searchers knocked out only one copy of the gene, they found the mice lived 18 percent longer than normal mice.
Whats more, the animals lived longer, even though they had characteristics that should shorten their livessuch as being overweight and having higher insulin levels in the blood, said White.
However, both sets of Irs2 knockout mice exhibited other characteristics that marked them as healthier. They were more active as they aged, and their glucose metabolism resembled that of younger mice.
The researchers also found that after eating, their brains showed higher levels of superoxide dismutase, an antioxidant enzyme that protects cells from damage by highly reactive chemicals called free radicals.
Our findings put a mechanism behind what your mother told when you were growing upeat a good diet and exercise, and it will keep you healthy, said White.
Diet, exercise and lower weight keep your peripheral tissues sensitive to insulin. That reduces the amount and duration of insulin secretion needed to keep your glucose under control when you eat. Therefore, the brain is exposed to less insulin. Since insulin turns on Irs2 in the brain, that means lower Irs2 activity, which weve linked to longer lifespan in the mouse.
The study was co-authored by Akiko Taguchi and Lynn Wartschow in Whites laboratory in the Division of Endocrinology at Childrens Hospital Boston and Harvard Medical School.
White speculated that the insulin-like signaling pathway in the brain might promote age-related brain diseases.
We are beginning to appreciate that obesity, insulin resistance, and high blood insulin levels are connected to Alzheimers disease, Huntingtons disease, and dementias in general, he said.
It might be that, in people who are genetically predisposed to these diseases, too much insulin overactivates Irs2 in the brain and accelerates disease proPage: 1 2 3 Related medicine news :1
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