Gastric and duodenal features of meals mediate controls of liquid gastric emptying during fill in rhesus monkeys

1999 ◽  
Vol 277 (5) ◽  
pp. R1282-R1290 ◽  
Author(s):  
Timothy H. Moran ◽  
Susan Knipp ◽  
Gary J. Schwartz
Keyword(s):  
Gastric Emptying ◽  
Negative Feedback ◽  
Glucose Concentration ◽  
Rhesus Monkeys ◽  
Physiological Saline ◽  
Gastric Volume ◽  
Feedback Controls ◽  
Lower Glucose ◽  
Concentration Dependency

To study the dynamics of liquid gastric emptying in rhesus monkeys under conditions that simulated gastric fill during a meal, we measured the gastric emptying of liquid glucose at various concentrations and volumes when administered intragastrically at rates ranging from 12.5 to 37.5 ml/min. Glucose gastric emptying was faster during than following the period of gastric fill. At a single glucose concentration, volume infused rather than the rate of filling determined the volume emptied. Lower glucose concentrations emptied more slowly than physiological saline. As glucose concentration increased, emptying during fill slowed. Duodenal glucose infusions greatly slowed the rate of saline emptying during fill, demonstrating duodenal feedback control. Although casein hydrolosate emptied more rapidly than glucose, the dynamics of volume and concentration dependency and the role of duodenal feedback were similar. These data reveal that both gastric volume and duodenal negative feedback controls important in gastric emptying following stomach filling also contribute to its control during fill.

scholarly journals Gastric Sensory and Motor Functions and Energy Intake in Health and Obesity—Therapeutic Implications

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1158
Author(s):  
Lizeth Cifuentes ◽  
Michael Camilleri ◽  
Andres Acosta
Keyword(s):  
Energy Consumption ◽  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Volume ◽  
Obesity Management ◽  
Bariatric Endoscopy ◽  
Motor Functions ◽  
Therapeutic Implications ◽  
Intestinal Functions

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.

Endogenous cholecystokinin in the control of gastric emptying of liquid nutrient loads in rhesus monkeys

1993 ◽  
Vol 265 (2) ◽  
pp. R371-R375 ◽  
Author(s):  
T. H. Moran ◽  
P. J. Ameglio ◽  
G. J. Schwartz ◽  
H. J. Peyton ◽  
P. R. McHugh
Keyword(s):  
Gastric Emptying ◽  
Rhesus Monkeys ◽  
Physiological Saline ◽  
Inhibitory Effect ◽  
Intragastric Administration ◽  
Nutrient Loads ◽  
Cck Receptor Antagonist ◽  
Quantitative Contribution ◽  
The Brain ◽  
Cck Antagonist

A role for the brain/gut peptide cholecystokinin (CCK) in the control of gastric emptying has been proposed. In the present studies, we have used a potent type A CCK-receptor antagonist (devazepide) to examine the quantitative contribution of endogenously released CCK in the control of liquid gastric emptying of 100 ml lipid, protein, and carbohydrate test loads in rhesus monkeys. Emptying was studied in conscious monkeys equipped with chronic indwelling gastric cannulas. Prior intragastric administration of devazepide (1.0-320 micrograms/kg) differentially affected the 10-min emptying of glucose (0.125/ml), peptone (4.5%), and Intralipid (4.5%). Glucose emptying was not affected by any dose of the CCK antagonist. The emptying of peptone was accelerated by doses of 10 micrograms/kg or higher. This effect, however, was only partial and plateaued at a dose of 100 micrograms/kg. The gastric emptying of Intralipid was accelerated at a dose of 32 micrograms/kg, and the inhibitory effect of the Intralipid was completely eliminated at a dose of 320 micrograms/kg. At this dose of devazepide, the Intralipid test meal emptied from the stomach at the same rate as physiological saline. These data demonstrate that in rhesus monkeys endogenously released CCK 1) does not play a role in the control of glucose emptying, 2) is a partial mediator of the inhibitory action of peptone on gastric emptying, and 3) is the primary inhibitory mediator in the control of the gastric emptying of Intralipid.

