Disabling enzyme allows mice to gorge without becoming obese, new s...(fferent organs and glands and travel thr...)

The new findings show that a large portion of the action is occurring within the actual fat tissue, mainly through the autocrine and paracrine action of PGE2 that acts locally within a cell or small group of cells.

The researchers caution that previous discoveries in fat metabolism and appetite regulation have not always translated well from mice to humans. Although some people have mutations in the gene that codes for AdPLA, it remains to be seen what effect these mutations have in humans, they said.

They also noted that inhibiting the expression of AdPLA in mice led to greater insulin resistance and a four-fold increase in fat content in the liver. However, tests of liver function were largely normal.

Nevertheless, AdPLA may become an attractive target in developing a treatment to combat obesity, the researchers said. If excess fat can be burned before it escapes the fat cell, it can never get into the bloodstream to negatively affect other organs, such as the heart.

"We believe that the effects in the liver are due to the extremely high rate of fat breakdown and drastic leanness in these mice, so we are looking to see if reducing rather than completely eliminating AdPLA can provide effective protection against obesity without secondary effects," said Duncan.

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