Sit back for a brief primer on where the money is going for diabetic drug research. Our small intestine has taste cells just like those of our tongue called “L” cells. So when “sweet” crosses this cell in the small intestine, these taste cells release a compound called GLP-1 that does all kinds of wonderful things in regards to helping our bodies handle sugar.
Initial drug development was on synthetic GLP-1 (ours gets broken down in about 2 mins, so human GLP-1 can’t be used), but that proved tricky. The next direction was to slow down the enzyme that breaks down our own GLP-1 so it will last longer than 2 minutes. This involved slowing down the enzyme dipeptidyl peptidase IV (DPP4).
Thus was born one of the most massive push for drug development since the PPAR class of drugs (this class, by the way, which contained drugs like Avandia and troglitazone, are largely off the market because they proved to create much greater harm than good) over a decade ago.
Given the massive push, the heavy utilization and the continued reliance of drugs instead of lifestyle changes I would strongly suggest any diabetic sit on the sidelines for a few years and wait to see what happens with this class of drugs. Almost without fail, when we move this fast in a brand new direction dealing with enzymes in the body we know little about, the results are disastrous. Think Vioxx.
This particular study done in mice suggests the alterations in the levels of DPP4 may change the way our immune system responds, and this response can vary depending upon the immune status of the individual. In other words, we really have no clue what a class of drugs that messes with DPP4 levels will do to our immune systems, but we’ve got some inklings that it does something.
As I said–best to sit on the sidelines for this one. In the meantime, exercise, cut back on calories, drink more tea and coffee and absolutely get away from artificial sweeteners.
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2222.2011.03778.x/abstract