Researchers from Mount Sinai School of Medicine have discovered a novel function of brain insulin, indicating that impaired brain insulin action may be the cause of the unrestrained lipolysis that initiates and worsens type 2 diabetes in humans.
The research team, led by Christoph Buettner, MD, Assistant Professor of Medicine in the Division of Endocrinology, Diabetes and Bone Disease at Mount Sinai School of Medicine, first infused a tiny amount of insulin into the brains of rats and then assessed glucose and lipid metabolism in the whole body. In doing so, they found that brain insulin suppressed lipolysis, a process during which triglycerides in fat are broken down 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 cells.
The research is published this month in the journal Cell Metabolism.
Source: Mount Sinai School of Medicine
