Relationship of plasma motilin concentration to fat ingestion, duodenal acidification and alkalinization, and migrating motor complexes in dogs

1981 ◽  
Vol 59 (2) ◽  
pp. 180-187 ◽  
Author(s):  
J. E. T. Fox ◽  
N. S. Track ◽  
E. E. Daniel

Plasma motilin concentrations were measured in dogs following duodenal acidification and alkalinization and gastric instillation of fat. Antral and duodenal motility were recorded concurrently using intraluminal manometry. Alkalinization of the duodenum produced an increase in antral and duodenal motility and a significant rise in plasma motilin. Alkaline infusions at 5 mL/min into the duodenum initiated phase III of a migrating motor complex both in the antrum and in the duodenum. Duodenal acid infusions produced no change in plasma motilin concentrations while inhibiting antral motility and stimulating duodenal motility for the duration of the infusion. Gastric instillation of 60 g fat produced a 25% increase above basal motilin levels at 50 min after instillation. Motilin levels monitored during spontaneous migrating motor complexes showed peak motilin levels occurring during maximal activity of the antral duodenal region in seven out of nine motor complexes examined but motilin peaks also occurred without migrating complexes being present in this area and, as well, complexes occurred when motilin was undetectable. These results taken together with our other studies in man confirm that a true species difference exists between man and dog in the hormonal motor response to duodenal alkalinization. Although a relationship appears to exist between the appearance of maximal migrating motor complex activity in the gastroduodenal area and plasma motilin concentrations in dogs as in humans, the motilin peaks are probably neither necessary nor sufficient to induce phase III activity.


1981 ◽  
Vol 59 (2) ◽  
pp. 173-179 ◽  
Author(s):  
E. E. Daniel ◽  
J. E. T. Fox ◽  
S. M. Collins ◽  
T. D. Lewis ◽  
M. Meghji ◽  
...  

The hypothesis that acid, emptied intermittently from the stomach during fasting, might initiate the duodenal phase of the migrating motor complex was tested in normal human subjects, in addition, the relationship between plasma motilin concentrations and the initiation of migrating motor complexes was examined. Migrating complexes occurred spontaneously in the absence of acid in the duodenal bulb and in the presence of duodenal bulb neutralization with sodium bicarbonate. Thus duodenal bulb acidification is not necessary for initiation of the duodenal phase of the migrating motor complexes. Further-more, cyclical increases in plasma motilin concentrations were not closely correlated with the initiation of the gastric phase of maximal activity of the migrating motor complexes. However, motilin concentrations were decreased significantly following onset of the duodenal phase III. We conclude that neither duodenal acidification nor increases in motilin concentration are necessary to initiate migrating motor complexes in man.



1983 ◽  
Vol 61 (11) ◽  
pp. 1289-1298 ◽  
Author(s):  
K. E. Hall ◽  
G. R. Greenberg ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant

The role of the vagus nerve in the control of fasting plasma pancreatic polypeptide (PP), gastrin, and motilin levels was investigated in conscious dogs. Lowest plasma levels of motilin (81 ± 8 pmol/L), PP (19 ± 1 pmol/L) and gastrin (5 ± 1 pmol/L) were observed during phase I of the migrating motor complex (MMC). Significant peaks in plasma motilin (127 ± 11 pmol/L, P < 0.005), PP (26 ± 2 pmol/L, P < 0.005), and gastrin (14 ± 2 pmol/L, P < 0.005) were seen, coinciding with the appearance of phase II (PP and gastrin) or phase III (motilin) of the migrating motor complex in the upper gut. Whereas bilateral vagal blockade abolished the peaks in PP and gastrin, a significant (P < 0.025) increment in plasma motilin remained, which correlated with the late phase III equivalent of the vagally independent complex (VIC) in the duodenum. This VIC-related motilin peak (170 ± 20 pmol/L) was significantly higher (P < 0.025) and the time course (9 ± 2 min) significantly shorter (P < 0.01) than the peak (127 ± 11 pmol/L) and duration (31 ± 9 min) observed without vagal blockade. Thus, in fasting, the cyclical increments of PP and gastrin are both dependent on excitatory vagal innervation, whereas excitatory pathways controlling phase III associated peak motilin release are nonvagal. In addition, the pattern of fasting motilin release and the amplitude of peak motilin secretion may be affected by vagal inhibition.



