Scientists have identified a single gene in yeast that can regulate the aging process, and many believe a similar gene plays a role in the aging of higher species as well.

Leonard Guarente, professor of biology at the Massachusetts Institute of Technology, gave a specialized lecture at Penn State last week on the connection of the Sirt1 gene with aging and calorie restriction in humans.

"The gene SIR2 dictates the life span of yeast organisms, and this relationship ought to be true for all descendents of this organism, including humans," said Guarente, who presented the Russell Marker Lectures in Genetic Engineering, sponsored by the Eberly College of Science. "It provides a crucial link between metabolism and aging."

Wendy Hanna-Rose, assistant professor of biochemistry and molecular biology, said the Sirt1 gene in humans and other mammals is the most similar to SIR2 in yeast.

"Currently, [scientists] are studying these genes in mice because they are more closely related to humans," said Hanna-Rose, who introduced Guarente at the lecture. "We know that if you take a mouse and give it a diet that is lower in calories, that mouse will live longer. The gene they study actually plays a role in regulating that process."

Guarente showed a video clip of two groups of the same strain of mice at 29 months old. The first group was fed a typical diet, while the second was put on a calorie-restricted diet.

"The [first group of] mice became fatter and are near the end of their lives," Guarente said. "The same strain on a calorie-restricted diet at 29 months are small, active, have sleek coats -- they look great."

He said the calorie-restricted group is expected to live 1.5 times as long as the first group.

There is empirical data that shows if one genetically engineers mice to be leaner, then they live longer, Guarente said.

"Somehow we have to get a message to all our organs about whether food is plentiful or scarce," he said. "The best strategy of the body is to store fat and burn carbohydrates, but if energy is limited, that equation changes and the body burns fat. Diet could be a signal to the whole body."

Guarente said that food limitation increases the regulation of Sirt1, which results in fat mobilization and dictates the pace of aging in the animal as a whole.

"Sirt1 is playing a critical role in diet and life span, and it becomes most important when food becomes scarce," he said. "The major effect is going to be to deliver the benefits of food scarcity on longevity."

Guarente added that starvation is not the same thing as long-term calorie restriction.

"You can't just stop eating," he said. "In rodents, we give them a nutrient-rich diet."

Sarah Ades, assistant professor of biochemistry and molecular biology, said that Guarente's research stands out because he has taken nutritional studies on this topic to the molecular and genetic level, and he has found a molecular basis for how calorie restriction expands life span.

"It seems like the Sirt1 genes in humans can affect the signaling process," Ades said. "Diseases like diabetes alter the secretion of insulin and [Guarente] has found that Sirt1 affects these [diseases] as well."

She said the research might result in drugs that could treat obesity and diabetes.

However, "that's only one part of aging," Ades said.

Researchers will "also keep on trying to understand what aging is and how it is controlled," she added.

Hanna-Rose said that if researchers can figure out what it is about calorie restriction that increases life span, they might learn how to manipulate the gene to make the body think calories were being restricted.

"Of course, all of this is in the future, but those are the implications," she said.