Role of acid secretory response to sham feeding in predicting recurrent ulceration after proximal gastric vagotomy

1994 ◽  
Vol 81 (7) ◽  
pp. 1002-1006 ◽  
Author(s):  
B. Stenquist ◽  
H. Forssell ◽  
L. Olbe ◽  
L. Lundell
1950 ◽  
Vol 16 (1) ◽  
pp. 104-116 ◽  
Author(s):  
Henry D. Janowitz ◽  
Franklin Hollander ◽  
David Orringer ◽  
Milton H. Levy ◽  
Asher Winkelstein ◽  
...  

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 355
Author(s):  
Ingo Rustenbeck ◽  
Torben Schulze ◽  
Mai Morsi ◽  
Mohammed Alshafei ◽  
Uwe Panten

The pancreatic beta-cell transduces the availability of nutrients into the secretion of insulin. While this process is extensively modified by hormones and neurotransmitters, it is the availability of nutrients, above all glucose, which sets the process of insulin synthesis and secretion in motion. The central role of the mitochondria in this process was identified decades ago, but how changes in mitochondrial activity are coupled to the exocytosis of insulin granules is still incompletely understood. The identification of ATP-sensitive K+-channels provided the link between the level of adenine nucleotides and the electrical activity of the beta cell, but the depolarization-induced Ca2+-influx into the beta cells, although necessary for stimulated secretion, is not sufficient to generate the secretion pattern as produced by glucose and other nutrient secretagogues. The metabolic amplification of insulin secretion is thus the sequence of events that enables the secretory response to a nutrient secretagogue to exceed the secretory response to a purely depolarizing stimulus and is thus of prime importance. Since the cataplerotic export of mitochondrial metabolites is involved in this signaling, an orienting overview on the topic of nutrient secretagogues beyond glucose is included. Their judicious use may help to define better the nature of the signals and their mechanism of action.


1967 ◽  
Vol 45 (4) ◽  
pp. 633-641 ◽  
Author(s):  
R. M. Preshaw

In conscious dogs with gastric fistulas the latency of both the gastric acid and pepsin responses to sham feeding was about 6 min. When a background secretion was induced with various closes of hog gastrin, the latency of the acid response to sham feeding was unchanged, but the latency of the pepsin response was shortened. The peak rates of acid and pepsin secretion after sham feeding were not altered by the infusion of gastrin.


The 3-cycles per minute (cpm) gastric pacesetter potential is a fundamental electrical phenomenon of the stomach. This low-frequency biorhythm is the basis for normal neuromuscular function of the stomach. In regard to the origins and the various neural and hormonal influences that affect the 3-cpm rhythm, many mysteries remain. Ongoing and future inquiries into the very nature of rhythmicity will provide deeper understanding of gastric myoelectrical activity and the electrical activity detected in the electrogastrogram (EGG). The role of knockout mice that lack interstitial cells of Cajal will be increasingly important in understanding the crucial role of rhythmic electrical events in normal and abnormal neuromuscular function of the stomach. These and other animal studies will also continue to help clinicians understand the deficits in gastric neuromuscular function caused by electrical dysrhythmias. A delicate balance maintains normal 3-cpm activity. Stomach electrical rhythmicity is rather unstable during fasting, for example, compared with the rhythmic 3-cpm electrical events and contractile events that occur in the postprandial period. What mechanisms produce these fasting and postprandial electrical changes? Are neural or hormonal circuits most critical? Are extrinsic or intrinsic nerves the most important? Studies of fasting and postprandial EGG activity may offer insights into sensations of hunger and satiety. The EGG signal is responsive to brain-gut interactions such as the cephalic-vagal reflex. Sham feeding studies with healthy subjects indicated that the sight, smell, and taste of food significantly increased 3- cpm activity. However, in subjects who indicated that the sham feeding experience was disgusting, no increase in 3-cpm activity occurred in this situation. Future studies of patients with eating disorders such as bulimia or anorexia nervosa using EGG recording methods may reveal new insights into the pathophysiology of eating disorders and be of value in monitoring the progress of treatment. Different EGG patterns induced by different meals reflect the different gastric neuromuscular work required to receive, mix, and empty the specific meal. Characteristics of the EGG signal from frequency to amplitude may also correlate with perceptions of stomach fullness, hunger, or satiety.


