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Cause-and-effect relationship between motilin and migrating myoelectric complexes
Abstract:
We investigated the cause-and-effect relationship between plasma motilin levels and migrating myoelectric complexes (MMCs). Each dog was implanted with a set of eight bipolar electrodes on the small intestine. Premature phase IIIs were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase IIIs were associated with peaks of plasma motilin, which always occurred after phase IIIs had started in the proximal duodenum. The plasma motilin level decreased consistently during phase I and started to increase again only after phase II had started in the duodenum. Either a meal or somatostatin infusion disrupted MMC cycling, but morphine boluses overcame this disruption and initiated phase IIIs that propagated distally. The phase IIIs thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase IIIs during the fed state or during somatostatin infusion. Our findings suggest that endogenous motilin does not initiate spontaneous MMCs. Instead, MMC contractions release motilin. The physiological role of motilin, thus released, may be to act as an endocrine agent to coordinate secretory and motor events with the start of phase III activity in the upper small intestine.
Insights
Plasma motilin levels increase after migrating myoelectric complexes (MMCs) begin, suggesting motilin doesn't initiate MMCs. Instead, MMC contractions release motilin to coordinate digestive events.
Area of Science:
- Gastroenterology
- Neurogastroenterology
- Digestive Physiology
Background:
- Migrating myoelectric complexes (MMCs) are essential for gut motility and preventing bacterial overgrowth.
- The role of plasma motilin in initiating or regulating MMCs remains incompletely understood.
Purpose of the Study:
- To investigate the causal relationship between plasma motilin levels and the initiation and propagation of MMCs.
- To determine if endogenous motilin initiates spontaneous MMCs or if it is released in response to MMC activity.
Main Methods:
- Electrode implantation in dogs to monitor small intestinal electrical activity.
- Induction of premature MMCs using morphine bolus injections.
- Assay of plasma samples for motilin and gastrin levels during different physiological states.
Main Results:
- Spontaneous and morphine-induced phase IIIs of MMCs were consistently associated with peaks in plasma motilin.
- Plasma motilin levels increased after phase IIIs commenced in the proximal duodenum.
- Exogenous motilin administration did not initiate phase IIIs, while MMC contractions led to motilin release.
Conclusions:
- Endogenous motilin does not initiate spontaneous MMCs; rather, MMC contractions stimulate motilin release.
- Released motilin may function as an endocrine signal coordinating digestive processes with the onset of phase III activity.