A steady flow of new scientific evidence continues to show that patients affected by obesity and type 2 diabestes metabolize fat very differently from lean people. We are responding to the obesity epidemic by advancing development of ZGN-1061, by restoring balance between the production and utilization of fat.
ZGN-1061 is designed to reduce the activity of these stress mediators, restoring balance to fat metabolism and reducing inflammation.
Once a person becomes obese, the body undergoes certain metabolic changes and becomes “programmed” to create and store more fat, making it much more difficult to reduce body weight. The metabolic adaptations that take place in obese people impair the normal release and breakdown of fatty acids from adipose tissue.
Simultaneously, the body becomes much more efficient in diverting calories from food and storing them as fat.
This means that in the setting of obesity, high circulating insulin concentrations and levels of fats and sugars lead to stress in the liver and adipose tissue. This cellular stress is propagated by stress signaling molecules such as extracellular regulated kinase (ERK). Activation of stress pathways leads to changes in fat and cholesterol metabolism, and to the stimulation of the body’s inflammation cascades. Together these stress pathways lead to the overproduction of fat and glucose by the liver and reduce the availability of fat stored in adipose tissue. The result is that the body locks away calories that otherwise could be used productively as an energy source, and blood glucose levels are harder to control.
Currently marketed treatments use existing mechanisms to block the absorption of fat, or impact the feeding centers in the hypothalamus involved in controlling hunger, with moderate success to date.