Jerusalem: Israeli and American researchers uncovered the role of a specific enzyme in managing blood sugar levels in a study that opens up new therapeutic possibilities for people with type 2 diabetes. Type 2 diabetes is a metabolic disorder characterized by insulin resistance, where the body's cells do not respond effectively to insulin. Over time, the pancreas may produce less insulin.
According to Philippines News Agency, researchers from the Hebrew University of Jerusalem, Hadassah Medical Center, and the University of Pennsylvania found that the enzyme Glucose-6-phosphatase 2 (G6PC2) helps manage blood sugar levels by regulating the secretion of glucagon, a hormone that raises blood sugar. The study was recently published in the peer-reviewed Science Translational Medicine.
Dr. Klaus H. Kaestner from the University of Pennsylvania stated, 'This research uncovers a critical mechanism that helps maintain blood sugar balance, moving us closer to understanding the complexities of diabetes and how we can address it more effectively.' Glucagon, produced by alpha (a) cells in the pancreas, works in tandem with insulin to maintain blood sugar balance. When blood sugar drops too low, glucagon raises it, ensuring stability. However, individuals with T2D often experience elevated glucagon levels, making it difficult to regulate blood sugar effectively. Until now, the way G6PC2 influences glucagon release was less understood.
The research team focused on the role of G6PC2 in defining the 'setpoint' at which glucose inhibits glucagon secretion. They discovered that variations in the G6PC2 gene affect its expression in a cells, altering glucagon regulation. In mice lacking the G6PC2 gene specifically in a cells, glucose more effectively suppressed glucagon secretion, underscoring the enzyme's role in this regulatory process. These findings were then replicated in human a cells.
Dr. Dana Avrahami-Tzfati of the Hebrew University explained, 'Our findings show that the enzyme G6PC2 helps control glucagon release by sensing glucose levels in a cells. This study offers a new therapeutic strategy of inhibiting G6PC2 to help control blood sugar in diabetics by simultaneously increasing insulin and reducing glucagon.' By influencing both insulin and glucagon, G6PC2 emerges as a potential target for innovative diabetes treatments.
Dr. Benjamin Glaser from the Hadassah Medical Center highlighted, 'Most current treatments focus on enhancing insulin action, often overlooking glucagon. Inhibiting G6PC2 offers a dual approach, targeting both hormones to potentially enhance therapeutic outcomes.' The findings pave the way for further exploration of G6PC2 and its therapeutic possibilities. Developing drugs to inhibit G6PC2 could simultaneously address imbalances in both insulin and glucagon, improving blood sugar control for people with type 2 diabetes (T2D).
By modulating G6PC2 activity, it may be possible to adjust the 'setpoint' for glucagon secretion, helping prevent hyperglycemia. Understanding genetic variations in the G6PC2 gene could enable personalized treatment strategies for T2D patients. Insights into how G6PC2 regulates glucagon secretion could benefit research into other metabolic disorders involving glucagon or insulin dysregulation, such as type 1 diabetes or certain forms of hypoglycemia.
