation (scored on 0-5 scale) was assessed every minute. IGP was measured as average pressure over 5 channels in the proximal stomach at least 1cm below the LES, with 5-minute baseline measured 10 minutes before ND start. Outcomes were compared with paired t-test or Wilcoxon test as appropriate. All data are expressed as mean ± SEM unless otherwise stated. Results: Baseline IGP prior to ND infusion was similar between DB and placebo (Table). After DB treatment, the nutrientinduced drop in IGP from baseline (baseline-nadir) was inhibited (p=0.056) and delayed (p=0.007) compared to placebo. The total area under the IGP curve during nutrient infusion was significantly smaller after DB (p=0.021), consistent with attenuation of the gastric accommodation response (Figure). Satiation score at nadir IGP tended to be higher after DB vs placebo (p=0.087). The volume of ND ingested and the duration of the nutrient infusion were not statistically different between groups. No adverse effects were noted after either agent. Conclusion: The potent bitter tastant DB inhibits gastric accommodation to a meal, independently of taste receptor stimulation in the tongue. Themechanism and receptors involved in this action warrant further study.

GLP-1 analogues as a new treatment option for hypothalamic obesity in adults: report of nine cases

Patients with hypothalamic pathology often develop morbid obesity, causing severe metabolic alterations resulting in increased morbidity and mortality. Glucagon-like peptide-1 (GLP-1) analogues improve glycaemic control in type 2 diabetic patients and cause weight loss in obese patients by yet unknown mechanisms. Here we tested whether GLP-1 analogues were also effective in the treatment of obesity and associated metabolic alterations in patients with hypothalamic disease. Nine patients (eight with type 2 diabetes mellitus) with moderate to severe hypothalamic obesity were treated with GLP-1 analogues for up to 51 months. Body weight, homeostasis model assessment - insulin resistance (HOMA-IR), HbA1c and lipids were assessed. Eight patients experienced substantial weight loss (-13.1±5.1 kg (range -9 to -22)). Insulin resistance (HOMA-IR -3.2±3.5 (range -9.1 to 0.8)) and HbA1c values (-1.3±1.4% (range -4.5 to 0.0)) improved under treatment (24.3±18.9 months (range 6 to 51)). Five patients reported increased satiation in response to the treatment. Two of the eight patients complained about nausea and vomiting and one of them abandoned therapy because of sustained gastrointestinal discomfort after 6 months. One patient suffered from intolerable nausea and vomiting and discontinued treatment within 2 weeks. GLP-1 analogues can cause substantial and sustained weight loss in obese patients with hypothalamic disease. This offers a new approach for medical treatment of moderate to severe hypothalamic obesity and associated metabolic alterations.

Stressful Events in Early Life Lead to Aberrant Ghrelin and Appetite Regulation to Stress in Adulthood

Background. Stressful events in early life pre- dispose to the development of eating disorders in adulthood. This study investigates how neonatal maternal separation (NMS) affects satiety and ghrelin secretion in adulthood. Methods. Sprague-Dawley rats underwent NMS and con- trols were without NMS. Experiments were conducted on day 60: (1) water avoidance stress (WAS); (2) feeding after overnight fasting; (3) feeding after overnight fasting and WAS. Blood samples, gastric and hypothalamic tissues expression were collected for ghrelin analysis. Results. (1) MS rats had a higher basal ghrelin. After WAS, MS rats had enhanced ghrelin. (2) A higher initial calorie intake and lower postprandial gastric ghrelin protein in MS are observed without difference in overall calorie intake. (3) MS had symptoms of binge eating and early satiation. Overall reduction of calorie intake was observed until 48 hours in MS. Conclusion. Stressful events in early life led to aberrant ghrelin profile and early satiation in response to stressful experience in adulthood.

Lack of CCK1R reduces satiation in response to dietary fat

Food intake is regulated by signals coming from the gastrointestinal tract and by the brain. There is good evidence that long term consumption of a high fat diet leads to desensitization in detection of dietary lipid, possibly by a decrease in vagal afferent sensitivity to cholecystokinin (CCK). We tested the hypothesize that CCK acting at CCK1 receptors is essential for response to a high fat diet using CCK1R−/ − mice. CCK1R−/ − mice or their wildtypes 129sv were maintained on isocaloric high fat (HF) or isocaloric normal fat (NF) diets for 4 weeks and meal pattern analysis was performed using the Habitest system. There was no significant difference in overall daily food intake or weight gain between the two groups. The CCK1R−/ − mice fed either the NF or the HF diet consumed significantly more food in the first meal compared to the wildtype controls (64% and 60% of total food intake vs. 51% and 46%). During the second meal, the CCK1R−/ − mice fed the HF diet consumed twice as much food as the controls; there was no difference between CCK1R−/ − or wildtype mice fed the NF diet. These results indicate that CCK1R−/ − mice fed a high fat diet are less satiated compared to wildtype mice. We conclude that the CCK1R is involved in satiation in response to a high fat diet.

