The incidence of obesity is reaching epidemic proportions in industrialized countries. Unfortunately, this is not merely a cosmetic problem, but also a major health problem. In particular, obesity is associated not only with the development of type 2 diabetes, but also with coronary heart disease, osteoarthritis, respiratory complications, and certain forms of cancer. The main drive of this “diabesity” epidemic is still incompletely understood, but it is obvious that the inadequate handling of the dietary lipid overload plays an important role. In addition to white adipose tissue (WAT), the liver is an important organ for handling excess lipid levels. Free fatty acids are taken up from the plasma and can either be oxidized or serve as precursors of hepatic triglyceride (TG) synthesis. However, ectopic deposition of FFA may lead to liver steatosis and insulin resistance.
Previous tracing studies in the NIN proved the existence of neural pathways between the brain and the liver, as well as clear effects of hypothalamic activity on hepatic glucose production. Our experiments are aimed at unraveling further the neural circuits within the brain that control hepatic lipid metabolism. We would like to test the hypothesis that an unbalanced output of the autonomic nervous system plays a role in hepatic steatosis.