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Gericke B, Amiri M, Naim HY. The multiple roles of sucrase-isomaltase in the intestinal physiology. Mol Cell Pediatr. 2016;3(1):2doi: 10.1186/s40348-016-0033-y.
Gericke, B., Amiri, M., & Naim, H. Y. (2016). The multiple roles of sucrase-isomaltase in the intestinal physiology. Molecular and cellular pediatrics, 3(1), 2. https://doi.org/10.1186/s40348-016-0033-y
Gericke, Birthe, et al. "The multiple roles of sucrase-isomaltase in the intestinal physiology." Molecular and cellular pediatrics vol. 3,1 (2016): 2. doi: https://doi.org/10.1186/s40348-016-0033-y
Gericke B, Amiri M, Naim HY. The multiple roles of sucrase-isomaltase in the intestinal physiology. Mol Cell Pediatr. 2016 Dec;3(1):2. doi: 10.1186/s40348-016-0033-y. Epub 2016 Jan 26. PMID: 26812950; PMCID: PMC4728165.
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Mol Cell Pediatr. 2016 Dec;3(1):2. doi: 10.1186/s40348-016-0033-y. Epub 2016 Jan 26.

The multiple roles of sucrase-isomaltase in the intestinal physiology.

Molecular and cellular pediatrics

Birthe Gericke, Mahdi Amiri, Hassan Y Naim

Affiliations

  1. Department of Physiological Chemistry, University of Veterinary Medicine Hannover, Buenteweg 17, 30559, Hannover, Germany.
  2. Department of Physiological Chemistry, University of Veterinary Medicine Hannover, Buenteweg 17, 30559, Hannover, Germany. [email protected].

PMID: 26812950 PMCID: PMC4728165 DOI: 10.1186/s40348-016-0033-y

Abstract

Osmotic diarrhea and abdominal pain in humans are oftentimes associated with carbohydrate malabsorption in the small intestine due to loss of function of microvillar disaccharidases. Disaccharidases are crucial for the digestion and the subsequent absorption of carbohydrates. This review focuses on sucrase-isomaltase as the most abundant intestinal disaccharidase and the primary or induced pathological conditions that affect its physiological function. Congenital defects are primary factors which directly influence the transport and function of sucrase-isomaltase in a healthy epithelium. Based on the mutation type and the pattern of inheritance, a mutation in the sucrase-isomaltase gene may exert a variety of symptoms ranging from mild to severe. However, structure and function of wild type sucrase-isomaltase can be also affected by secondary factors which influence its structure and function either specifically via certain inhibitors and therapeutic agents or generally as a part of intestinal pathogenesis, for example in the inflammatory responses. Diagnosis of sucrase-isomaltase deficiency and discriminating it from other gastrointestinal intolerances can be latent in the patients because of common symptoms observed in all of these cases.Here, we summarize the disorders that implicate the digestive function of sucrase-isomaltase as well as the diagnostic and therapeutic strategies utilized to restore normal intestinal function.

Keywords: Carbohydrate maldigestion; Congenital sucrase-isomaltase deficiency; Gastrointestinal intolerance; Gut microbiota; Inflammation; Sucrase-isomaltase

References

  1. Curr Opin Gastroenterol. 2008 Sep;24(5):631-7 - PubMed
  2. Infect Immun. 2004 Jun;72(6):3536-42 - PubMed
  3. Curr Opin Gastroenterol. 2012 Mar;28(2):104-12 - PubMed
  4. Hum Mutat. 2006 Jan;27(1):119 - PubMed
  5. Curr Opin Cell Biol. 2011 Apr;23(2):176-83 - PubMed
  6. Drug Metab Lett. 2009 Jan;3(1):58-60 - PubMed
  7. J Virol. 1998 Sep;72(9):7228-36 - PubMed
  8. Hum Pathol. 1992 Jul;23(7):774-9 - PubMed
  9. Arch Pharm Res. 2000 Jun;23(3):261-6 - PubMed
  10. Curr Biol. 1999 Jun 3;9(11):593-6 - PubMed
  11. Mol Cell Biochem. 2006 Feb;283(1-2):85-92 - PubMed
  12. Am J Gastroenterol. 2008 Jan;103(1):162-9 - PubMed
  13. J Infect Dis. 1994 May;169(5):1116-20 - PubMed
  14. Int J Vitam Nutr Res. 1998;68(5):281-6 - PubMed
  15. J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 2):e348-52 - PubMed
  16. Scand J Gastroenterol. 2001 May;36(5):507-10 - PubMed
  17. J Inherit Metab Dis. 2012 Nov;35(6):949-54 - PubMed
  18. J Pediatr Gastroenterol Nutr. 2012 Nov;55 Suppl 2:S7-13 - PubMed
  19. Scand J Gastroenterol. 2000 Jun;35(6):599-606 - PubMed
  20. Curr Opin Gastroenterol. 2004 Mar;20(2):146-55 - PubMed
  21. J Biol Chem. 1996 Jan 12;271(2):1237-42 - PubMed
  22. Gastroenterology. 1990 Jun;98(6):1401-7 - PubMed
  23. Nat Rev Gastroenterol Hepatol. 2015 Sep;12(9):527-36 - PubMed
  24. J Enzyme Inhib Med Chem. 2012 Aug;27(4):553-7 - PubMed
  25. Am J Physiol Gastrointest Liver Physiol. 2005 Dec;289(6):G1108-14 - PubMed
  26. Scand J Gastroenterol. 2001 Feb;36(2):163-8 - PubMed
  27. Gut. 1999 Jul;45(1):70-6 - PubMed
  28. Clin Exp Immunol. 2015 Mar;179(3):363-77 - PubMed
  29. Int J Mol Med. 2006 Oct;18(4):721-7 - PubMed
  30. Immunol Rev. 2003 Oct;195:178-89 - PubMed
  31. Pediatr Res. 1988 Aug;24(2):233-7 - PubMed
  32. Parasitol Res. 1995;81(2):143-7 - PubMed
  33. Scand J Gastroenterol. 1995 Mar;30(3):235-41 - PubMed
  34. J Biol Chem. 1988 May 25;263(15):7242-53 - PubMed
  35. Eur J Clin Nutr. 2007 Dec;61 Suppl 1:S132-7 - PubMed
  36. Clin Gastroenterol Hepatol. 2006 Mar;4(3):276-87 - PubMed
  37. BMC Pediatr. 2002 Apr 25;2:4 - PubMed
  38. Exp Cell Res. 2009 Oct 15;315(17):2871-8 - PubMed
  39. J Pediatr Gastroenterol Nutr. 2012 Nov;55 Suppl 2:S34-5 - PubMed
  40. J Lab Clin Med. 1970 Jun;75(6):937-45 - PubMed
  41. J Pediatr Gastroenterol Nutr. 2012 Nov;55 Suppl 2:S13-20 - PubMed
  42. Am J Pathol. 2007 Dec;171(6):1952-65 - PubMed
  43. Nat Rev Immunol. 2014 May;14(5):329-42 - PubMed
  44. Am J Physiol Gastrointest Liver Physiol. 2007 May;292(5):G1228-32 - PubMed
  45. Pediatr Res. 1982 Apr;16(4 Pt 1):318-23 - PubMed
  46. Acta Biochim Pol. 2012;59(4):631-8 - PubMed

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