12/22/2010 PERMALINK
Mammalian aging process linked to overactive cellular pathway. Whitehead Institute researchers have linked hyperactivity in the mechanistic target of rapamycin complex 1 cellular pathway to reduced ketone production in the liver, which is a well-defined physiological trait of aging in mice. During sleep or other times of low carbohydrate intake, the liver converts fatty acids to ketones, which are vital sources of energy during fasting, especially for the heart and brain. As animals age, their ability to produce ketones in response to fasting declines. One cellular pathway, the mTORC1 pathway, is known to coordinate cell growth with nutrient availability and other growth factors. Previous research has shown that when this pathway is inhibited, a variety of animals, including worms, flies, and mice tend to live longer. When researchers turned off the mTORC1 pathway in very young mice, these mice did not experience the normal decline in ketogenesis as they aged. In old age, their ketogenesis levels remained similar to younger mice, confirming that continual inhibition of the mTORC1 pathway prevented the aging-induced decline in ketone production.