A team of researchers from the Van Andel Institute in Grand Rapids has found that surplus sugar — with the average American eating around 22 teaspoons of added sugar per day — may cause our mitochondria, or cellular powerhouses, to becomes less efficient, reducing their overall energy output.
The findings were published in Cell Reports and highlight the cellular implications of excessive sugar consumption and provide a new model to study the initial metabolic events that may contribute to the development of diabetes.
“The body needs sugar, or glucose, to survive, but, as the saying goes: ‘All good things in moderation,’” says Ning Wu, an assistant professor at Van Andel Institute and corresponding author of the study. “We found that too much glucose in cells, which is directly linked to the amount of sugar consumed in one’s diet, affects lipid composition throughout the body, which in turn affects the integrity of mitochondria. The overall effect is a loss of optimal function.”
Overconsumption of sugar is known to cause contribute to diabetes and other disorders, but until now, the ways in which overconsumption sets the stage for metabolic diseases on a cellular level has been relatively unclear.
Using the new model, Wu and her colleagues demonstrated that excess glucose reduces the concertation of polyunsaturated fatty acids (PUFAs) in the mitochondrial membrane, making them less efficient.
According to the American Heart Association, from a chemical standpoint, polyunsaturated fats are fat molecules that have more than one unsaturated carbon bond in the molecule. Omega-6 and omega-3 fatty acids are essential to the human body’s function but are not produced by the body. PUFAs support mitochondrial function and mediate a host of other biological processes such as inflammation, blood pressure, and cellular communication.
Instead, excess glucose is synthesized into a different form of fatty acid that isn’t as efficient or flexible as PUFAs. This upends the lipid composition of the membrane and puts stress on the mitochondria, damaging them and impacting their performance.
“Although we may not always notice the difference in mitochondrial performance right away, our bodies do,” says Wu. “If the lipid balance is thrown off for long enough, we may begin to feel subtle changes, such as tiring more quickly. While our study does not offer medical recommendations, it does illuminate the early stages of metabolic disease and provides insights that may shape future prevention and therapeutic efforts.”
The team was able to reverse the detrimental effect overconsumption of sugar by feeding a low-sugar ketogenic diet to the mouse models used in the research. This suggests reducing glucose and restoring normal membrane lipid composition supports healthy mitochondrial integrity and function. They also found that consuming excess carbohydrates reduces the beneficial effect of PUFA supplements.
Other authors include Althea N. Waldhart, Brejnev Muhire, Ben Johnson, Dean Pettinga, Zachary B. Madaj, Emily Wolfrum, Vanessa Wegert, and J. Andrew Pospisilik of VAI; and Xianlin Han of the Sam and Ann Barshop Institute for Longevity and Aging Studies and the Department of Medicine at UT Health San Antonio.
Established in Grand Rapids in 1996 by the Van Andel family, VAI is now home to more than 400 scientists, educators, and support staff, who work with a growing number of national and international collaborators to foster discovery.