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Recently, the research team at Cologne and Bonn University in Germany discovered how protein aggregation affects the glucose metabolism process regulated by insulin receptors, triggering body aging.
Our longevity depends not only on our way of life, but also on our genetic material. The genetic program in which insulin receptors regulate plays an important role. Recently, the research team at the University of Cologne and Bonn in Germany discovered how protein aggregation affects this genetic process, triggering body aging. Related articles were published in the April 21 issue of Cell.
Insulin receptor is an expected life brake
In the early stages of our evolution, sugar intake is closely related to the length of life, and in the relationship between sugar and life, insulin plays a crucial role. By binding to cell surface receptors, insulin can rapidly and efficiently regulate blood sugar levels, but many survival-related processes are shut down at the same time. This is not necessary for the body when the food supply is sufficient, although this is a long-term reduction in life expectancy. Insulin receptors are like brakes of life expectancy, and experimental animals inactivated by insulin receptors actually live longer than normal experimental animals.
But how does insulin receptors usually remain in our cells and tissues? A recent study by scientists at the University of Cologne and Bonn focused on this fundamental question.
Anti-aging effect of CHIP protein
The researchers found that a protein called CHIP, a ubiquitin ligase, plays a crucial role here. Its behavior is like a helper of the cell surface insulin receptor cycle renewal. It promotes the degradation of the insulin receptor through ubiquitination, and transfers the insulin receptor into the cell for decomposition and cyclic renewal. The brakes of the life expectancy of the body - the insulin receptor is thus "released" without braking, and CHIP also plays an anti-aging function.
The author of the article, Thorsten Hoppe, a professor at the University of Cologne, explains: "The CHIP protein has a similar function in the worms, fruit flies and human cells. This protein is increasingly stimulating our research interest."
Insufficient CHIP protein leads to premature aging
The initial results of the study were very surprising, and CHIP also performed its function in a completely different way. In particular, CHIP also promotes the degradation of misfolded and structurally damaged proteins. With age, the accumulation of protein misfolding can lead to dementia and muscle weakness. The researchers found that when the intracellular CHIP protein is severely deficient, similar degenerative diseases can be caused in both nematodes and human cells, and insulin receptor turnover is inhibited, leading to premature aging of cells.
Can the dream of Laoquan really be realized? Another author of the article, Jorg Hohfeld, a researcher from the University of Bonn, said: "In fact, it is not that simple." When the number of CHIP is too large, normal proteins are also forced to be recycled, which leads to the destruction of the body's homeostasis. However, researchers are already looking for ways to degrade the insulin receptor using CHIP, hoping to apply it to clinical treatment.
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