Sci. Aging Knowl. Environ., 19 November 2003
The "Fly Die" Diet
Coenzyme Q-less banquet that prolongs worm lives doesn't work for fruit flies
Key Words: CoQ ubiquinone
Like the fine print in a late-night infomercial for a miracle supplement, new work suggests that with a life-extending diet, "results may vary." Rations that lengthen worm life span hasten fruit fly demise, new research shows. The victuals lack a component of mitochondria, the cell's power plants. The diet quickened the pace of mitochondrial decay, a problem that exists in human disease, suggesting that fruit flies might mimic age-related decline of human mitochondrial function better than worms do.
Damage from reactive oxygen species (ROS), byproducts of metabolism, might promote aging (see "The Two Faces of Oxygen"). For example, Caenorhabditis elegans adults that cannot make a compound called coenzyme Q, which helps produce ROS in the mitochondria, live longer than normal animals do. Even reducing the amount of Q that worms eat translates to longer life: Normal worms that snarf bacteria lacking Q live 59% longer than squigglers that nibble Q-dribbled kibble (see "Eschew Beaucoup Q"). Life-extending methods that work in different organisms can reveal general mechanisms of aging, so evolutionary biologist Michael Palmer and biochemist Timothy Sackton of Brown University in Providence, Rhode Island, tested whether a Q-less diet would also lengthen life in Drosophila melanogaster.
To do so, the researchers fed 13,700 adult fruit flies one of three diets and waited for them to die. One food regime consisted of standard yeast-based meals. The second consisted of yeast that lacked the gene that makes coenzyme Q. Based on the results from worms, the team expected that flies chowing down on the Q-less grub would live longer, but they died almost 30% earlier, on average, than flies eating the well-rounded fare. Although this result suggested that the flies must consume Q, flies in the third group munched a diet with Q but without another component of the mitochondrial energy factory, and they also died about 30% earlier than normal. The observations imply that fly longevity doesn't depend on the presence or absence of Q in these menus.
No one knows why the dietary regime promotes longevity in worms but not flies. Life extension by a Q-less diet "might be an artifact of the C. elegans system," says Palmer. In a pinch, roundworms can generate power through fermentation, a process that squeezes a little bit of energy from food but doesn't involve coenzyme Q or the production of ROS. Perhaps when Q is unavailable, roundworms switch to this ROS-free process, says Palmer. Flies can't ferment, so the Q-less diet might simply cripple their overall energy production. Alternatively, yeast with broken power plants--from a lack of Q or another mitochondrial component--might produce a toxic compound that kills flies, says geneticist Pamela Larsen of the University of Texas Health Science Center in San Antonio.
Because fly mitochondria suffer without dietary Q, perhaps insects mimic human metabolic behavior better than worms do, says molecular gerontologist Simon Melov of the Buck Institute for Age Research in Novato, California. He points out that people who carry malfunctioning coenzyme Q-synthesizing genes suffer severe diseases that involve fatigue, cognitive deficiencies, and seizures. Humans might need to exercise care when taking dietary advice from a worm.
November 19, 2003
Science of Aging Knowledge Environment. ISSN 1539-6150