Gastric distension, gastric capacity, gastric balloons, and food intake

2019 ◽  
Vol 208 ◽  
pp. 112560 ◽  
Author(s):  
Allan Geliebter
Keyword(s):  
Food Intake ◽  
Gastric Distension ◽  
Gastric Capacity

Interaction of GLP-1 with gastric distension in regulating food intake and satiety in humans

2001 ◽  
Vol 120 (5) ◽  
pp. A208-A208
Author(s):  
L DEGEN ◽  
D MATZINGER ◽  
B FISCHER ◽  
F ZIMMERLI ◽  
M KNUPP ◽  
...  
Keyword(s):  
Food Intake ◽  
Gastric Distension

Effect of gastric distension on food intake and satiety in healthy human subjects

2000 ◽  
Vol 118 (4) ◽  
pp. A1071 ◽  
Author(s):  
Daniel Matzinger ◽  
Lukas Degen ◽  
Daniel Fronterotta ◽  
Christoph Beglinger
Keyword(s):  
Food Intake ◽  
Human Subjects ◽  
Gastric Distension ◽  
Healthy Human ◽  
Healthy Human Subjects

Capsaicin attenuates hindbrain neuron responses to circulating cholecystokinin

1989 ◽  
Vol 257 (5) ◽  
pp. R1162-R1168 ◽  
Author(s):  
R. C. Ritter ◽  
S. Ritter ◽  
W. R. Ewart ◽  
D. L. Wingate
Keyword(s):  
Food Intake ◽  
Sensory Neurons ◽  
Gastric Distension ◽  
Extracellular Recordings ◽  
Cholecystokinin Octapeptide ◽  
Unmyelinated Axons ◽  
Sensory Modalities ◽  
Afferent Inputs ◽  
Dorsal Hindbrain ◽  
The Brain

Capsaicin is a neurotoxin that destroys small sensory neurons with unmyelinated axons, including a subpopulation of vagal sensory neurons. Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension. However, both gastric distension and intravascular CCK alter the discharge of dorsal hindbrain neurons by a vagal mechanism. Therefore, it is plausible that some hindbrain neurons receive convergent input from capsaicin-sensitive vagal neurons that are responsive to CCK and also from capsaicin-insensitive neurons that are responsive to gastric distension. To investigate this possibility we made extracellular recordings from gastric distension-responsive hindbrain neurons during intra-arterial cholecystokinin octapeptide (CCK-8) administration in anesthetized intact and capsaicin-pretreated rats. We found that capsaicin-pretreated rats exhibit attenuated neuronal discharge responses to CCK-8 but not to gastric distension. These results are consistent with the existence of convergent CCK-sensitive and gastric distension-sensitive afferent inputs to hindbrain neurons and suggest that various gastrointestinal sensory modalities may be communicated to the brain by populations of neurons that can be distinguished by their sensitivity to neurotoxins.

Gastric loads potentiate inhibition of food intake produced by a cholecystokinin analogue

1991 ◽  
Vol 261 (5) ◽  
pp. R1141-R1146 ◽  
Author(s):  
G. J. Schwartz ◽  
L. A. Netterville ◽  
P. R. McHugh ◽  
T. H. Moran
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Threshold Dose ◽  
Gastric Distension ◽  
Cck Receptors ◽  
Load Combination ◽  
Glucose Intake ◽  
Dose Dependent Fashion ◽  
Inhibit Food Intake ◽  
Long Acting

We have proposed that cholecystokinin's (CCK) inhibition of gastric emptying contributes to its ability to inhibit food intake. To directly test this hypothesis in rats, the effect of the presence of a 5-ml gastric saline load on the ability of a long-acting cholecystokinin analogue U-67827E (0.1-10.0 nmol/kg) to inhibit intake of a 0.5 kcal/ml glucose solution was measured. The CCK analogue alone inhibited intake at a threshold dose of 2.5 nmol/kg. Although lower doses of the CCK analogue alone had no effect on subsequent glucose intake, when combined with the gastric load such doses did significantly inhibit intake. Thus the presence of a gastric load reduced the threshold dose of the CCK analogue required to inhibit intake. Furthermore, at suprathreshold doses, the peptide-load combination suppressed intake more than the peptide alone. In addition, administration of 0.5 and 5.0 nmol/kg doses of the CCK analogue inhibited gastric emptying at 10, 20, and 30 min in a dose-dependent fashion. The CCK analogue's inhibition of food intake and gastric emptying were reversed by pretreatment with 100 micrograms/kg L364,718, indicating that the analogue was having its effects by interacting with specific type A CCK receptors. Together these data support the notion that CCK satiety derives from an integration of the visceral afferent signals generated by CCK's promotion of gastric distension and those produced directly by CCK.

