advertisement
 

  Back to Ask the Diabetes Team Ask the Diabetes Team
Question:

From New York, USA:

I am wondering, when an autoimmune attack takes place on the endocrine pancreas, are the alpha cells destroyed in addition to the beta cells? If so, does this make hypoglycemia a greater risk? What cells make amylin? Are these destroyed in the same attack that produces diabetes, or not? Or, is the amylin deficiency not explained yet?

Answer:

The autoimmune attack is aimed at the islets, but mostly the beta cells. Most of the other cells are also attacked but not as vigorously in most studies. However, the communication from one cell to the others also seems to be damaged in this process and, thus, the other cells hormone production is altered, much like a damaged thermostat that can over- and under-react. High sugar levels may contribute to this over time as well as the initial autoimmune attack itself.

SB

[Editor's comment: For additional information on amylin, see The role of amylin in the physiology of glycemic control.; Amylin inhibits glucose-induced insulin secretion in a dose-dependent manner. Study in the perfused rat pancreas.; Amylin and insulin co-replacement therapy for insulin-dependent (type I) diabetes mellitus.; and Effects of amylin and the amylin agonist pramlintide on glucose metabolism. BH]

DTQ-20070209003436
Original posting 17 Feb 2007
Posted to Research: Other Research

  
advertisement


                 
  Home Return to Top

Last Updated: Tuesday April 06, 2010 15:10:12
This Internet site provides information of a general nature and is designed for educational purposes only. If you have any concerns about your own health or the health of your child, you should always consult with a physician or other health care professional.

This site is published by T-1 Today, Inc. (d/b/a Children with Diabetes), a 501c3 not-for-profit organization, which is responsible for its contents.
By using this site, you agree to our Terms of Use, Legal Notice, and Privacy Policy.
© Children with Diabetes, Inc. 1995-2015. Comments and Feedback.