A Nobel Prize in Medicine belongs to whoever (whomever?) figures out how to reliably and affordably protect and preserve beta cell function starting early in the course of type 2 diabetes. Or type 1 diabetes, for that matter.
Dietary carbohydrates lead to secretion of insulin into the bloodstream by the pancreas’s beta cells. The insulin limits and reverses the rise in blood sugar that results from digestion of carbohydrates. If blood sugar rises too high, it damages our bodies.
Type 2 diabetes is a disorder of carbohydrate metabolism. Insulin from the beta cells isn’t doing its job adequately because tissues that should be taking up bloodstream sugar are resistant to insulin’s effect of driving sugar into the cells. The beta cells pump out increasing amounts of insulin, trying to overcome the resistance of the tissues. Eventually the beta cells become exhausted or “burned out,” reflected in diminished beta cell mass. This situation has usually been present for years before type 2 diabetes is formally diagnosed. This scenario is a leading theory of the development of type 2 diabetes.
Type 2 diabetes is considered by most physicians to be a progressive illness, requiring more and more drugs to control as the years pass. That’s because the beta cells are dying off or otherwise becoming totally nonfunctional. Once they’re gone, it’s hard (impossible?) to get them back. If diabetes could be diagnosed early on, we’d find healthier beta cells to work with. Perhaps we could strengthen or protect them. This is what beta cell preservation is all about. Keep them working as nature intended, avoiding the expense and risks of drug therapy.
So I was excited to find an article entitled “Effects of exenatide on measures of beta cell function after three years in metformin-treated patients with type 2 diabetes.” Exenatide is sold in the U.S. as Byetta. It’s a GLP-1 analogue.
European researchers studied 36 type 2 diabetics for three years. All were taking metformin. Sixteen of them also took exenatide, whereas 20 also took insulin glargine (e.g., Lantus in the U.S.).
What Did They Find?
Both groups achieved similar levels of blood sugar control after three years. Exanatide users lost 5.7 kg (12.5 lb) while glargine users gained 2.1 kg (4.6 lb).
After three years of drug use, the subjects were told to stop exenatide and glargine while continuing metformin. After four weeks off-drug:
- insulin sensitivity improved significantly in the exenatide group while glargine had no effect
- first-phase insulin secretion improved by a small amount in the exenatide group
However, 12 weeks after stopping the study drugs, hemoglobin A1c and fasting blood sugars returned to pretreatment levels in both groups. (Hemoglobin A1c is a blood test of overall diabetes control over the preceeding three months.)
You have to wonder if the improved insulin sensitivity in the exenatide group simply reflects their weight loss as compared to the weight gain in the insulin glargine group. Improved insulin sensitivity is good, any way you can get it.
When measured 12 weeks after stopping the study drugs, hemoglobin A1c and fasting blood sugar levels were no better than baseline levels three years earlier. Very disappointing. If exanatide or glargine preserved beta cell function, you’d want to see better post-treatment numbers. The search for beta cell preservation continues.
Reference: Bunck, M., Corner, A., Eliasson, B., Heine, R., Shaginian, R., Taskinen, M., Smith, U., Yki-Jarvinen, H., & Diamant, M. (2011). Effects of Exenatide on Measures of Beta-Cell Function After 3 Years in Metformin-Treated Patients With Type 2 Diabetes Diabetes Care, 34 (9), 2041-2047 DOI: 10.2337/dc11-0291
PS: In case it matters to you, this study was funded at least partially by Amylin Pharmaceuticals and Eli Lilly and Company.