Insulin May Actually Slow Progression of Atherosclerosis, not Increase It

Insulin may actually protect patients with diabetes against artery damage, rather than worsening the damage that occurs, new research from the Joslin Diabetes Center shows.

Senior author George L. King, MD, Joslin’s Chief Scientific Officer, and his research team found that mice whose insulin receptor had been knocked out developed cholesterol plaques that were more than twice the size of the plaques found in control animals. The insulin receptor was only knocked out in the endothelial cells of mice, rendering these cells unresponsive to the hormone. However, the two groups of mice showed similar levels of other factors that impact one’s risk for cardiovascular disease, such as blood pressure, glucose metabolism, and lipid levels in the blood.

After further investigation, the researchers discovered that the faster rate of artery damage was due to increased expression of the VCAM-1 adhesion molecule in the mice with the knocked-out insulin receptor. This condition was reversed when a VCAM-1 antibody was given to the mice.

Writing in Cell Metabolism, the authors conclude: “These results provide definitive evidence that loss of insulin signaling in endothelium, in the absence of competing systemic risk factors, accelerates atherosclerosis. Therefore, improving insulin sensitivity in the endothelium of patients with insulin resistance or type 2 diabetes may prevent cardiovascular complications.”

According to King, extrapolating these results to humans “would suggest that physicians should not be so wary of prescribing insulin to patients with diabetes.”

“It also raises the exciting possibility of designing special insulins that interact directly with blood vessels, potentially slowing atherosclerosis in these patients,” King continued.