Anti-aging: Glycine Treatment May Be Key To ‘Fountain Of Youth’
Japanese scientists have found that skin aging may be reversed by reprogramming the skin cells to an embryonic stem cell-like state. This may sound complicated but the only key to this process is glycine treatment that scientists found to be capable of reversing the degeneration of the skin.
Skin-aging may be reversed
A team of scientists led by Professor Jun-Ichi hayashi from the University of Tsukuba in Japan disproved theory that damages to the skin due to aging are caused my mutations in the mitochondrial DNA of the skin. They found that aging of the skin rather is brought by another form of genetic regulation called the epigenetic regulation.
“Epigenetic regulation refers to changes, such as the addition of chemical structures or
proteins, which alter the physical structure of the DNA, resulting in genes turning on or off,” the scientists wrote in their report. Unlike mutations, epigenetic changes do not affect the DNA sequence of the skin itself.
Scientists found genes that reverse skin aging
In their study, the researchers got skin cell samples from both young and elderly people. They then reprogrammed the human fibroblast cell lines derived from their skin to an embryonic stem cell-like state. The result showed that reversal of the skin cell sample to its most basic state erased all skin damages, irrespective whether the sample was gotten from the young or the elderly.
Having discovered this reversal skin property, the scientists then looked for what might control the epigenetic regulation of the skin. They then found that genes capable of regulating the glycine production in the skin can also regulate the epigenetic regulation. Hence, they identified two genes with glycine properties.
For 10 days the scientists cultured the skin cell sample from a 97-year-old with glycine treatment. The end result was compelling as the aging process of the skin sample was totally reversed.
Read the full scientific report: Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects
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