(Ivanhoe Newswire) -- Flies fed an "anti-Atkins" low protein diet live longer because their mitochondria function better, according to a new study from the Buck Institute for Age Research in California. The research shows that the molecular mechanisms responsible for the lifespan extension in the flies have important implications for human aging and diseases such as obesity, diabetes and cancer.

Mitochondria act as the "powerhouse" of the cells. It is well known that mitochondrial function worsens with age in many species, and especially in humans with Type II diabetes and obesity. "Our study shows that dietary restriction can enhance mitochondrial function, hence offsetting the age-related decline in its performance," Buck faculty member Pankaj Kapahi, PhD, lead author of the study, is quoted as saying.

The research calls into question the health benefits of the high-protein diets often used to lose weight. Kapahi said that while the long-term impacts of such diets have not been examined in humans, he believes they are likely to be harmful. "In flies, we see that the long-lived diet is a low protein diet and what we have found here is a mechanism for how that may be working," he said.

The researchers reported that while there is a reduction in protein synthesis with the low protein diet, the activity of specific genes involved in generating energy in the mitochondria are increased. That activity -- conversion of RNA to protein -- is important for the protective effects of dietary restriction, said Kapahi. "There have been correlative studies that show mitochondria change with dietary restriction, [and] this research provides a causal relationship between diet and mitochondrial function."
 
The study describes the mechanism by which mitochondrial genes are converted from RNA to protein by a particular protein (d4EBP). Flies fed a low protein diet showed an uptick in activity of d4EBP, which mediates cell growth in response to nutrient availability. The research showed that d4EBP is necessary for lifespan extension.

When the activity of the protein was genetically "knocked out" the flies did not live longer, even when fed the low protein diet. When the activity of d4EBP was enhanced, lifespan was extended, even when the flies ate a rich diet.
 
The Buck Institute study provides a significant advance in understanding the role of 4EBP, said Kapahi, and implies an important role for 4EBP and mitochondrial function as excellent targets to explore their role in lifespan extension in mammals.

SOURCE: Cell, October 2, 2009