Calorie Restriction Boosts Cell Components Recycling

Calorie restriction extends life in most animals which have been studied well on calorie restricted diets. Calorie restriction is the only consistent way to extend life in lab animals that has been found to date. Some University of Florida scientists found that rats on low calorie diets might live longer because the calorie restriction causes cells to more rapidly chew up and recycle cellular components such as energy-producing mitochondria.

And a University of Florida study shows just how much the body benefits when it goes green, at least if youre a rat: Cutting calories helps rodents live longer by boosting cells ability to recycle damaged parts so they can maintain efficient energy production. Caloric restriction is a way to extend life in animals. If you give them less food, the stress of this healthy habit actually makes them live longer, said Christiaan Leeuwenburgh, Ph.D., chief of the division of biology of aging in UFs Institute on Aging. Understanding how the process works at the cellular level in rodents could help scientists develop drugs that mimic the process in humans, Leeuwenburgh added.

Some biogerontologists theorize that aging damaged mitochondria displace healthy mitochondria. Then those damaged mitochondria spew out free radicals that damage cells. These University of Florida researchers are speculating that if cells more aggressively chew up damaged mitochondria then those bad mitochondria won't take over and squeeze out healthier mitochondria.

Fortunately, younger cells are adept at reducing, recycling and rebuilding. In this process, damaged mitochondria are quickly swallowed up and degraded. The broken down pieces are then recycled and used to build new mitochondria. However, older cells are less adept at this process, so damaged mitochondria tend to accumulate and contribute to aging.

Here is their core finding. Calorie restriction accelerated autophagy, the recycling of damaged cellular components.

UF scientists studied 22 young and old rats, comparing those allowed to eat freely with those fed a low-calorie, nutritious diet. The stress of a low-calorie diet was enough to boost cellular cleaning in the hearts of older rats by 120 percent over levels seen in rats that were allowed to eat what they wanted. The diet had little or no effect on younger rats.

If drugs could be found that enhance autophagy (the chewing up of damaged cellular components) then those drugs might slow down the aging process by preventing bad damaged mitochondria from taking over cells and spewing free radicals into cells and into the environment around cells.

Autophagy is a housekeeping mechanism that keeps cells free of damaged and thereby detrimental mitochondria and other toxic materials while recycling their building blocks  nutrients needed by the cell, said Stephanie Wohlgemuth, Ph.D., a lecturer in UFs department of aging and geriatrics and the studys lead author. So if that process is maintained with age  or even increased  that can only be beneficial.

Gene therapy that could fix mitochondrial DNA might some day deliver an even bigger anti-aging benefit by fixing damaged mitochondria that spew free radicals.