The inhibitory effect of GLP-1 on food intake is augmented by gastric distension in healthy human subjects

2000 ◽  
Vol 118 (4) ◽  
pp. A74-A75 ◽  
Author(s):  
Daniel Matzinger ◽  
Lukas Degen ◽  
Markus Knupp ◽  
Christoph Beglinger
Keyword(s):  
Food Intake ◽  
Human Subjects ◽  
Inhibitory Effect ◽  
Gastric Distension ◽  
Healthy Human ◽  
Healthy Human Subjects

scholarly journals Leptin and the Control of Food Intake: Neurons in the Nucleus of the Solitary Tract Are Activated by Both Gastric Distension and Leptin

Endocrinology ◽  
2007 ◽  
Vol 148 (5) ◽  
pp. 2189-2197 ◽  
Author(s):  
Lihong Huo ◽  
Lisa Maeng ◽  
Christian Bjørbæk ◽  
Harvey J. Grill
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Significant Proportion ◽  
Gastric Distension ◽  
Reduce Food Intake ◽  
Signal Transducer ◽  
Electrophysiological Response ◽  
Fluorescent Immunohistochemistry ◽  
Transcription 3

Leptin reduces food intake by an unspecified mechanism. Studies show that forebrain ventricular leptin delivery increases the inhibitory effects of gastrointestinal (GI) stimulation on intake and amplifies the electrophysiological response to gastric distension in neurons of the medial subnucleus of the nucleus tractus solitarius (mNTS). However, forebrain ventricular delivery leaves unspecified the neuroanatomical site(s) mediating leptin’s effect on intake. Detailed anatomical analysis in rats and mice by phosphorylated signal transducer and activator of transcription 3 immunohistochemistry shows that hindbrain leptin-responsive neurons are located exclusively within the mNTS. Here, we investigate 1) whether leptin and gastric distension affect the same mNTS neurons and 2) whether the intake-inhibitory action of gastric distension is potentiated by hindbrain leptin delivery. Twenty-five minutes after gastric balloon distension or sham distension, rats were injected with leptin or vehicle and killed 35 min later. Double-fluorescent immunohistochemistry for phosphorylated signal transducer and activator of transcription 3 and c-Fos revealed that about 40% of leptin-responsive cells also respond to gastric distension. A paradigm was then developed to examine the relationship between leptin and gastric distension volume on intake inhibition. At subthreshold levels, hindbrain ventricular leptin or distension volume were without effect. When combined, an interaction occurred that significantly reduced food intake. We conclude that 1) leptin-responsive neurons in the hindbrain are primarily located in the mNTS at the level of the area postrema, a key vagal afferent projection zone of the GI system; 2) a significant proportion of leptin-responsive neurons in the mNTS are activated by stomach distension; and 3) leptin delivered to the hindbrain is sufficient to potentiate the intake-suppressive effects of an otherwise ineffective volume of gastric distension. These results are consistent with the hypothesis that leptin acts directly on neurons within the mNTS to reduce food intake through an interaction with GI signal processing.

Effect of gastric distension prior to eating on food intake and feelings of satiety in humans

2006 ◽  
Vol 87 (5) ◽  
pp. 903-910 ◽  
Author(s):  
Sibylle Oesch ◽  
Cornelia Rüegg ◽  
Barbora Fischer ◽  
Lukas Degen ◽  
Christoph Beglinger
Keyword(s):  
Food Intake ◽  
Gastric Distension

scholarly journals Repeated gastric distension alters food intake and neuroendocrine profiles in rats

2012 ◽  
Vol 105 (4) ◽  
pp. 975-981 ◽  
Author(s):  
Sara L. Hargrave ◽  
Kimberly P. Kinzig
Keyword(s):  
Food Intake ◽  
Gastric Distension

Comparative effects of CCK-8 on feeding, sham feeding, and exocrine pancreatic secretion in rats

1986 ◽  
Vol 251 (1) ◽  
pp. R97-R105 ◽  
Author(s):  
R. D. Reidelberger ◽  
T. E. Solomon
Keyword(s):  
Food Intake ◽  
Pancreatic Secretion ◽  
Gastric Distension ◽  
Exocrine Pancreatic Secretion ◽  
Humoral Factors ◽  
Sham Feeding ◽  
Hormonal Mechanism ◽  
Satiety Hormone ◽  
Feeding Effect ◽  
Normal Feeding

Cholecystokinin (CCK) is thought to be a hormonal regulator of exocrine pancreatic secretion and is postulated to be a satiety hormone. We compared the dose-response effects of CCK octapeptide (CCK-8) on feeding, sham feeding, and pancreatic secretion to gauge whether the feeding effect might be physiological. Pancreatic responses to intravenous CCK-8 (40, 200, 1,000, or 4,000 pmol . kg-1 . h-1) in fasted unanesthetized rats were compared with effects of CCK-8 (0, 200, 1,000, or 4,000 pmol . kg-1 . h-1) on ingestion of liquid diet in fasted rats with gastric cannulas either closed (normal feeding) or open (sham feeding). Maximal pancreatic amylase output occurred at 200 pmol . kg-1 . h-1 of CCK-8; output declined at higher doses. Food intake was significantly inhibited only at 1,000 and 4,000 pmol . kg-1 . h-1 of CCK-8; the effect was similar when gastric cannulas were closed and open. These results, together with available data on the low postprandial levels of plasma CCK, suggest that circulating levels of CCK normally present after food intake are not sufficient to produce satiety. Furthermore, suppression of feeding by CCK does not appear to be mediated solely by a mechanism that senses gastric distension, because CCK-8 had similar effects in the presence and absence of gastric distension. Whether CCK interacts with other neural or humoral factors to produce satiety by a hormonal mechanism remains to be determined.

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