Biology:Migrating motor complex

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Short description: Physiological phenomenon

Migrating motor complex, also known as migrating myoelectric complex, migratory motor complex, migratory myoelectric complex and MMC, is a pattern of electrical activity observed in the gastrointestinal tract in a regular cycle during fasting. MMC was discovered and characterized in fasting dogs in 1969 by Dr. Joseph H. Szurszewski at the Mayo Clinic.[1] He also showed that this activity stops upon eating a meal, and suggested that it induces a motor activity that acts as a "interdigestive housekeeper" in the small intestine.[1] These motor complexes trigger peristaltic waves, which facilitate transportation of indigestible substances such as bone, fiber, and foreign bodies from the stomach, through the small intestine, past the ileocecal sphincter, and into the colon. MMC activity varies widely across individuals and within an individual when measured on different days. The MMC occurs every 90–230 minutes during the interdigestive phase (i.e., between meals) and is responsible for the rumbling experienced when hungry.[2][3] It also serves to transport bacteria from the small intestine to the large intestine and to inhibit the migration of colonic bacteria into the terminal ileum; an impairment to the MMC typically results in small intestinal bacterial overgrowth.[4]

Phases

The MMC originates mostly in the stomach—although ~25% will arise from the duodenum or proximal jejunum—and can travel to the distal end of the ileum.[5] They consist of four distinct phases:

  • Phase I – A prolonged period of quiescence (40–60% of total time);
  • Phase II – Increased frequency of action potentials and smooth muscle contractility (20–30% of total time);
  • Phase III – A few minutes of peak electrical and mechanical activity (5–10 minutes);
  • Phase IV – Declining activity which merges with the next Phase I.[5]

Regulation

Movements of the small bowel are believed to be controlled by the central and enteric nervous systems, intestinal muscles, and numerous peptides and hormones. For example, the MMC is thought to be initiated by motilin, and it does not directly depend on extrinsic nerves.[6] Additionally, gastrin, insulin, cholecystokinin, glucagon, and secretin have been reported to disrupt the MMC.

Eating interrupts the MMC. For example, one study found that a continental breakfast of 450 Kcal causes the MMC to disappear for 213 ± 48 minutes.[7] The number of calories and nature of food determine the length of the disruption with fats causing a longer disruption than carbohydrates which in turn cause a longer disruption than protein.[8]

Most of the cleaning waves in the MMC happen at night while we are asleep. For many people this will be sufficient enough to help maintain a healthy, balanced environment in the digestive tract. For others, it may be beneficial to space out food intake to allow for a couple cleaning waves to occur between meals throughout the day as well.[9]

Impairment

Autoimmunity following infection by a pathogen producing CdtB, such as C. jejuni, may be the leading cause of MMC impairment.[10] Narcotics are also known to impair the MMC.[11] Stress has been shown to reduce MMC activity as well.[12]

Patients with SIBO and IBS have on average a third as many MMC phase III events with those events being roughly 30% shorter on average.[13]

Therapeutic stimuli

Drugs used to enhance gastrointestinal motility are generally referred to as prokinetics. Serotonin induces phase III of the MMC, and so serotonin receptor agonists are commonly administered as prokinetics.[14] Motilin administration causes phase III contractions, and so motilin agonists are another common prokinetic.[15]

Eradication of bacterial overgrowth has been shown to partially restore MMC activity.[13]

An elemental diet has been hypothesized to partially restore MMC function.[16]

References

  1. ↑ 1.0 1.1 Szurszewski, Joseph H. (1969-12-01). "A migrating electric complex of canine small intestine" (in en). American Journal of Physiology. Legacy Content 217 (6): 1757–1763. doi:10.1152/ajplegacy.1969.217.6.1757. ISSN 0002-9513. https://www.physiology.org/doi/10.1152/ajplegacy.1969.217.6.1757. 
  2. ↑ "Variability of migrating motor complex in humans". Digestive Diseases and Sciences 37 (5): 723–8. May 1992. doi:10.1007/BF01296429. PMID 1563314. 
  3. ↑ "Mechanism of interdigestive migrating motor complex". Journal of Neurogastroenterology and Motility 18 (3): 246–57. July 2012. doi:10.5056/jnm.2012.18.3.246. PMID 22837872. 
  4. ↑ Hasler, William (2006). Physiology of the Gastrointestinal Tract (Fourth ed.). 
  5. ↑ 5.0 5.1 Boron, Walter F; Boulpaep, Emile Louis Jean Baptiste (2012). Medical physiology : a cellular and molecular approach (Updated second ed.). Philadelphia, Pa.: Saunders. ISBN 978-1-4377-1753-2. 
  6. ↑ "Motilin". Current Opinion in Endocrinology, Diabetes and Obesity 15 (1): 54–7. February 2008. doi:10.1097/MED.0b013e3282f370af. PMID 18185063. 
  7. ↑ "The interdigestive motor complex of normal subjects and patients with bacterial overgrowth of the small intestine". The Journal of Clinical Investigation 59 (6): 1158–66. June 1977. doi:10.1172/JCI108740. PMID 864008. 
  8. ↑ "The migrating motor complex". The Medical Clinics of North America 65 (6): 1311–29. November 1981. doi:10.1016/S0025-7125(16)31474-2. PMID 7035768. 
  9. ↑ "Bloating, Gut Health, and the Migrating Motor Complex" (in en). http://www.synergynutrition.ca/1/post/2021/08/bloating-gut-health-and-the-migrating-motor-complex.html. 
  10. ↑ "Autoimmunity Links Vinculin to the Pathophysiology of Chronic Functional Bowel Changes Following Campylobacter jejuni Infection in a Rat Model". Digestive Diseases and Sciences 60 (5): 1195–205. May 2015. doi:10.1007/s10620-014-3435-5. PMID 25424202. 
  11. ↑ "Effect of total parenteral nutrition plus morphine on bacterial translocation in rats" (in en). Annals of Surgery 217 (3): 286–92. March 1993. doi:10.1097/00000658-199303000-00011. PMID 8452407. PMC 1242782. http://insights.ovid.com/. 
  12. ↑ "The irritable bowel syndrome: a paroxysmal motor disorder". Lancet 2 (8462): 973–7. November 1985. doi:10.1016/S0140-6736(85)90525-2. PMID 2865504. 
  13. ↑ 13.0 13.1 "Lower frequency of MMC is found in IBS subjects with abnormal lactulose breath test, suggesting bacterial overgrowth". Digestive Diseases and Sciences 47 (12): 2639–43. December 2002. doi:10.1023/A:1021039032413. PMID 12498278. 
  14. ↑ "Serotonin induces phase III of the MMC, VIA 5-HT3-receptors dependent on cholinergic mechanisms in the small intestine". Gastroenterology 114: A795. 1998-04-15. doi:10.1016/S0016-5085(98)83246-0. 
  15. ↑ "The activity front of the migrating motor complex of the human stomach but not of the small intestine is motilin-dependent". Regulatory Peptides 6 (4): 363–9. August 1983. doi:10.1016/0167-0115(83)90265-3. PMID 6635258. 
  16. ↑ "A 14-day elemental diet is highly effective in normalizing the lactulose breath test". Digestive Diseases and Sciences 49 (1): 73–7. January 2004. doi:10.1023/B:DDAS.0000011605.43979.e1. PMID 14992438. 

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