A new study has identified the hormone adrenomedullin as a key player in insulin resistance associated with obesity-related type 2 diabetes. Researchers found that adrenomedullin disrupts insulin signaling in blood vessel cells, contributing to metabolic dysfunction. Blocking its effects restored insulin sensitivity and improved glucose control in a mouse model, suggesting a potential therapeutic target for obesity-induced diabetes.
Type 2 diabetes remains a major global health challenge, driving illness, mortality, and rising healthcare costs. The condition is largely driven by obesity-induced insulin resistance, which impairs glucose metabolism in skeletal muscle, fat tissue, and the liver. However, emerging evidence suggests that endothelial cells lining blood vessels also play a crucial role in metabolic regulation through insulin signaling. While previous studies have implicated endothelial insulin resistance in type 2 diabetes, the precise mechanisms remain unclear.
In research led by Haaglim Cho, scientists discovered that obese mice and humans exhibit elevated levels of adrenomedullin and complement factor H (CFH), a protein that enhances adrenomedullin’s effects. Experiments on human endothelial cells revealed that adrenomedullin impairs insulin signaling by triggering a biochemical cascade that deactivates insulin receptors. This suggests that increased adrenomedullin and CFH levels in obesity contribute to vascular insulin resistance, exacerbating systemic metabolic dysfunction.
Further investigation demonstrated that administering adrenomedullin to lean mice induced insulin resistance and poor glucose regulation, mimicking obesity-related diabetes. However, mice lacking adrenomedullin receptors in their blood vessels were protected from these effects, confirming that the hormone exerts its influence through vascular receptors.
Crucially, blocking adrenomedullin signaling improved insulin function in blood vessels, enhanced muscle blood flow, and prevented insulin resistance in obese mice. These findings underscore adrenomedullin’s role as a key driver of metabolic dysfunction in obesity-related diabetes and highlight its potential as a novel therapeutic target.
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