Gastric Satiety Research Articles

Acute Strength Exercise Decreases Satiety by Modifying Blood Cytokines Levels in Physically Active Men

Abstract Aim: Exercise elicits adaptations in several physiological systems, such as the gastrointestinal tract. We evaluated the effects of an acute strength exercise (acute-SE) on gastric satiety and its correlation with creatinine kinase (CK), lactate, and plasma cytokine levels in humans. Methods: Anthropometric parameters, body composition, muscular strength, and satiety (drink test protocol) at rest and exercise were assessed. Results: In the squat, bench press, and T-bar row exercises, we observed a significant decrease (p<0.05) in muscular strength in the second, third, and fourth sets compared with that in the first set. Compared with rest, we observed a significant increase (p<0.05) in CK and lactate levels after acute-SE. In the drink test, acute-SE significantly increased (p <0.05) the total intake, calories ingested, and a total time of ingestion. Concerning cytokines, there was a significant increase (p<0.05) after acute-SE of IL-1β and IL-6 levels at the beginning of the test and a decrease in IL-6, -10, -13, and TNF-α levels after acute-SE at the end of the test (p<0.05). There was a correlation between CK, lactate, and total intake after acute-SE (p<0.05) as well as between IL-6, 13, TNF-α, and volume ingested in the last score of the drink test after acute-SE (p<0.05). Conclusion: Acute-SE decreases satiety associated with changes in lactate, CK, and plasma cytokine levels in healthy humans.

The first of the viscoceuticals? A shear thickening gum induces gastric satiety in rats.

We examined the effect of gavage of 4 ml of a viscous shear-thickening polysaccharide solution (15% w/w) extracted from the fronds of the mamaku tree fern (Cythea medullaris) in reducing appetite and delaying gastric emptying in twenty six Sprague Dawley rats. After two weeks habituation to a pelleted chow, the rats were gavaged on alternate days with either the mamaku extract or with the same volume of deionised water for a total of five times over a period of two weeks. The body mass and food intake of each rat were determined daily and the weights of their stomach contents determined on euthanasia two hours after the final gavage. The rats gavaged with the mamaku gum consumed significantly lower quantities of chow on the day of gavage. The weights of the stomach contents of rats two hours after gavage with mamaku extract were significantly greater than those following gavage with water. The failure of the rats dosed with mamaku to lose body weight likely resulted from the overall adverse effect of gavage on food intake, the limited numbers of doses of the gum and the rebound hyperphagia on days when the rats were not gavaged. Together the results indicate that gavage with mamaku gum delayed gastric emptying with respect to that of rats dosed with water and supressed appetite for 12-24 hours after dosage.

Obesity induced suppression of gastric satiety signals are only partially reversed by dietary change

Obesity induced suppression of gastric satiety signals are only partially reversed by dietary change

Diet‐induced adaptation of vagal afferent function

Afferent signals from the stomach play an important role in inhibition of food intake during a meal. The gastric hormone ghrelin can influence gastric satiety signalling by altering the sensitivity of gastric vagal afferents. Changes in diet, including food restriction and high fat diet (HFD) alter satiety signalling. We hypothesised that the function of gastric vagal afferent endings are affected by both a period of food restriction and a high fat diet, and that the inhibitory effect of ghrelin on vagal afferents is influenced by the different feeding conditions. We found that both fasting and HFD reduced the responses of gastric vagal tension receptors to distension, but not responses of mucosal receptors to mucosal contact. We traced vagal afferents anterogradely to their terminals in the mucosa where we found they were in close apposition to ghrelin-containing cells. Ghrelin receptor mRNA was expressed in vagal afferent cell bodies of the nodose ganglia, and increased in response to caloric restriction, but decreased in HFD mice. In control mice, ghrelin decreased the sensitivity of tension but not mucosal receptors. After caloric restriction or high fat diet, ghrelin inhibited mucosal receptors, and the inhibition of mechanosensitive tension receptors was enhanced. Therefore, both caloric restriction and HFD decrease mechanosensory vagal afferent signals, and augment the inhibitory effect of ghrelin on vagal afferents, but different mechanisms mediate the short- and longer-term changes.

Ethanol-induced Coma after Therapeutic Ethanol Injection of a Hepatic Cyst

Ethanol-induced Coma after Therapeutic Ethanol Injection of a Hepatic Cyst

Review article: the gastrointestinal tract: neuroendocrine regulation of satiety and food intake

The gastrointestinal tract elicits numerous signals regulating food intake and satiety, and recently many studies have been performed to elucidate the mechanisms regulating these signals. To describe the effects of the gastrointestinal tract on satiety, satiation and food intake. A PubMed search was performed to identify and select the relevant literature using search terms including 'gastric satiety, intestine + satiety, satiation, cholecystokinin, ghrelin, peptide YY, glucagon-like peptide-1 and ileal brake'. Satiation, satiety and food intake result, among other factors, from signals originating in the stomach caused by distension and signals from the small intestine. These intestinal signals result from nutrient sensing in the gut and activate neural and humoral pathways. Activation of the distal part of the gut, the so called ileal brake, leads to reduction in hunger and food intake, and models of chronic ileal brake activation lead to massive weight loss. Gastrointestinal signals are crucial for the regulation of food intake, satiety and satiation. The ileal brake deserves special attention, as both ileal intubation studies and surgical studies demonstrate that activation of the ileal brake reduces food intake. In the surgical models, weight loss occurs without adaptation to the anorectic effects of ileal brake activation.

