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Migrating motor complex

From Wikipedia, the free encyclopedia

Migrating motor complex, also known as migrating myoelectric complex, migratory motor complex, migratory myoelectric complex and MMC, is a cyclic, recurring motility pattern that occurs in the stomach and small bowel during fasting; it is interrupted by feeding.[1] A pattern of electrical activity is also observed in the gastrointestinal tract in a regular cycle during this interdigestive period.

MMC was discovered and characterized in fasting dogs in 1969 by Dr. Joseph H. Szurszewski at the Mayo Clinic.[2] He also showed that this activity stops upon eating a meal, and suggested that it induces a motor activity that acts as an "interdigestive housekeeper" in the small intestine.[2] 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.[3][4] 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.[5]

Phases

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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.[6] 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.[6]

Regulation

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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.[7] 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.[8] 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.[9]

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.[10]

Impairment

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Autoimmunity following infection by a pathogen producing CdtB, such as C. jejuni, may be the leading cause of MMC impairment.[11] Narcotics are also known to impair the MMC.[12] Stress has been shown to reduce MMC activity as well.[13]

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.[14]

Therapeutic stimuli

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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.[15] Motilin administration causes phase III contractions, and so motilin agonists are another common prokinetic.[16]

Eradication of bacterial overgrowth has been shown to partially restore MMC activity.[14]

An elemental diet has been hypothesized to partially restore MMC function.[17]

References

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  1. ^ Deloose E, Janssen P, Depoortere I, Tack J. The migrating motor complex: control mechanisms and its role in health and disease. Nat Rev Gastroenterol Hepatol. 2012;9(5):271-285. Published 2012 Mar 27. doi:10.1038/nrgastro.2012.57
  2. ^ a b Szurszewski, Joseph H. (1969-12-01). "A migrating electric complex of canine small intestine". American Journal of Physiology. Legacy Content. 217 (6): 1757–1763. doi:10.1152/ajplegacy.1969.217.6.1757. ISSN 0002-9513.
  3. ^ Dooley CP, Di Lorenzo C, Valenzuela JE (May 1992). "Variability of migrating motor complex in humans". Digestive Diseases and Sciences. 37 (5): 723–8. doi:10.1007/BF01296429. PMID 1563314.
  4. ^ Takahashi T (July 2012). "Mechanism of interdigestive migrating motor complex". Journal of Neurogastroenterology and Motility. 18 (3): 246–57. doi:10.5056/jnm.2012.18.3.246. PMC 3400812. PMID 22837872.
  5. ^ Hasler W (2006). Physiology of the Gastrointestinal Tract (Fourth ed.).
  6. ^ a b Boron WF, Boulpaep EL (2012). Medical physiology : a cellular and molecular approach (Updated second ed.). Philadelphia, Pa.: Saunders. ISBN 978-1-4377-1753-2.
  7. ^ Poitras P, Peeters TL (February 2008). "Motilin". Current Opinion in Endocrinology, Diabetes and Obesity. 15 (1): 54–7. doi:10.1097/MED.0b013e3282f370af. PMID 18185063.
  8. ^ Vantrappen G, Janssens J, Hellemans J, Ghoos Y (June 1977). "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. doi:10.1172/JCI108740. PMC 372329. PMID 864008.
  9. ^ Vantrappen G, Janssens J, Peeters TL (November 1981). "The migrating motor complex". The Medical Clinics of North America. 65 (6): 1311–29. doi:10.1016/S0025-7125(16)31474-2. PMID 7035768.
  10. ^ "Bloating, Gut Health, and the Migrating Motor Complex". Synergy Nutrition. Retrieved 2022-07-19.
  11. ^ Pimentel M, Morales W, Pokkunuri V, Brikos C, Kim SM, Kim SE, et al. (May 2015). "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. doi:10.1007/s10620-014-3435-5. PMID 25424202.
  12. ^ Kueppers PM, Miller TA, Chen CY, Smith GS, Rodriguez LF, Moody FG (March 1993). "Effect of total parenteral nutrition plus morphine on bacterial translocation in rats". Annals of Surgery. 217 (3): 286–92. doi:10.1097/00000658-199303000-00011. PMC 1242782. PMID 8452407.
  13. ^ Kumar D, Wingate DL (November 1985). "The irritable bowel syndrome: a paroxysmal motor disorder". Lancet. 2 (8462): 973–7. doi:10.1016/S0140-6736(85)90525-2. PMID 2865504.
  14. ^ a b Pimentel M, Soffer EE, Chow EJ, Kong Y, Lin HC (December 2002). "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. doi:10.1023/A:1021039032413. PMID 12498278.
  15. ^ Lördal M, Hellström PM (1998-04-15). "Serotonin induces phase III of the MMC, VIA 5-HT3-receptors dependent on cholinergic mechanisms in the small intestine". Gastroenterology. 114: A795. doi:10.1016/S0016-5085(98)83246-0.
  16. ^ Janssens J, Vantrappen G, Peeters TL (August 1983). "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. doi:10.1016/0167-0115(83)90265-3. PMID 6635258.
  17. ^ Pimentel M, Constantino T, Kong Y, Bajwa M, Rezaei A, Park S (January 2004). "A 14-day elemental diet is highly effective in normalizing the lactulose breath test". Digestive Diseases and Sciences. 49 (1): 73–7. doi:10.1023/B:DDAS.0000011605.43979.e1. PMID 14992438.
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