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Insulin resistance may begin with sugar consumption
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A recent study suggests that excessive sugar consumption may activate a protein in the liver to produce excessive glucose and subsequently lead to insulin resistance and diabetes.
Researchers hypothesize that insulin resistance may not be caused by defects in signaling, but rather in the triggering of carbohydrate-responsive element-binding protein (ChREBP), which is prompted by excess sugar in the liver to keep making glucose, according to a news release from Duke University.
“For the past several decades, investigators have suggested that there must be a problem in the way the liver senses insulin, and that is why insulin-resistant people make too much glucose,” Mark Herman, MD, assistant professor in the division of endocrinology, metabolism, and nutrition at Duke University School of Medicine, said in the release.
Researchers studied mice that were genetically altered so that their insulin-signaling pathways were fully activated and should have been unable to produce glucose. When the mice consumed fructose, ChREBP was triggered, causing it to make more glucose despite insulin signals to stop.
“We found that no matter how much insulin the pancreas made, it couldn’t override the processes started by this protein, ChREBP, to stimulate glucose production. This would ultimately cause blood sugar and insulin levels to increase, which over time can lead to insulin resistance elsewhere in the body.”
These findings could lead to better understanding of the development of prediabetes and eventually to drugs targeting the disease, according to Herman.