Research Provides New Theory on Insulin Resistance
Is too much sugar consumption to blame for type 2 diabetes? New research adds to the growing scientific evidence linking too much sugar, particularly fructose, to the prevalence of metabolic disease worldwide.
In the present study, scientists uncovered a metabolic process that could upend previous ideas about how the body becomes resistant to insulin and eventually develops diabetes. While there has been numerous claims that high sugar consumption can lead to diabetes, some expert say that commonly consumed amounts of sugar do not contribute to this epidemic.
"While others are convinced that excessive sugar ingestion is a major cause. This paper reveals a specific mechanism by which consuming fructose in large amounts, such as in soda, can cause problems." said senior author Mark Herman, M.D., assistant professor in the Division of Endocrinology, Metabolism, and Nutrition at Duke University School of Medicine.
Type 2 diabetes begins when the body develops insulin resistance. Insulin is a key hormone that regulates glucose the body consumes. Insulin resistance occurs when the body’s metabolic tissues stop responding normally to insulin.
But the new study suggests that the cause of insulin resistance may have little to do with defects in insulin signalling and might actually be caused by a separate process triggered by excess sugar in the liver that activates a molecular factor known as carbohydrate-responsive element-binding protein, or ChREBP.
The research found that fructose initiates a process that causes the liver to keep making glucose and raising blood glucose levels, even as insulin tries to keep glucose production in check.
"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," Herman said.
"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."
While more studies are needed, scientists say they better understand a key mechanism leading to pre-diabetes and can now explore how to possibly interrupt that chain of events.
The finding could also help scientists one day diagnose metabolic disorders earlier on, potentially allowing patients to make changes to their diets and lifestyles sooner to prevent more serious complications.
"You could eat three apples and not get the same amount of fructose you might get from a 20-ounce sugar-sweetened beverage," Herman said. "The major sources of excessive fructose are in foods like sodas and many processed foods, which are foods most doctors would say to limit in your diet."
The new findings were published in the Journal of Clinical Investigation.
Source of this article:
ChREBP regulates fructose-induced glucose production independently of insulin signaling
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