Inhibition of gastric emptying and feeding by fenfluramine

1986 ◽  
Vol 250 (5) ◽  
pp. R764-R769 ◽  
Author(s):  
P. H. Robinson ◽  
T. H. Moran ◽  
P. R. McHugh
Keyword(s):  
Gastric Emptying ◽  
Macaca Mulatta ◽  
Normal Saline ◽  
Rhesus Monkeys ◽  
Glucose Solution ◽  
Gastric Volume ◽  
Dilution Technique ◽  
Glucose Test ◽  
Anorectic Agent ◽  
Initial Bolus

To assess the mechanism by which the anorectic agent fenfluramine influences feeding, we examined in Macaca mulatta the effect of intragastric fenfluramine (2 mg/kg) on both feeding and the gastric emptying of saline and glucose test meals. Gastric emptying was measured by the dye-dilution technique, using chronic indwelling intragastric cannulas. The emptying of normal saline was inhibited by fenfluramine as was the initial bolus phase of the emptying of glucose. In contrast, the subsequent controlled phase of glucose emptying was unaffected in two out of four animals, slightly inhibited in one, and strongly inhibited in only one monkey. Rhesus monkeys trained to drink a glucose solution to satiety drank, on average, 21% less after fenfluramine. The emptying of the consumed glucose solution from the stomach was reduced by 39%, whereas gastric volume at satiety was reduced by only 10%. The reduction of intake was strongly related to the degree of inhibition of gastric emptying. These results support an important role for the inhibition of gastric emptying in fenfluramine-induced suppression of feeding.

Gastric branch vagotomy blocks nutrient and cholecystokinin-induced suppression of gastric emptying

1993 ◽  
Vol 264 (3) ◽  
pp. R630-R637 ◽  
Author(s):  
G. J. Schwartz ◽  
G. Berkow ◽  
P. R. McHugh ◽  
T. H. Moran
Keyword(s):  
Gastric Emptying ◽  
Intraperitoneal Administration ◽  
Physiological Saline ◽  
Male Rats ◽  
Caloric Content ◽  
Vagus Nerves ◽  
Acidic Solutions ◽  
Caloric Density ◽  
The Brain

A role for the vagus nerve in the emptying of intragastric nutrients and the gastric inhibitory actions of the brain-gut peptide cholecystokinin (CCK) has been proposed. To directly assess the role of the gastric vagal branches in these actions, we compared the emptying of 5-ml nutrient and nonnutrient gastric loads in male rats in which both branches of the gastric vagus nerves were cut (GVX, n = 7) with emptying in surgical control (n = 8) rats. Gastric emptying of saline was also examined in both groups after intraperitoneal administration of 8 micrograms/kg CCK. In control rats, high osmolarity, low pH, and caloric density all significantly decreased gastric emptying compared with the emptying of physiological saline. In addition, fat (oleic acid) and protein (peptone) loads emptied significantly more slowly than isocaloric carbohydrate (glucose) loads. Gastric branch vagotomy completely blocked the suppression of emptying produced by fat, protein, carbohydrate, and acid loads. In addition, GVX attenuated the ability of hyperosmotic nutrient and nonnutrient loads to inhibit emptying to the same degree, irrespective of their caloric content. Finally, in intact rats, CCK significantly inhibited the emptying of physiological saline, and gastric vagotomy abolished this suppression. Taken together, these results are consistent with the proposals that 1) the controlled emptying of caloric, hyperosmotic, and acidic solutions is dependent on gastric vagal branches, and 2) exogenous CCK relies on an intact vagal pathway in the control of gastric emptying.

