Researchers at the David Geffen School of Medicine at UCLA added protease inhibitors to cultures of both mouse and human cells.

They saw that the drugs inhibited an enzyme called ZMPSTE24, which helps convert prelamin A to mature lamin A, an important molecule in the structural scaffolding that supports the cell nucleus.

In AIDS patients, the cellular defect usually produces metabolic syndrome -- a diabetic precursor condition -- as well as a loss of body fat.

About a third of AIDS patients on protease inhibitors develop these side effects, the researchers said.

They said they plan to study the phenomenon more closely because the defect is similar to the defect found in the rare premature aging disease called progeria and could produce clues about how that problem might be solved and deeper understanding of aging in general.

The study appears in the July 16 early edition of the Proceedings of the National Academy of Sciences.