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Consensus statement calls for more beta cell research in type 2 diabetes
Leahy JL. J Clin Endocrinol Metab. 2010;95:4206-4216.
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Because of evidence that beta-cell failure occurs earlier and more severely in patients with type 2 diabetes, a new consensus statement suggests that greater emphasis be placed on regular glycemic screening. It is also recommended that greater emphasis be placed on early identification of patients at metabolic risk and on prompt and aggressive intervention.
The consensus statement, published in the Journal of Clinical Endocrinology & Metabolism, was written by a group of researchers, clinical endocrinologists and primary care physicians who convened to consider updated information about how pancreatic beta-cell defects should alter the treatment for diabetes. The Endocrine Society organized the group.
Animal and human studies have shown that dysfunctional beta cells are an underlying cause of type 2 diabetes. The cells cannot change insulin secretion to make up for the increasing insulin resistance. More evidence shows that beta-cell dysfunction occurs early in diabetes development, and that the decline in function can be reversed.
“There is widespread evidence that conventional approaches to the management of type 2 diabetes have been inadequate,” Jack L. Leahy, MD, professor of medicine and chief of the Endocrinology, Diabetes and Metabolism Unit at the University of Vermont, and one of the consensus working group members, said in a press release. “Studies have increasingly shown that beta cells have an important role in the progression of diabetes. If we could gain a better understanding of that role, we may be able to develop new and effective means of treatment.”
The researchers also recommend additional studies to determine the clinical value of pharmacological therapies that target beta-cell function. They also proposed further research into genetic subtypes of type 2 diabetes to find whether they are susceptible to individualized therapy designed to slow or reverse beta-cell decline. They also proposed studies to determine the link between beta-cell function and insulin resistance. – by Melissa Foster and Emily Shafer
The article published in the Journal of Clinical Endocrinology & Metabolism focuses on a very important problem for patients with type 2 diabetes: dysfunction of pancreatic beta cells. A fundamental problem appears to be a deficiency in the number of cells, which is coupled with an important dysfunction of secretion, whereby this reduced number of beta cells puts out less insulin per cell than in a normal situation. There is much we need to know about beta cells. We must not only understand the secretory mechanisms but also the basic biology of beta-cell birth and death and how this might vary between different individuals. This information is important because there seems to be a turnover of beta cells, although it is very slow. We should determine why beta cells die at a particular rate and whether some pharmaceutical approach has the potential to slow the process and replenish these cells. It will also be important to determine why a person with insulin resistance does or does not develop diabetes — why do the beta cells of only some people fail?
This research should have a therapeutic payoff at some point in the future, and hopefully the research discussed in the consensus statement will advance our knowledge and lead to the development of new therapeutic approaches.
– Gordon C. Weir, MD
Senior Investigator,
Joslin Diabetes Center
Professor of Medicine, Harvard Medical School
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