Recently, a research report published in the international magazine Diabetes entitled "Acute Nitric Oxide Synthase Inhibition Accelerates Transendothelial Insulin Efflux In Vivo", scientists from Vanderbilt University discovered through research A new type of insulin "accelerator".
When the body's insulin level rises after eating, it sends a signal to promote the absorption of circulating glucose by the skeletal muscle. In the body of diabetic patients, the process is often damaged. This condition is called insulin. Insulin resistance.
Insulin must reach the skeletal muscle through the inner wall of endothelial cells or small blood vessels, and induce glucose uptake by skeletal muscle. Nitric oxide (NO) is a key regulator of endothelial cell function, which can stimulate arterial vasodilation and increase insulin exchange. Available surface area. In the article, the researcher Dr. David Wasserman and his colleagues found that when a compound called L-NAME blocks the function of nitric oxide synthase and reduces the level of nitric oxide in the mouse, it passes through endothelial cells. The activity of insulin is increased, as is the blood sugar lowering caused by insulin stimulation.
The investigators concluded that the urgent pharmacological inhibition of nitric oxide synthase increases the permeability of capillaries to insulin and increases the effects of insulin, thereby offsetting the acute effects of other organisms and reducing blood flow to capillaries. This may reveal a new mechanism for treating insulin resistance, and it can also help researchers develop new treatments for patients with diabetes later. (Bio Valley Bioon.com)
Original source:
Ian M. Williams, P. Mason McClatchey, Deanna P. Bracy, et al. Acute Nitric Oxide Synthase Inhibition Accelerates Transendothelial Insulin Efflux In Vivo, Diabetes (2018). DOI: 10.2337/db18-0288
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