Diabetes is a disease diagnosed by the inability to regulate blood glucose concentration. A primary cause of diabetes is loss of insulin-producing pancreatic cells, or beta cells, which permanently affects insulin production capacity. For this reason, small molecules that can induce healthy, endogenous beta cell proliferation and regeneration have become the subject of vigorous research as of late. Studies in this thesis indicate that dual specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A) inhibitors such as harmine and harmine-derived analogs, or “harmalogs,” promote beta cell replication in mouse and human islets in vivo. Furthermore, co-treatment with harmine and transforming growth factor beta (TGF-beta) inhibitors further induce robust beta cell proliferation in vivo. These results suggest a potential future therapy for promoting beta cell regeneration and the recovery of glycemic control in diabetic patients.
|Advisor:||Garcia Ocaña, Adolfo|
|Commitee:||Vasavada, Rupangi, Scott, Donald|
|School:||Icahn School of Medicine at Mount Sinai|
|School Location:||United States -- New York|
|Source:||MAI 81/2(E), Masters Abstracts International|
|Subjects:||Medicine, Biology, Nutrition|
|Keywords:||Beta cell, Diabetes, DYRK1A, Harmalog, Harmine|
Copyright in each Dissertation and Thesis is retained by the author. All Rights Reserved
dissertation or thesis. The supplemental files are provided "AS IS" without warranty. ProQuest is not responsible for the
content, format or impact on the supplemental file(s) on our system. in some cases, the file type may be unknown or
may be a .exe file. We recommend caution as you open such files.
supplemental files is subject to the ProQuest Terms and Conditions of use.