A dietary regimen that is the opposite of the high protein Atkins diet was associated with a longer lifespan and improved mitochondrial function in research conducted with flies at the Buck Institute for Age Research in Novato, California. Reduced functioning of the mitochondria, which are the power plants of the cells, occurs with aging and is associated with such diseases such as type 2 diabetes and Parkinson’s disease.
In the October 2, 2009 issue of the journal Cell, Pankaj Kapahi, PhD and colleagues identify the mechanism of the extension of life span observed in flies whose diets were modified by lowering the level of yeast relative to sucrose (the source of carbohydrates in the flies’ diets). By examining the expression of genes in restricted flies, Dr Kapahi and his associates found that, although protein synthesis was reduced on a global level, the activity of specific genes involved in the production of energy within the mitochondria increased. According to Dr Kapahi, this activity, which occurs at the level of conversion of RNA to protein, is involved in dietary restriction’s protective effects. Flies receiving low protein diets showed increased activity of a protein known as d4EBP, which is part of a signaling pathway called TOR (target of rapamycin) that influences cell growth in response to the availability of nutrients. (Rapamycin, a drug that has many medical uses, was recently shown to increase the lifespan of aged mice.) While flies on a low protein diet experienced a significant extension of lifespan compared to flies whose diets were nonrestricted, knocking out the gene for d4EBP diminished the effect, and restoring d4EBP expression enhanced it.
The findings question the wisdom of popular high protein weight loss diets. “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.” Dr Kapahi stated.
The study is the first genome-wide investigation of how proteins are translated in dietary restricted organisms. “Our study shows that dietary restriction can enhance mitochondrial function hence offsetting the age-related decline in its performance,” Dr Kapahi concluded. “There have been correlative studies that show mitochondria change with dietary restriction; this research provides a causal relationship between diet and mitochondrial function.”