Gliclazide friend or foe ?

　
How it works.

Gliclazide binds to sulfonylurea receptors on the surface of the Beta islet cells found in the pancreas. This binding effectively closes the K+ ion channels. This decreases the efflux of potassium from the cell which leads to the depolarization of the cell. This causes voltage dependent Ca++ ion channels to open increasing the Ca++ influx. The calcium can then bind to and activate calmodulin which in turn leads to exocystosis of insulin vesicles leading to insulin release.

Pretty impressive eh.

That was a copy and paste job from Wikipedia, oh that I could recite that sort of jargon without notes. So the bottom line is, Gliclazide works by forcing the already damaged and overworked pancreas into outputting more insulin. It does this even if more insulin is not required to bring down blood glucose levels, hence the often reported hypos. A heavily overweight type two diabetic often has three times the serum insulin levels as a slim non diabetic, the last thing many type two overweight diabetics need, is more insulin sloshing around their system. More insulin inhibits stored fat burning and very often increases weight, thus reducing insulin sensitivity, and the vicious circle continues.

So apart from knocking out the pancreas, causing hypos and very often increasing weight, it’s not got a lot going for it. It will come as no surprise to some that world renowned diabetes expert Dr. Richard Bernstein refuses to prescribe Gliclazide. As with many type two diabetes medications, there is often a high price to pay for only a modest reduction in HbA1c. Other than insulin, nothing comes close to reducing blood glucose numbers compared with diet and exercise. To date, I can find no downside or side effects in the consumption of quality non factory produced food and a brisk two mile walk.

Eddie