Researchers Pinpoint Link Between Caloric Restriction and Longevity

When under stress, two genes within mitochondria guard against cell death

By Jeffrey Perkel
HealthDay Reporter

Related Encyclopedia • Alzheimer's Disease • Ginkgo Biloba • Hip Replacement • Hurthle Cell Carcinoma More... Related Healthscout Videos Importance of Good Nutrition Controlling Incontinence Preventing Heart Disease the Easy Way Lifestyle Changes for Heart Disease Prevention and Treatment More... Related Animations • Alzheimer's Disease Video Animation • Erectile Dysfunction • What is a Heart Attack? More... Related Drug Information • Actonel • Coumadin • Detrol LA • Ditropan XL More... Related News Articles • Health Tip: Helping a Loved One Heal • Thumbs Down on Beta Blockers for High Blood Pressure • Prosthetic Ears Boost Hearing After Injury • Stem Cells Ease Stroke-Like Brain Damage in Mice More...

THURSDAY, Sept. 20 (HealthDay News) -- Harvard researchers report they have uncovered a molecular clue that seems to explain why cutting calories might lengthen your life.

It turns out that mitochondria guard against cell death, and two specific genes within the mitochondria actually carry out that task, the scientists say. Mitochondria are compartments within a cell that are dedicated to energy production, and their loss is thought to be a major cause of aging.

Text Continues Below

---

The research also identifies two potential drug targets that could be exploited to slow down the aging process, said lead researcher David Sinclair, director of the Paul F. Glenn Laboratories for Aging Research at Harvard Medical School.

Sinclair and his colleagues found that, when either rat or human cells were deprived of nutrients (as in a caloric-restriction diet), the overall cellular concentration of a compound known as NAD dropped precipitously -- but not within mitochondria. Indeed, following any kind of cellular stress, mitochondrial NAD concentration actually increased.

Sinclair's team found that mitochondria can synthesize their own NAD to withstand stress, thereby helping the cells stay alive long enough to repair themselves.

Two members of a family of genes called sirtuins were required for this effect to occur, the authors found. Those proteins, SIRT3 and SIRT4, both reside within the mitochondria, and they need NAD to do their jobs.

"We were able to mimic calorie restriction in a dish," said Sinclair, "and that's important, because for decades, people knew calorie restriction made the cells less prone to death, but not how it worked, and we tracked it down to the mitochondria and to SIRT3 and SIRT4."

The findings were published in the Sept. 21 issue of Cell.

"This is really a great paper, and it basically provides very new knowledge about how NAD biosynthesis is regulated in our cells," said Dr. Shin-ichiro Imai, an assistant professor of molecular biology and pharmacology at the Washington University School of Medicine, in St. Louis.

Page:  1 | 2 | Next >>