Enteroglucagon is a peptide hormone derived from preproglucagon. It is a gastrointestinal hormone, secreted from mucosal cells primarily of the colon and terminal ileum.[1] It consists of 37 amino acids. Enteroglucagon is released when fats and glucose are present in the small intestine; which decrease the motility to allow sufficient time for these nutrients to be absorbed.

Discovery

In 1948, Sutherland and De Duve identified a gastrointestinal glucagon-like material in gastric mucosa,[2] the term "enteroglucagon" was used to describe this material that shared a similar immunoreactivity with glucagon.[3] A half-century later, Brubaker and Drucker[4] studied proglucagon gene expression, they discovered the function of enteroglucagon is related to the growth of intestinal epithelium.[5]

Function

Enteroglucagon is a proglucagon-derived peptide or enteroendocrine cells derived peptide in the small intestine. Preproglucagon undergoes post translational modification to release glucagon-like peptides (GLP-1 and GLP-2) and other molecules derived from L-cells of intestine. GLP-1 is derived from a class of intestinal hormones called incretin and the molecule exists in two forms GLP-1(7-37) and GLP-1(7-36) amide.[6] GLP-1 form of incretin starts circulating in response to a high blood glucose level. Incretin effect is a negative feedback loop between glucose and insulin level, it promotes insulin release from beta cells of pancreas islet and suppresses glucagon when the glucose level is high.[7] In vertebrate mammals, GLP-2 sequences are highly conversed in the intestine.[2] The molecule functions as apart of adaptive response, such that contributes intestinal growth, proliferation effect, intestinal dilation (increases the mucosal blood flow) and reduces the chance of apoptosis.[2]

Clinical Significance

GLP-1 is effective at reducing blood glucose levels. GLP-1 analogs have a significant therapeutic effect and high efficacy on diabetes treatments and hypoglycemia prevention.[8] Proliferation effect and trophic effect on the small intestine, GLP-2 is used as a therapy to support patients with short-bowel syndrome and other underlying intestinal conditions.[9]

See also

References

  1. ^ Holst, J. J. (1997). "Enteroglucagon". Annual Review of Physiology. 59: 257–71. doi:10.1146/annurev.physiol.59.1.257. PMID 9074764.
  2. ^ a b c Dunphy, J. L.; Fuller, P. J. (1997-09-19). "Enteroglucagon, bowel growth and GLP-2". Molecular and Cellular Endocrinology. 132 (1–2): 7–11. doi:10.1016/s0303-7207(97)00137-8. ISSN 0303-7207. PMID 9324041. S2CID 8182049.
  3. ^ Sarwal, Dhruv; Bordoni, Bruno (2021), "Physiology, Enteroglucagon", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31971745, retrieved 2021-05-02
  4. ^ Drucker, Daniel J.; Shi, Qing; Crivici, Anna; Sumner-Smith, Martin; Tavares, Wendy; Hill, Mary; DeForest, Lorraine; Cooper, Sari; Brubaker, Patricia L. (July 1997). "Regulation of the biological activity of glucagon-like peptide 2 in vivo by dipeptidyl peptidase IV". Nature Biotechnology. 15 (7): 673–677. doi:10.1038/nbt0797-673. ISSN 1546-1696. PMID 9219272. S2CID 35172107.
  5. ^ Drucker, D J; Erlich, P; Asa, S L; Brubaker, P L (1996-07-23). "Induction of intestinal epithelial proliferation by glucagon-like peptide 2". Proceedings of the National Academy of Sciences of the United States of America. 93 (15): 7911–7916. Bibcode:1996PNAS...93.7911D. doi:10.1073/pnas.93.15.7911. ISSN 0027-8424. PMC 38848. PMID 8755576.
  6. ^ Deacon, Carolyn F. (September 2007). "Incretin-based treatment of type 2 diabetes: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors". Diabetes, Obesity & Metabolism. 9 Suppl 1: 23–31. doi:10.1111/j.1463-1326.2007.00765.x. ISSN 1462-8902. PMID 17877544. S2CID 12334916.
  7. ^ Sarwal, Dhruv; Bordoni, Bruno (2021), "Physiology, Enteroglucagon", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31971745, retrieved 2021-04-30
  8. ^ Trujillo, Jennifer M.; Nuffer, Wesley; Ellis, Samuel L. (February 2015). "GLP-1 receptor agonists: a review of head-to-head clinical studies". Therapeutic Advances in Endocrinology and Metabolism. 6 (1): 19–28. doi:10.1177/2042018814559725. ISSN 2042-0188. PMC 4321870. PMID 25678953.
  9. ^ Jeppesen, P. B. (November 2003). "Clinical significance of GLP-2 in short-bowel syndrome". The Journal of Nutrition. 133 (11): 3721–3724. doi:10.1093/jn/133.11.3721. ISSN 0022-3166. PMID 14608103.