Unlocking longer life spans: Improved glucose uptake and diet restrictions in fruit flies

Fruit flies live longer when they eat better and have a higher glucose intake in their brain

Researchers at Tokyo Metropolitan University discovered that fruit fly genetically modified to increase glucose uptake had significantly longer lives. They found that by examining the brain cells in aging flies they could see how better glucose uptake compensated for age-related declines in motor function and resulted to a longer lifespan. This effect was even more prominent when combined with dietary restrictions. This suggests that improved glucose uptake by the brain and healthier eating could lead to longer lifespans.

The brain is one of the most power-hungry parts of our body, using up 20% of oxygen and 25% of glucose. It’s important to keep it powered by using glucose to create adenosine triphosphate (ATP), which is the \”energy messenger\” of the human body. This chemical reaction, called glycolysis, occurs in the intracellular fluid as well as a portion of the cell known as mitochondria. As we age, brain cells are less adept at producing ATP. This correlates to a lower glucose supply. This could suggest that eating more to get more glucose is a good idea. A healthier diet is also known to lead to a longer life. It may be possible to better understand how people can live longer and healthier by unraveling the mystery of these contradictory facts.

This problem was studied by a team of Drosophila fruit fly researchers led by Associate Prof. Kanae Ando. Firstly, the team confirmed that older flies had lower levels of ATP and glucose uptake. This was specifically attributed to lower levels of enzymes required for glycolysis. To counteract the effect, they genetically manipulated flies so that more of a protein transporting glucose called hGut3 was produced. This increase in glucose uptake, it was found, was enough to improve the amount ATP in cells. They found that increased hGut3 caused a decrease in enzyme production, which counteracted the age-related decline. Although this did not improve the age-related damage of mitochondria, it did result in a lessening in locomotor function.


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