The effect of short‐term, low‐dose tricyclic and tetracyclic antidepressant treatment on satiation, postnutrient load gastrointestinal symptoms and gastric emptying: a double‐blind, randomized, placebo‐controlled trial

Antidepressants are commonly prescribed for patients with functional dyspepsia. However, the effect of tricyclic antidepressants on satiation and gastric emptying remains unclear, and there are no data for tetracyclic compounds. To compare the effects of nortriptyline (maximum dose: 50 mg daily) and mirtazapine (30 mg daily) vs placebo on gastric emptying, gastric satiation and postprandial symptoms after a nutrient load in healthy volunteers. Randomized, double-blind, placebo-controlled study evaluated gastric function before and after 14 days of nortriptyline (n = 13), mirtazapine (n = 13), or placebo (n = 14) in healthy volunteers. Validated methods were used to study gastric emptying ((13)C-octanoate) and satiation postnutrient drink test. The three arms were comparable with regard to age, gender, body mass index and hospital anxiety/depression scale. There were no statistically significant effects of mirtazapine or nortriptyline on gastric emptying compared to placebo (P = 0.34). Maximum tolerated volume was similar on drug and placebo (P = 0.56). Aggregate symptom score 30 min postmaximum tolerated volume after nutrient drink challenge on placebo was 132 (+/-21), vs 165 (+/-21) on mirtazapine, and 126 (+/-21) on nortriptyline 50 mg respectively (P = 0.28). Tricyclic and tetracyclic antidepressant agents do not appear to have significant effects on gastric motor or satiation postnutrient challenge in healthy individuals at the doses tested.

Comparison of Anterior Gastric Wall and Greater Gastric Curvature Invaginations for Weight Loss in Rats

Many bariatric endoscopic or surgical procedures performed today reduce gastric capacity and/or induce an early sensation of gastric satiety, alone or in combination with a distal enteric intervention. A form of prosthetic wrap of the folded stomach was used in the past for treating obesity with a high rate of prosthesis-related reintervention. Nissen gastric fundoplication used in the treatment of gastroesophageal reflux disease induces a small but significant weight loss without gastric stapling, partitioning, or prosthesis-related morbidity. We recently reported greater gastric curvature invagination without stapling, partitioning or prosthesis use, for weight loss in rats. We now compare anterior gastric wall and greater gastric curvature invaginations for weight loss. The anterior invagination would be technically easier, should it be tested in humans. 20 rats were randomized in 2 groups. The anterior gastric wall of 10 rats was invaginated in the first group (AGW). The greater gastric curvature of 10 rats was invaginated in the second group (GGC). All animals were weighed weekly for 4 weeks. They were then autopsied on the 28th day. The mean body weight of the GGC group became statistically less than the AGW group at 21 days. The mean weight of the peritesticular fat pad and the mean gastric volume were not statistically different at 28 days (autopsy). Greater gastric curvature invagination significantly reduces body weight compared to anterior gastric wall invagination at 21 days.

Lack of interaction between peripheral injection of CCK and obestatin in the regulation of gastric satiety signaling in rodents

Obestatin is a new peptide for which anorexigenic effects were recently reported in mice. We investigate whether peripheral injection of obestatin or co-injection with cholecystokinin (CCK) can modulate food intake, gastric motor function (intragastric pressure and emptying) and gastric vagal afferent activity in rodents. Obestatin (30, 100 and 300 μg/kg, i.p.) did not influence cumulative food intake for the 2 h post-injection in rats or mice nor gastric emptying in rats. In rats, obestatin (300 μg/kg) did not modify CCK (1 μg/kg, i.p.)-induced significant decrease in food intake (36.6%) and gastric emptying (31.0%). Furthermore, while rats injected with CCK (0.3 μg/kg, i.v.) displayed gastric relaxation, no change in gastric intraluminal pressure was elicited by obestatin (300 μg/kg, i.v.) pre- or post-CCK administration. In in vitro rat gastric vagal afferent preparations, 20 units that had non-significant changes in basal activity after obestatin at 30 μg responded to CCK at 10 ng by a 182% increase. These data show that obestatin neither influences cumulative food intake, gastric motility or vagal afferent activity nor CCK-induced satiety signaling

Serotonin-3 receptors in gastric mechanisms of cholecystokinin-induced satiety

our understanding of the controls of food intake has increased substantially during the last 30 years. Important in this has been the recognition of the meal as a controlled, physiologically relevant unit of energy intake. During a meal, ingested nutrients accumulate in the stomach and gradually

Gastric satiation is volumetric, intestinal satiation is nutritive

Gerry Smith's thoughtful survey in his book Satiation (1998) outlined the established principles of gastric and intestinal satiation and delineated several questions still requiring clarification. Experiments since the time of the review have addressed some of these questions. A synthesis of the principles outlined in the Gerry Smith survey and the subsequent experimental results indicates that the direct controls, or neural feedback signals from the GI tract, that limit meal size consist of gastric volumetric signals and intestinal nutritive signals. The two types of negative feedback synergize in the control of feeding, and both are carried by vagal afferents.

