Differential brain responses to gradual intragastric nutrient infusion and gastric balloon distension: A role for gut peptides?

NeuroImage ◽  
2017 ◽  
Vol 144 ◽  
pp. 101-112 ◽  
Author(s):  
Huynh Giao Ly ◽  
Patrick Dupont ◽  
Koen Van Laere ◽  
Inge Depoortere ◽  
Jan Tack ◽  
...  
2006 ◽  
Vol 291 (1) ◽  
pp. R115-R123 ◽  
Author(s):  
Matthew R. Hayes ◽  
Fiona M. Chory ◽  
Claire A. Gallagher ◽  
Mihai Covasa

We have previously shown that serotonin type-3 (5-HT3) receptors mediate cholecystokinin (CCK)-induced satiation and that this effect is dependent on postoropharyngeal feedback. However, the independent contributions of gastric and intestinal feedback in 5-HT3 receptor mediation of suppression of food intake by CCK have not been determined. Using a sham-feeding preparation combined with intraduodenal sucrose infusion, we show that blockade of 5-HT3 receptors by ondansetron (1 mg/kg ip) had no effect on suppression of sham feeding by intraduodenal 15% sucrose infusion (4 ml/10 min), CCK (2 μg/kg ip) administration, or the combination of the two treatments. In separate experiments consisting of either sham-feeding rats that received gastric distension with the use of a balloon or real-feeding rats whose stomachs were distended using gastric loads of saline after the occlusion of the pylorus, we tested the hypothesis that gastric feedback signals are necessary for activation of 5-HT3 receptors. Ondansetron significantly attenuated suppression of sham sucrose intake after a 10-ml gastric balloon distension (30.5 ± 2.2 vs. 20.2 ± 2.2 ml, respectively) and gastric distension combined with CCK (21.9 ± 1.4 vs. 12.0 ± 1.7 ml, respectively). When intestinal feedback was eliminated in a real-feeding paradigm by closing the pylorus using a cuff preparation, ondansetron attenuated suppression of sucrose intake produced by a 10-ml saline gastric load (6.8 ± 0.7 vs. 4.2 ± 0.4 ml, respectively). Finally, when CCK (1 μg/kg) was administered in combination with a 5-ml saline gastric load in a real-feeding preparation, ondansetron significantly attenuated suppression of sucrose intake by CCK (9.0 ± 0.9 vs. 6.3 ± 0.5 ml, respectively), as well as the enhanced suppression of intake by CCK plus gastric load (6.9 ± 0.6 vs. 4.6 ± 0.5 ml, respectively). These findings demonstrate that CCK-induced activation of 5-HT3 receptors requires gastric, but not intestinal feedback.


1990 ◽  
Vol 259 (3) ◽  
pp. G402-G409
Author(s):  
C. J. Yeo ◽  
J. A. Bastidas ◽  
R. E. Schmieg ◽  
M. J. Zinner

After a meal, the absorption of water and electrolytes from the jejunal lumen increases. This meal-induced jejunal absorption occurs in jejunal segments out of normal gastrointestinal continuity. The experimental model used 25-cm proximal jejunal Thiry-Vella loops in awake dogs (n = 72 observations) to evaluate the mechanisms involved in meal-induced jejunal absorption, seeking to define the source or sources of the proabsorptive signal. Specifically, we evaluated the jejunal absorptive response to a standard meal, a standard meal plus cholinergic blockage using atropine, a sham-fed meal, a gavage-fed meal, and gastric distension with balloon and gavage water. Both the standard meal and the gavage-fed meal induced a prompt, sustained, and significant (P less than 0.0001) increase in the absorption of H2O, Na+, and Cl-. Atropine significantly reduced the magnitude of the postmeal absorptive response (P less than 0.05) compared with the standard meal alone. The sham-fed meal, gastric balloon distension, and gavage water did not alter jejunal absorption. Vagal nerve integrity after cervical esophageal manipulation was verified by gastric acid output and gastrin response to stimuli. These data support a role for cholinergic modulation of meal-stimulated jejunal absorption via a cephalic-phase-independent and gastric-distension-independent mechanism.


Digestion ◽  
2003 ◽  
Vol 68 (2-3) ◽  
pp. 161-168 ◽  
Author(s):  
E.M.H. Mathus-Vliegen ◽  
M. van Weeren ◽  
P.V. van Eerten

Diabetes Care ◽  
2016 ◽  
Vol 39 (10) ◽  
pp. 1787-1795 ◽  
Author(s):  
Katharine F. Hunt ◽  
Joel T. Dunn ◽  
Carel W. le Roux ◽  
Laurence J. Reed ◽  
Paul K. Marsden ◽  
...  

2010 ◽  
Vol 24 (2) ◽  
pp. 76-82 ◽  
Author(s):  
Martin M. Monti ◽  
Adrian M. Owen

Recent evidence has suggested that functional neuroimaging may play a crucial role in assessing residual cognition and awareness in brain injury survivors. In particular, brain insults that compromise the patient’s ability to produce motor output may render standard clinical testing ineffective. Indeed, if patients were aware but unable to signal so via motor behavior, they would be impossible to distinguish, at the bedside, from vegetative patients. Considering the alarming rate with which minimally conscious patients are misdiagnosed as vegetative, and the severe medical, legal, and ethical implications of such decisions, novel tools are urgently required to complement current clinical-assessment protocols. Functional neuroimaging may be particularly suited to this aim by providing a window on brain function without requiring patients to produce any motor output. Specifically, the possibility of detecting signs of willful behavior by directly observing brain activity (i.e., “brain behavior”), rather than motoric output, allows this approach to reach beyond what is observable at the bedside with standard clinical assessments. In addition, several neuroimaging studies have already highlighted neuroimaging protocols that can distinguish automatic brain responses from willful brain activity, making it possible to employ willful brain activations as an index of awareness. Certainly, neuroimaging in patient populations faces some theoretical and experimental difficulties, but willful, task-dependent, brain activation may be the only way to discriminate the conscious, but immobile, patient from the unconscious one.


2007 ◽  
Author(s):  
Francis J. McClernon ◽  
Rachel V. Kozink ◽  
Jed E. Rose

2017 ◽  
Vol 2017 ◽  
pp. 104-104
Author(s):  
Hanah Choi ◽  
◽  
DongHyun Kim ◽  
EunJu Lee ◽  
Eunju Ko

2018 ◽  
Vol 2018 ◽  
pp. 693-695
Author(s):  
Eun-Ju Lee ◽  
◽  
Kyeong Cheon Cha ◽  
Minah Suh

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