Coffee connects an important anti -aging switch

by Andrea
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Drink coffee to live longer: everything is in routine

Coffee connects an important anti -aging switch

A new study has revealed that caffeine triggers an important anti -aging cellular mechanism.

Known to keep us awake and bring some health benefits, the Caffeine also moves cell behavior.

One of the main actors that can influence is the TORC1a kind of cell growth switch, which tells the cells “grow now!” or “stop!”, Depending on energy and nutrient levels.

As it refers to, this sign controls energy responses and stress in living beings for over 500 million years.

Some studies suggest that caffeine can slow down this sign of growth, possibly explaining its connection to a longer cell life. But, as the same magazine writes, there is a mystery here: it is not yet known if caffeine wages directly to Torc1 or gets there through secondary ways.

But a new study, published in the June edition, revealed that the Caffeine does not turn off directly to Torc1 how it was thought.

Instead, Active to Ampkan old cellular fuel sensor that is like a biological.

Ampk is activated when cells miss energy. When caffeine triggers this switch, AMPK naturally reduces Torc1, slowing growth and potentially promoting longevity.

Metformin, a medicine widely used for type 2 diabetes, activates Ampk, helping cells improve their energy balance.

Scientists used a yeast to find out how caffeine affects Ampk. In cells with ampk mutations, caffeine seems to increase sensitivity to DNA damage, but not due to its effects on cell division (mitosis), as you can expect.

Instead, researchers have found that caffeine acts in conjunction with other agents that damage DNA to make this effect stronger.

Interestingly, the caffeine accelerates how speed with which cells are divided and helps prolong your life (Known as chronological life time, or CLS), and this benefit is linked to Ampk’s way.

“These findings help explain why caffeine can be beneficial to health and longevity”He told New Atlas John-Patrick Alaoleader of the investigation, the laboratory Cellular Ageing and Senescence do Centre for Molecular Cell Biology and Queen Mary University of London.

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