1991 ◽  
Vol 261 (2) ◽  
pp. G327-G331 ◽  
Author(s):  
M. A. Ballesteros ◽  
J. D. Wolosin ◽  
D. L. Hogan ◽  
M. A. Koss ◽  
J. I. Isenberg

Cephalic-vagal stimulation affects a number of upper gastrointestinal secretory and motility events. The purpose of this study was to examine the role of vagal-cholinergic regulation on human proximal duodenal mucosal HCO-3 secretion. The duodenal bulb was isolated between balloons and perfused with 154 mM NaCl, and HCO-3 secretion was measured. Although cholinergic stimulation with bethanechol (50 micrograms.kg-1.h-1 iv) produced systemic effects, resting HCO-3 secretion was unchanged. Cephalic-vagal stimulation, induced by sham feeding, significantly increased duodenal HCO-3 secretion from a basal of 177 +/- 17 to 240 +/- 19 mumols.cm-1.h-1 (P less than 0.02). The response to sham feeding was approximately 50% of the peak response to acid-stimulated HCO-3 output. Atropine (22 micrograms/kg iv) inhibited basal HCO-3 secretion significantly (79 +/- 5%). However, the net incremental increases in duodenal mucosal HCO-3 secretion in response to luminal acidification and vagal stimulation were unaltered by atropine pretreatment. Additionally, indomethacin (100 mg po) failed to modify the response to vagal-stimulated HCO-3 secretion. These findings indicate that basal human proximal duodenal mucosal HCO-3 secretion is maintained largely by resting cholinergic innervation and is stimulated by cephalic-vagal stimulation. Furthermore, since the incremental HCO-3 responses to cephalic-vagal stimulation and luminal acidification were unaltered by atropine pretreatment, each is likely mediated by noncholinergic mechanisms.


1978 ◽  
Vol 74 (4) ◽  
pp. 704-707 ◽  
Author(s):  
Jonathan E. Clain ◽  
Vay Liang W. Go ◽  
Juan-R. Malagelada

2014 ◽  
Vol 307 (9) ◽  
pp. R1167-R1179 ◽  
Author(s):  
Ilan M. Ruhr ◽  
Charlotte Bodinier ◽  
Edward M. Mager ◽  
Andrew J. Esbaugh ◽  
Cameron Williams ◽  
...  

The physiological effects of guanylin (GN) and uroguanylin (UGN) on fluid and electrolyte transport in the teleost fish intestine have yet to be thoroughly investigated. In the present study, the effects of GN, UGN, and renoguanylin (RGN; a GN and UGN homolog) on short-circuit current ( Isc) and the transport of Cl−, Na+, bicarbonate (HCO3−), and fluid in the Gulf toadfish ( Opsanus beta) intestine were determined using Ussing chambers, pH-stat titration, and intestinal sac experiments. GN, UGN, and RGN reversed the Isc of the posterior intestine (absorptive-to-secretory), but not of the anterior intestine. RGN decreased baseline HCO3− secretion, but increased Cl− and fluid secretion in the posterior intestine. The secretory response of the posterior intestine coincides with the presence of basolateral NKCC1 and apical cystic fibrosis transmembrane conductance regulator (CFTR), the latter of which is lacking in the anterior intestine and is not permeable to HCO3− in the posterior intestine. However, the response to RGN by the posterior intestine is counterintuitive given the known role of the marine teleost intestine as a salt- and water-absorbing organ. These data demonstrate that marine teleosts possess a tissue-specific secretory response, apparently associated with seawater adaptation, the exact role of which remains to be determined.


1991 ◽  
Vol 101 (4) ◽  
pp. 954-961 ◽  
Author(s):  
Koji Takeuchi ◽  
Jiro Matsumoto ◽  
Koji Ueshima ◽  
Susumu Okabe

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