Regeneration Research in Diabetes

In both type 1 diabetes and advanced type 2 diabetes, insulin-producing beta cells lose their ability to function or perish completely. As a result, no or insufficient insulin is produced, resulting in permanently high blood glucose levels. Despite modern drug therapies, it is not always possible to completely normalize and prevent fluctuations in blood glucose levels. None of today's therapies stops the course of the disease or leads to the cure of the various forms of diabetes. As a result, up to fifty percent of patients still suffer from chronic secondary diseases and serious complications such as stroke, chronic renal failure, coronary heart disease, nerve and eye disease.


In brief:

The aim of regeneration research in diabetes is to preserve or replace beta cells. If insulin is distributed as needed, this prevents secondary diseases.

To prevent such secondary diseases, researchers around the world are looking for ways to preserve or restore beta-cell mass in order to normalize insulin secretion. Promising approaches include

  • Cell replacement therapy: Insulin-producing islet cells are to be generated from stem cells.
  • The regeneration of the body's own beta cells. Scientists are working on techniques to regenerate or preserve remaining beta cells.

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Regenerative Therapies give opportunities for cure - for Type-1- and also for Type-2-Diabetes. Prof. Heiko Lickert, head of the Institute of Diabetes and Regeneration Research at Helmholtz Zentrum München, explains the different strategies in a video-interview. Length: 2.33 Minutes

REGENERATION: BASICS: The beta cells are the insulin-producing cells in the pancreas. They are not distributed throughout the tissue, but are grouped in specific regions of the organ more

REGENERATION: FUTURE APPLICATION AREAS: Stem cells are the hope of modern medicine. They possess a high self-renewal rate more

REGENERATION: RESEARCH: There are already a number of promising research approaches in regenerative diabetes research more

Informationen zum Inhalt


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  • Bastidas-Ponce, A. et al.: Cellular and molecular mechanisms coordinating pancreas development. In: Development. 2017 Aug 15;144(16):2873-2888. doi: 10.1242/dev.140756.
  • Bastidas-Ponce, A.: Foxa2 and Pdx1 cooperatively regulate postnatal maturation of pancreatic β-cells. In: Mol Metab., 2017, 6(6):524-534. doi: 10.1016/j.molmet.2017.03.007. eCollection 2017 Jun.
  • Lickert, H., Kaestner, K.H.: Islet biology. In: Mol Metab., 2017, 6(9):vi. doi: 10.1016/j.molmet.2017.06.005. eCollection 2017 Sep 
  • Kleinert, M. et al.: Animal models of obesity and diabetes mellitus. In: Nat Rev Endocrinol., 2018, 14(3):140-162. doi: 10.1038/nrendo.2017.161.
  • Wang, X. et al: Genome-wide analysis of PDX1 target genes in human pancreatic progenitors. In: Mol Metab., 2018, 9:57-68. doi: 10.1016/j.molmet.2018.01.011.
  • Wang, X. et al.: Generation of a human induced pluripotent stem cell (iPSC) line from a patient with family history of diabetes carrying a C18R mutation in the PDX1 gene. In: Stem Cell Res., 2016, 17(2):292-295. doi: 10.1016/j.scr.2016.08.005.
  • Wang, X. et al: Generation of a human induced pluripotent stem cell (iPSC) line from a patient carrying a P33T mutation in the PDX1 gene. In: Stem Cell Res., 2016, 17(2):273-276. doi: 10.1016/j.scr.2016.08.004. Epub 2016 Aug 5.
  • Roscioni, S.S. et al.: Impact of islet architecture on β-cell heterogeneity, plasticity and function. In: Nat Rev Endocrinol., 2016, 12(12):695-709. doi: 10.1038/nrendo.2016.147. Epub 2016 Sep 2.
  • Migliorini, A. et al.: Targeting insulin-producing beta cells for regenerative therapy. In: Diabetologia. 2016 Sep;59(9):1838-42. doi: 10.1007/s00125-016-3949-9.
  • Bader, E. et al: Identification of proliferative and mature β-cells in the islets of Langerhans. In: Nature. 2016 Jul 21;535(7612):430-4. Epub 2016 Jul 11.
  • Willmann S.J. et al.: The global gene expression profile of the secondary transition during pancreatic development. In: Mech Dev. 2016 Feb;139:51-64. doi: 10.1016/j.mod.2015.11.004. 

Scientific advice: Prof. Dr. Heiko Lickert

Last Change

December, 13, 2018

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