Diabetes and Obesity Neurobiology

Through advances in molecular and neurobiology, we are beginning today to understand how the complex control circuit for the control of food intake and energy balance may work. Whether it is possible the findings, which were mostly obtained from animal experiments to humans, is not clear.

Participants will discuss a set-point model, which is aimed at the weight differences heading up or down to a fundamental value. Some results about the very complex control mechanisms include:

Leptin, a hormone that is produced in fat cells. The more fat there is in the fat cells, the higher the leptin concentration.  Primarily, it informs the CNS, whether the body is just starved to death.  It also inhibits the appetite.

Most overweight people seem to suffer from leptin resistance. There are now two possible explanations: a defect in leptin transport across the blood-brain barrier and a defective leptin receptor. Insulin is produced in the pancreas.  It regulates the glucose concentration in the blood. Mice whose neurons do not possess insulin receptors, are suffering from mild obesity.

PYY, GLP-1, and CCK Oxyntomodulin are produced in the gut and reduce hunger.

Ghrelin is a peptide that, among other things, is formed in the stomach. It stimulates the appetite. All this information is processed in the central nervous system and regulates appetite, energy use, the hormone levels and growth.