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Diabetes Medication

Byetta Regenerates Islet Cells

Now, for the first time, medical research has shown that a diabetes drug “has direct beneficial actions on human T2DM [type 2 diabetes] islet cells.” The researchers, a group of nine doctors in Pisa, Italy, call the drug exendin-4, but we know it as Byetta.

They found that it can “induce the expression of beta-cell genes…involved in cell differentiation and proliferation in human T2DM islets.” Earlier research with beta-cell lines and rodent islets indicated that exendin-4 promotes islet cell regeneration.But the new research exposed pancreatic islets prepared from 11 non-diabetic controls and seven people with type 2 diabetes

to exendin-4 for 48 hours. The amount of insulin released in response to 16.7 mmol/l glucose was 258.0 pmol/l from control islets and 150.6 from type 2 cells. That’s a significant difference.

Piero Marchetti, MD, PhD, of the department of endocrinology and metabolism of Cisanello Hospital, in Pisa, Italy, is the corresponding author of the new study. When I asked him for a copy of the full-text, he send me the uncorrected proof of the report, “Effects of exendin-4 on islets from type 2 diabetes patients” scheduled to be published in a forthcoming issue of the journal Diabetes, Obesity and Metabolism. The abstract of the report is in MEDLINE.Most researchers won’t come right out and say it, but islet cell regeneration has to be the Holy Grail of diabetes research. The better angels of diabetes research rightly fear to tread too close to any claim that smacks of the word “cure.”

And regeneration is close. However, it’s not the same thing as a cure for type 2 diabetes, because this is what’s known as a “two-hit disease.” First comes insulin resistance and then beta-cell dysfunction. Regenerating those errant beta cells may take care of the dysfunction, but the underlying insulin resistance will remain unless we do something else about it.

That something else can be getting A1C’s down to normal and eventually learning to control the inflammatory processes that generate insulin resistance. We don’t yet know that for sure. But that’s my hope.


This article is based on an earlier version of my article published by HealthCentral.

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