Explained the molecular process for the phenomenon of ‘metabolic memory’ — the process whereby previous episodes of poor glucose control lead to cardiovascular injury in diabetes.
Human cells have a long memory. Even after blood glucose levels are brought under control in someone living with diabetes, the damage caused by earlier periods of poor control can persist — and continue to cause harm. This phenomenon is known as metabolic memory, and for a long time, exactly how it worked was unknown.
Baker Institute researchers helped answer that question. They identified a specific enzyme, Set7, that regulates the expression of genes responsible for proteins that cause injury to the heart, blood vessels and kidneys. The mechanism is epigenetic — meaning it involves an environmental influence on gene expression, with glucose interacting with genes in a way that leaves a kind of molecular imprint, even after conditions improve.
The clinical implications are significant. This research helps explain why people who have previously managed their diabetes poorly can continue to experience organ damage even after their glucose levels are stabilised. It also points to possible therapeutic targets — blocking these epigenetic pathways may reduce organ injury.
More broadly, the findings reinforce the critical importance of early, consistent diabetes management. Prevention of the initial damage — through the partnership of patients and clinicians working together — remains the most powerful intervention available.
