Scientists have discovered a new function of insulin in the brain.
Researchers at Mount Sinai School of Medicine have found that impaired insulin action in the brain may be the result of unbridled lipolysis trigger and exacerbate type 2 diabetes in humans.
Conducted by Christoph Buettner, assistant professor of medicine, Division of Endocrinology, Diabetes and Bone Disease Mount Sinai School of Medicine, the research team first injected a small amount of insulin in the brain of rats and then assessed glucose metabolism lipids in the body. In doing so, found that brain insulin suppresses lipolysis, a process in which triglycerides are broken down into fatty acids and fatty acids are released.
Furthermore, in mice that lacked the brain insulin receptor, lipolysis was unrestrained. While fatty acids are important energy sources during fasting, they can worsen diabetes, especially when they are released after the person has eaten, as happens in people with diabetes. Researchers previously believed that insulin’s ability to suppress lipolysis was entirely mediated through insulin receptors expressed on adipocytes, or fat tissue order lexapro cells.
“The major lipolysis-inducing pathway in our bodies is the sympathetic nervous system and here the studies showed that brain insulin reduces sympathetic nervous system activity in fat tissue. In patients who are obese or have diabetes, insulin fails to inhibit lipolysis and fatty acid levels are increased. The low-grade inflammation throughout the body’s tissue that is commonly present in these conditions is believed to be mainly a consequence of these increased fatty acid levels.”
Buettner added, “When brain insulin function is impaired, the release of fatty acids is increased. This induces inflammation, which can further worsen insulin resistance, the core defect in type 2 diabetes. Therefore, impaired brain insulin signaling can start a vicious cycle since inflammation can impair brain insulin signaling.
“This cycle has been preserved and can lead to type 2 diabetes. Our study raises the possibility that the increase in insulin signaling in the brain may have therapeutic benefit of the lower risk of complications of insulin therapy, which is the ‘ hypoglycemia. ”