Higher blood glucose levels were linked to greater pancreatic beta cell dysfunction in adults with type 2 diabetes who took only metformin as a drug treatment, according to the results of a study published in the Journal of Diabetes and Its Complications.
While these results may not seem surprising — after all, it seems logical that glucose levels would be higher in people whose pancreases aren’t producing enough insulin — they highlight the widespread problem of pancreatic beta cell dysfunction in people with type 2, and suggest that therapies beyond just metformin may be useful to help maintain the pancreas’s ability to produce insulin.
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Unlike type 1 diabetes, in type 2, it’s usually not a lack of available insulin in the body that causes elevated blood glucose, at least at first. Instead, high glucose levels in type 2 are typically caused by insulin resistance, or the body’s inability to efficiently use insulin to reduce blood glucose. But as type 2 diabetes progresses, many people lose the ability to produce as much insulin as they previously did, and it’s often necessary to start taking insulin when this happens.
For the latest study, the participants a group of 3,108 adults with type 2 diabetes for less than 10 years, all of whom took metformin alone as a diabetes treatment. Researchers looked at at how they responded to a 2-hour oral glucose tolerance test, and compared their blood glucose response with a number of other measurements, including their insulin response, insulin sensitivity, C-peptide (a substance produced along with insulin that stays in the blood longer), pancreatic beta cell function, and A1C (a measure of long-term blood glucose control). Not surprisingly, they found that participants’ insulin and C-peptide responses to oral glucose tended to be greater in people with lower insulin sensitivity, and smaller in those with higher insulin sensitivity. Also as expected, glucose levels tended to be higher when a participant’s insulin and C-peptide response was lower, and vice versa.
Higher glucose more strongly tied to beta cell dysfunction than insulin resistance
But a few findings were notable, including the fact that there was only a modest relationship between A1C and measured pancreatic beta cell function. Higher blood glucose levels in response to oral glucose, on the other hand, was strongly linked to beta cell dysfunction — demonstrating that the effects of this dysfunction aren’t always apparent in A1C, but tend to be seen in an oral glucose tolerance test. So for doctors to screen patients for possible beta cell dysfunction, A1C might not be the best place to start.
And another important finding was that higher glucose was more strongly tied to beta cell dysfunction than to insulin resistance. So addressing beta cell dysfunction — possibly through additional treatments that help improve pancreatic function — could be a more effective treatment strategy to reduce glucose levels than simply addressing insulin resistance, as some treatments for type 2 diabetes do. The study authors endorsed this idea, concluding that in people with high blood glucose, “Efforts to improve glycemia should focus on interventions aimed at improving [beta] cell function.”
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