Epigenetics describes ways in which DNA in the cells can be modified leading to ‘cellular memory’. The phenomenon of ‘metabolic memory’ was described in the DCCT:EDIC study, where those participants with early, tight blood glucose control showed a decreased occurrence of diabetic eye disease (and other complications) compared to the group with poor control, for over a decade after the trial ended. It is assumed that cells ‘remember’ good or poor blood sugar control, but the mechanisms for this are unknown. JDRF is working to better understand the factors leading to complications resistance and susceptibility. In this paper, changes to the DNA coding for a specific compound involved in this cellular memory were shown to affect risk of diabetic retinopathy. This finding has not been fully explained but offers an intriguing genetic link between mechanisms of cellular memory, and diabetes complications risk.
Genetic Examination of SETD7 and SUV39H1/H2 Methyltransferases and the Risk of Diabetes Complications in Patients with Type 1 Diabetes. Tiitu A, El-Osta A, Forsblom C, Sandholm N, Parkkonen M, Tarnow L, Parving HH, McKnight AJ, Maxwell AP, Cooper ME, Groop PH; on the behalf of the FinnDiane Study Group. Diabetes. 2011, 60:3073-3080.
Ramifications for Individuals with Type 1 Diabetes:
This work is at a very early stage, so direct translation to a drug is not in the near term. However, increasing our understanding of this metabolic memory may identify ways in which damage from glucose may be reversed and complications averted.
JDRF did not fund this work although have funded several related projects in epigenetics and metabolic memory.