Central nervous system injection of dynorphin-(1-13) overrides gastric satiety factors in sheep

Signals from the gastrointestinal (GI) tract, arising during ingestion and digestion of food, are important in the termination of feeding. This study was carried out to determine whether the satiety triggered by specific GI stimuli in sheep could be reversed by central nervous system (CNS) administration of dynorphin, a putative endogenous kappa-opiate receptor ligand, which has been shown to be a potent feed-intake stimulant in many species. Rumen distension and increased intraruminal concentration of propionic acid (an energy substrate produced during fermentation in the rumen) both significantly decreased feed intake in fasted sheep. When either of these stimuli were combined with continuous 60-min lateral cerebroventricular injection of [D-Ala2]dynorphin A-(1-13) (0.32 nmol/min), feed intake returned to control levels. Increasing feed intake in food-producing animals is an important way of improving production efficiency. The findings of these experiments illustrate how manipulation of a CNS opioid system can modify the effects of feed intake-limiting factors generated by ingestion of a meal, thereby promoting greater feed intake.

Gastric balloons: A plea for sanity in the midst of balloonacy

Intragastric balloons have been suggested as a treatment for severe obesity, a degree of obesity associated with a relatively greater eating disorder or lack of control of energy balance. The premises that 250–500-ml balloons are able to simulate “satiety” in a 1700-ml stomach sufficiently to cause weight loss, that the stomach will not stretch to accommodate such a besoar (with or without ulcerating), and that behavioral modification is cost-effective in weight control in this population have not been corroborated. Experience from gastric restrictive surgery has demonstrated the conceptual failure of gastric satiety as a means of achieving and sustaining weight loss in a substantial percentage of morbidly obese patients. Other methods are needed to reduce the increased morbidity and mortality of severe obesity.

Endogenous and exogenous cholecystokinin may reduce food intake by different mechanisms.

To determine whether exogenous cholecystokinin (CCK) and endogenous CCK evoke different gastrointestinal motor responses, we investigated the motility induced by CCK by use of standard manometric methods. Injection (ip) of 500 ng/kg CCK caused immediate profound gastric inhibition and duodenal phasic excitation that did not resemble the postprandial pattern. Similar profound gastric inhibition has been associated with nausea. The contribution of endogenous CCK to the fed pattern of motility was investigated using proglumide; intraperitoneal injection of the antagonist before feeding caused no change, but injection before a second meal induced a decrease (P less than 0.025, n = 6) in gastric pressure with no accompanying duodenal change. This suggests that CCK causes an increase in gastric pressure that could result from a delay in gastric emptying. In support of this hypothesis, we have previously demonstrated, by use of proglumide, that endogenous CCK delays gastric emptying. Therefore exogenous CCK may reduce food intake by evoking an abnormal gastrointestinal motor pattern that may induce malaise, whereas endogenous CCK may decrease food intake by delaying gastric emptying, thus prolonging gastric satiety signals.

Gut peptides and food in the gut produce similar satiety effects

We compared the satiety effects and mechanisms of action of food stimuli delivered to anatomically restricted areas of the gut with the satiety effects and mechanisms of action of the gut peptides cholecystokinin (CCK) and bombesin (BBS). When food is limited to contact with the pregastric and gastric gut surfaces at a test meal, rats stop eating and display the fixed sequence of postprandial behaviors which characterizes normal satiety. This “gastric satiety” effect is unaffected by total abdominal vagotomy. Intraperitoneal administration of BBS produces a large, specific, and dose-related inhibition of food intake at a test meal; this action, like the gastric satiety effect of food, is unaffected by total abdominal vagotomy. Since a BBS-like peptide is present in high concentration in the stomach, these parallels between gastric satiety and BBS-induced satiety suggest that an endogenous BBS-like peptide plays a role in gastric satiety. When small amounts of food are infused directly into the small intestine of sham feeding rats, they stop eating and display the behavioral satiety sequence. This “intestinal satiety” effect requires the synergistic input of oropharyngeal food stimulation in close temporal association. Intraperitoneal administration of CCK alone to sham feeding rats stops eating and elicits the behavioral satiety sequence; this action, like the intestinal satiety effect of food, requires the synergistic input of oropharyngeal food stimulation in close temporal association. Since CCK is present in high concentration in the upper small intestine, and is released into the circulation by food at this site, the parallels between intestinal satiety and CCK-induced satiety suggest that endogenous CCK plays a role in intestinal satiety.