Interactions between gastric volume and duodenal nutrients in the control of liquid gastric emptying

1999 ◽  
Vol 276 (4) ◽  
pp. R997-R1002 ◽  
Author(s):  
Timothy H. Moran ◽  
James B. Wirth ◽  
Gary J. Schwartz ◽  
Paul R. McHugh
Keyword(s):  
Gastric Emptying ◽  
Adult Male ◽  
Rhesus Monkeys ◽  
Gastric Volume ◽  
Glucose Load ◽  
The Relationship ◽  
Male Rhesus

We examined the relationships between gastric volume and duodenal glucose load in the regulation of gastric emptying in adult male rhesus monkeys. Intragastric glucose loads (0.125 g/ml) of volumes ranging from 150 to 375 ml empty from the stomach at the same rate from 20 to 120 min. However, to achieve these equivalent emptying rates, progressively larger volumes were emptied in the initial 20 min with increasing gastric volume. Duodenal glucose infusions dose dependently inhibited the 10-min emptying of various volumes of intragastric saline. Although increasing gastric volume resulted in increased emptying, duodenal glucose right-shifted the relationship between initial gastric volume and volume emptied. These data demonstrate that liquid nutrient gastric emptying represents an interaction between gastric volume and nutrient-induced duodenal feedback. For controlled duodenal caloric delivery rates to be established, sufficient nutrient emptying must occur to increase the magnitude of duodenal feedback to withhold a given gastric volume.

scholarly journals Mechanistic role of antioxidants in rescuing delayed gastric emptying in high fat diet induced diabetic female mice

2021 ◽  
Vol 137 ◽  
pp. 111370
Author(s):  
Chethan Sampath ◽  
Derek Wilus ◽  
Mohammad Tabatabai ◽  
Michael L. Freeman ◽  
Pandu R. Gangula
Keyword(s):  
Gastric Emptying ◽  
High Fat Diet ◽  
Delayed Gastric Emptying ◽  
High Fat ◽  
Female Mice

scholarly journals Suppression of personality variation in boldness during foraging in three-spined sticklebacks

2021 ◽  
Vol 75 (4) ◽  
Author(s):  
Hannah E. A. MacGregor ◽  
Aislinn Cottage ◽  
Christos C. Ioannou
Keyword(s):  
Negative Feedback ◽  
Risk Taking ◽  
Positive Feedback ◽  
Gasterosteus Aculeatus ◽  
Control Treatment ◽  
Refuge Use ◽  
Individual Level ◽  
Behavioural Type ◽  
State Behaviour

Abstract Consistent inter-individual variation in behaviour within a population, widely referred to as personality variation, can be affected by environmental context. Feedbacks between an individual’s behaviour and state can strengthen (positive feedback) or weaken (negative feedback) individual differences when experiences such as predator encounters or winning contests are dependent on behavioural type. We examined the influence of foraging on individual-level consistency in refuge use (a measure of risk-taking, i.e. boldness) in three-spined sticklebacks, Gasterosteus aculeatus, and particularly whether changes in refuge use depended on boldness measured under control conditions. In the control treatment trials with no food, individuals were repeatable in refuge use across repeated trials, and this behavioural consistency did not differ between the start and end of these trials. In contrast, when food was available, individuals showed a higher degree of consistency in refuge use at the start of the trials versus controls but this consistency significantly reduced by the end of the trials. The effect of the opportunity to forage was dependent on behavioural type, with bolder fish varying more in their refuge use between the start and the end of the feeding trials than shyer fish, and boldness positively predicted the likelihood of feeding at the start but not at the end of the trials. This suggests a state-behaviour feedback, but there was no overall trend in how bolder individuals changed their behaviour. Our study shows that personality variation can be suppressed in foraging contexts and a potential but unpredictable role of feedbacks between state and behaviour. Significance statement In this experimental study, we examined how foraging influences consistency in risk-taking in individual three-spined sticklebacks. We show that bolder individuals become less consistent in their risk-taking behaviour than shyer individuals during foraging. Some bolder individuals reinforce their risk-taking behaviour, suggesting a positive feedback between state and behaviour, while others converge on the behaviour of shyer individuals, suggesting a negative feedback. In support of a role of satiation in driving negative feedback effects, we found that bolder individuals were more likely to feed at the start but not at the end of the trials. Overall, our findings suggest that foraging can influence personality variation in risk-taking behaviour; however, the role of feedbacks may be unpredictable.