The Use of Suggestion and Behavioral Methods in the Treatment of Aerophagia

Aerophagia is a stereotypic air swallowing that is rarely observed among non retarded children and adults. A possible explanation for aerophagia lies in the concept of automatic reinforcement. Repeated air swallowing produces outcomes that, if perceived as pleasant or relieving, could serve as reinforcing stimuli. A number of behavioral approaches have been used to reduce or eliminate this symptom. Partial positive results have been reported using response satiation, overcorrecting, DRO, response cost and contingent visual screening. Two cases of treating aerophagia in children are presented. In the first, treatment combined suggestions, covert desensitization and positive reinforcement of non aerophagic behavior. Four meetings resulted in complete elimination of the symptom. In the second case, the child was taught a response that was incompatible with air swallowing. Differential reinforcements were used for the “correct” versus the aerophagic response. Daily practice of 2-4 hours resulted in meaningful reduction of the aerophagic response. Treatment is continuing meanwhile, using the same procedure.

Using decelerative contingencies to reduce the self-injurious behavior of people with multiple handicaps: The effects of response satiation?

The response satiation model of instrumental performance was used to establish contingencies to reduce the self-injurious behavior (SIB) of two adults with profound mental retardation and multiple handicaps. In Experiment 1, withdrawal designs indicated behavior reductions of 68% and 82%, respectively, when contingencies were implemented that required the participants to engage in leisure activities at greater than baseline levels if they continued to perform the SIB at their baseline level. Experiment 2 involved the transfer of the treatment to the participants' respective living areas using staff as trainers. The largest reductions in behavior were associated with treatment packages that contained response satiation contingencies, and generality of the treatment packages across locations and trainers occured. The limitations of this study as an analysis of response satiation theory were noted; however, it was concluded that the response satiation approach to establishing contingencies for reducing SIB was worthy of future investigation.

Clinical effects of response deprivation and response satiation procedures

The present study used procedures prescribed by the response deprivation/satiation hypothesis to modify the occurrence of clinically relevant behaviors in two hospitalized, adult schizophrenics. By arranging contingencies which satisfied the conditions for response deprivation and response satiation, the same contingent response produced clinically significant increases in appropriate social behaviors and clinically significant decreases in inappropriate behaviors, respectively, in both participants. These results extend the findings of Konarski, Crowell, Johnson, and Whitman (1982) by demonstrating the applied usefulness of response deprivation procedures with a different clinical population. Moreover, this is the first study demonstrating the clinical usefulness of response satiation procedures.

Response deprivation and response satiation as determinants of instrumental performance: Some data and theory

Sixteen human subjects were presented with an instrumental task in which pressing a button to produce a visual stimulus was followed by an auditory stimulus. Half of the subjects were assigned to a condition under which pressing the button at the subject’s operant level produced less of the auditory stimulus than the subject would normally choose to receive. For the others, pressing the button at operant level produced more of the auditory stimulus than the subject would choose. Subjects in the former condition showed increases in instrumental performance; those in the latter showed decreases. The results indicated that the rewarding or punishing effects of an event depend upon the relation of the instrumental contingency to the subject’s unconstrained behavior.

Semantic satiation and word association

Forty Ss gave word associations to 12 common English words after undergoing a semantic satiation treatment for six of the words. For half the Ss the satiation treatment was of the stimulus material in the word association test while half were satiated for responses (the most common word association to items on the list underwent satiation treatment.) Satiation treatment retarded association speed when stimuli were satiated but had a tendency to facilitate association speed when response satiation was attempted.

Meaning change and retroactive effects following low meaningful stimulus and response satiation

Retroactive effects of satiation treatment were studied using nonsense verbal items. Response recall was facilitated by interpolated response satiation but was not affected by stimulus satiation. Some evidence for an interaction of instructions with regression effect was noticed in the case of Ss’ semantic ratings.

Effects of variations in amount of verbal repetition on meaning and paired-associate learning

The effects of varying the amount of continuous verbal repetition on meaning change and learning were investigated in the present experiment. Six groups of 10 Ss each were matched on the basis of trials to learn an initial paired-associate learning task. In the main test, three of these groups served as experimental groups and three as controls. An experimental and a control group were assigned to 5-, 15-, and 25-sec repetition conditions. All groups learned a second paired-associate list, but immediately before learning, the three experimental groups were given the repetition treatment for words that were to be used as response members for periods of either 5, 15, or 25 sec, and the corresponding control groups were given the repetition treatment for words that were not to be used as response members. It was found that: (a) the over-all effect of the repetition treatment is to reduce the intensity of the meaning of these highly meaningful words; (b) no reliable differences were obtained between the 5-, 15-, and 25-sec repetition conditions; (c) the rate of learning is slower after response satiation than after satiation of control words; and (d) the amounts of repetition do not produce any significant change in the rate of learning.

Paired-associate learning as a function of stimulus and response satiation.

Two experiments, one using highly meaningful pairs and the other using low meaningful pairs, were performed to determine the effects of stimulus and response satiation in paired‐associate learning. Results indicated that: (a) satiation treatment of highly meaningful words produces a decrease in their meaning, whereas similar treatment of low meaningful words does not produce significant semantic change; (b) with highly meaningful S‐R pairs, pre‐learning satiation of either the stimulus or the response words retards subsequent learning, whereas with low meaningful S—R pairs only stimulus satiation produces such retardation. Results are explained in terms of two factors involved in the satiation procedure: a meaning decrement and the development of a word‐word habit. The importance of these two factors for stimulus and response positions is discussed.