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Friday October 3, 2008 (foodconsumer.org) -- Researchers at the University of Wisconsin-Madison might have found a key target that can be used to prevent overeating, obesity or treat diseases related to obesity.

Reported in the Oct. 3, 2008 issue of Cell, Dr. Dongsheng Cai at the UW School of Medicine and Public Health said there is a messaging system in the brain that controls food intake and body weight.

Cai and colleagues found at the hypothalamus in the brain a cell-signaling pathway that is known to be associated with inflammation affects the regulation of food intake.

When the pathway is stimulated, animals like humans increase their energy consumption when suppressed they maintain normal food intake and body weight.

Obesity, which is caused by overeating, is commonly associated with a range of diseases such as heart disease and type 2 diabetes, which is most commonly found in developed countries where food is so cheap and so delicious that people can’t help, but eat more than what they need.

Cai's research was meant to provide some explanation how food and energy consumption affects metabolic inflammation, which is associated with an array of metabolic disorders.

Early studies at Harvard led by Cai and colleagues already found a compound known as IKKbeta activates a protein complex called NF-kappaB, inducing inflammatory reaction in many cells.

The pathway that can be activated by high-sugar and high-fat diet interrupts sugar, fat, or protein metabolism in tissues like liver, fat and skeletal muscle.

In the current study of mice, Cai and colleagues found for the first time that the pathway involving IKKbeta/NF-kappaB also exists in specific neurons in the hypothalamus, but is normally inactive.

They found that over-nutrition by overeating high-fat diet activated the pathway, specifically in neurons in the hypothalamus.

When NF-kappaB activity was suppressed for example by knocking out the IKKbeta gene and thus eliminating the production of IKKbeta, the mice were significantly protected from energy over consumption and obesity development.

This suggests that a drug that can suppress IKKbeta gene may be used to prevent overeating and or obesity.

Cai and his term also found a cell component called the endoplasmic reticulum (ER), shown recently to be involved in metabolic diseases involving over-nutrition can also play a role in over-nutrition activating IKKbeta/NF-kappaB in the hypothalamus.

Over-nutrition led to ER stress which forced activation of NF-kappaB, promoting increased food intake and obesity development, the study found.

"The ultimate goal will certainly be to identify a selective and effective suppressor of the pathway to target related neurons," Cai said.