When you have diabetes, you don’t have enough functioning beta cells, which store and release insulin. People with Type 1 diabetes have quickly lost almost all of these cells, and if you have Type 2, you will typically experience a progressive decline in the number and size of your beta cells.
One type of diabetes drug has been shown in animal studies to stop this loss of cells. However, because the drug is so new, researchers don’t know if it will have the same effect on human cells.
The technical name for this drug class is a mouthful: glucagon-like peptide-1 receptor agonists. Researchers often shorten it to GLP-1 receptor agonist, or even just GLP-1. The newest brand is Trulicity. Others available in the United States are Tanzeum, Victoza, Bydureon, and Byetta, which was the first of this class.
Only available for a decade
These drugs have been available for just over 10 years. While they haven’t been approved for people with Type 1 diabetes, some of these people apparently benefit when their doctors prescribe them "off-label."
As someone with type 2 diabetes, as soon as my health insurance began to cover the first of these drugs in early 2006, I took it to manage my blood glucose and my weight at the same time. This worked so well that I stopped taking it after less than two years because I no longer needed any drug for either condition.
Ever since then, I’ve been able to keep my A1C level down to about 5.5 or less without drugs – what the American Diabetes Association calls “complete remission.” I’ve often wondered how I could be so lucky, when the experts keep telling us that diabetes keeps getting progressively worse.
Keeping the balance
The answer may be in studies showing that this drug can maintain the balance between the birth of new beta cells and the death of old ones from apoptosis, which is the normal and controlled dying off of old cells. Accelerated apoptosis is the main reason why Type 2 diabetes tends to get progressively worse.
A recent study in The Journal of Pathology reviewed many animal studies, mostly on rodents, showing that GLP-1 drugs increase the number and size of beta cells. Human cells studied in vitro, like those in a test tube, largely support the findings of animal studies. But because there are important differences between rodents and humans – in the rates and capacity for islet cell turnover and growth, for example – “it is not a reliable assumption to extend the findings from animal studies to human studies,” as Dr. Alan Garber noted in a 2011 journal article. Garber is a professor of medicine at Baylor University and president of the American College of Endocrinology.
We don’t know for sure yet if taking GLP-1 drugs will preserve our beta cell function. Only when researchers do long-term studies can we be certain that they will maintain the balance between the birth and death of beta cells for a long time, Dr. Garber writes.
But the research to date makes it seem likely that these drugs may well be able to help at least some of us do even more than reduce our blood glucose level and our weight. It’s a good bet that GLP-1 can also stop the typical progression of diabetes from bad to worse by helping us to maintain our beta cell mass.
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David Mendosa is a journalist who learned in 1994 that he has Type 2 diabetes, which he now writes about exclusively. He has written thousands of diabetes articles, two books about it, created one of the first diabetes websites, and publishes the month newsletter, “Diabetes Update.” His very low-carbohydrate diet, current A1C level of 5.3, and BMI of 19.8 keeps his diabetes in remission without any drugs.
David Mendosa was a journalist who learned in 1994 that he had type 2 diabetes, which he wrote about exclusively. He died in May 2017 after a short illness unrelated to diabetes. He wrote thousands of diabetes articles, two books about it, created one of the first diabetes websites, and published a monthly newsletter, “Diabetes Update.” His very low-carbohydrate diet, A1C level of 5.3, and BMI of 19.8 kept his diabetes in remission without any drugs until his death.