1983 ◽  
Vol 245 (2) ◽  
pp. G178-G185 ◽  
Author(s):  
K. E. Hall ◽  
N. E. Diamant ◽  
T. Y. El-Sharkawy ◽  
G. R. Greenberg

A potential role of pancreatic polypeptide (PP) in the regulation of phase III of the migrating motor complex (MMC) was investigated in conscious dogs before and during bilateral vagal blockade. After a control fasting period, cyclical increments in plasma PP occurred with peak levels of 45 +/- 8 pmol/l coinciding with late phase II MMC motility. By contrast, after food a substantially higher (approximately five times peak fasting concentrations) and more prolonged elevation of PP was observed, in association with a postprandial pattern of activity. To approximate fasting plasma PP concentrations, porcine PP was infused at 100 pmol X kg-1 X h-1, which produced levels of plasma PP of 99 +/- 8 pmol/l. At this dose PP had no effect on phase III activity. However, at a dose of 400 pmol X kg-1 X h-1, which achieved plasma PP concentrations (283 +/- 33 pmol/l) similar to postprandial levels, there was a specific inhibition of phase III in the lower esophageal sphincter, stomach, duodenum, and upper jejunum. The phase III-associated increment of plasma motilin was also inhibited by this dose of PP. These inhibitory effects at the 400 pmol X kg-1 X h-1 dose of PP were also observed after bilateral blockade of the vagus nerves. Our results suggest that PP has no significant role in the modulation of phase III of the fasting MMC nor does it induce a typical feeding motor pattern. The selective inhibition of both phase III and the associated rise in plasma motilin by PP plasma levels similar to postprandial concentrations does, however, point to a possible role for pancreatic polypeptide in the postprandial inhibition of phase III of the MMC.



1986 ◽  
Vol 250 (5) ◽  
pp. G570-G574
Author(s):  
S. J. Konturek ◽  
P. J. Thor ◽  
J. Bilski ◽  
W. Bielanski ◽  
J. Laskiewicz

A relationship between duodenal myoelectric or motor activity and exocrine pancreatic secretion as well as plasma gut hormone levels has been investigated in fasted dogs, fed dogs, and dogs that were stimulated with exogenous gut hormones. Pancreatic secretion showed typical periodicity in phase with the myoelectric or motor activity of the duodenum. Fasting pancreatic bicarbonate and protein secretion reached peaks during phase III of the interdigestive migrating motor complex (MMC) cycle that were significantly larger than nadir levels occurring during phase I of the cycle. These fasting bicarbonate and protein peaks reached, respectively, approximately 9 and 30% of the highest postprandial outputs and 4 and 14% of the maximal secretory capacity elicited by secretin or CCK. They were accompanied by a significant rise in plasma motilin, gastrin, and pancreatic polypeptide (PP), but only exogenous motilin given in physiological dose induced motility pattern and pancreatic secretion similar to those observed during phase III. Feeding interrupted both motor and secretory MMC cycle, increased the pancreatic secretion to approximately 40-60% of the maximal secretory capacity, and was accompanied by increments in plasma gastrin, cholecystokinin (CCK), secretin, and PP. None of these hormones applied alone in physiological dose was capable of reproducing the postprandial inhibition of MMC cycles. We conclude that the pancreatic secretion in fasted dogs fluctuates periodically in phase with duodenal motility, but the phase III peak secretory outputs represent only minute fractions of the maximal secretory capacity and can therefore be ignored in regular testing of pancreatic secretion.



2002 ◽  
Vol 14 (4) ◽  
pp. 331-338 ◽  
Author(s):  
J. M. Andrews ◽  
D. G. O'donovan ◽  
G. S. Hebbard ◽  
C. H. Malbert ◽  
S. M. Doran ◽  
...  


2014 ◽  
Vol 27 (1) ◽  
pp. 63-71 ◽  
Author(s):  
E. Deloose ◽  
R. Vos ◽  
M. Corsetti ◽  
I. Depoortere ◽  
J. Tack


1987 ◽  
Vol 253 (3) ◽  
pp. G259-G267 ◽  
Author(s):  
H. J. Ehrlein ◽  
M. Schemann ◽  
M. L. Siegle

In the canine small intestine several simple (S) and complex (C) patterns of propulsive and nonpropulsive activities were found. The nonpropulsive activity consisted of 1) stationary individual contractions (S) and 2) stationary clusters of contractions (C). Patterns leading to aboral propulsion of luminal contents were 1) propagating contractions (S), 2) propagating power contractions (S), 3) phase III of the migrating motor complex (C), and 4) migrating clusters of contractions (C). The propagation velocities of the propulsive motor patterns differed markedly; they increased in the following order: phase III, migrating clustered contractions, propagating power contractions, propagating contractions. A retrograde transport of luminal contents was produced by two different activities: 1) retrograde propagating contractions (S) and 2) retrograde power contractions (S). They were accompanied with enterogastric reflux.



1994 ◽  
Vol 107 (4) ◽  
pp. 1234
Author(s):  
P. Pouderoux ◽  
M. Veyrac ◽  
H Michel


1998 ◽  
Vol 114 ◽  
pp. A769
Author(s):  
E. Husebye ◽  
R. Wackerbauer ◽  
J. Bondi ◽  
M. Skard Heier


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