scholarly journals Smad2/3 Activation Regulates Smad1/5/8 Signaling via a Negative Feedback Loop to Inhibit 3T3-L1 Adipogenesis

2021 ◽  
Vol 22 (16) ◽  
pp. 8472
Author(s):  
Senem Aykul ◽  
Jordan Maust ◽  
Vijayalakshmi Thamilselvan ◽  
Monique Floer ◽  
Erik Martinez-Hackert
Keyword(s):  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Adipose Tissues ◽  
Family Growth ◽  
Simultaneous Activation ◽  
Adipocyte Hypertrophy ◽  
Adipocyte Development ◽  
Energy Surplus

Adipose tissues (AT) expand in response to energy surplus through adipocyte hypertrophy and hyperplasia. The latter, also known as adipogenesis, is a process by which multipotent precursors differentiate to form mature adipocytes. This process is directed by developmental cues that include members of the TGF-β family. Our goal here was to elucidate, using the 3T3-L1 adipogenesis model, how TGF-β family growth factors and inhibitors regulate adipocyte development. We show that ligands of the Activin and TGF-β families, several ligand traps, and the SMAD1/5/8 signaling inhibitor LDN-193189 profoundly suppressed 3T3-L1 adipogenesis. Strikingly, anti-adipogenic traps and ligands engaged the same mechanism of action involving the simultaneous activation of SMAD2/3 and inhibition of SMAD1/5/8 signaling. This effect was rescued by the SMAD2/3 signaling inhibitor SB-431542. By contrast, although LDN-193189 also suppressed SMAD1/5/8 signaling and adipogenesis, its effect could not be rescued by SB-431542. Collectively, these findings reveal the fundamental role of SMAD1/5/8 for 3T3-L1 adipogenesis, and potentially identify a negative feedback loop that links SMAD2/3 activation with SMAD1/5/8 inhibition in adipogenic precursors.

Reflux aspiration associated with oesophageal dysmotility but not delayed liquid gastric emptying

2020 ◽  
Author(s):  
Oleksandr Khoma ◽  
Maite Jeanne Mendu ◽  
Amita Nandini Sen ◽  
Hans Van der Wall ◽  
Gregory Leighton Falk
Keyword(s):  
Gastric Emptying ◽  
Reflux Disease ◽  
Inclusion Criteria ◽  
Treatment Resistant ◽  
Oesophageal Motility ◽  
Oesophageal Manometry ◽  
Oesophageal Dysmotility ◽  
The Relationship ◽  
Clinical Subtype

Abstract Introduction Severe oesophageal dysmotility is associated with treatment resistant reflux and pulmonary reflux aspiration. Delayed solid gastric emptying (SGE) has been associated with oesophageal dysmotility, however the role of delayed liquid gastric emptying (LGE) in the pathophysiology of severe reflux disease remains unknown. The purpose of this study is to examine the relationship between delayed LGE, reflux aspiration and oesophageal dysmotility. Methods Data was extracted from a prospectively populated database of patients with severe treatment resistant gastro-oesophageal reflux disease (GORD). All patients with validated reflux aspiration scintigraphy (RASP) and oesophageal manometry were included in the analysis. Patients were classified by predominant clinical subtype as gastro-oesophageal (GOR) or laryngo-pharyngeal (LPR) reflux. LGE time of 22 minutes or longer was considered delayed. Results Inclusion criteria were met by 631 patients. Normal LGE time was found in 450 patients, whilst 181 had evidence of delayed LGE. Mean liquid half-clearance was 22.81min. Refux aspiration was evident in 240 patients (38%). Difference in the aspiration rates between delayed LGE (42%) and normal LGE (36%) was not significant (p=0.16). Severe ineffective oesophageal motility (IOM) was found in 70 patients (35%) and was independent of LGE time. Severe IOM was strongly associated with reflux aspiration (p<0.001). GOR dominant symptoms were more common in patients with delayed LGE (p=0.03). Conclusion Severe IOM was strongly associated with reflux aspiration. Delayed LGE is not associated with reflux aspiration or severe IOM. Delayed LGE is more prevalent in patients presenting with GOR dominant symptoms.

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