Dimitry,please contact me at [email protected]. I would suggest you some comment. I remain. Elio Conte 

Dear Colleaga,

It is difficult to answer your question because the characteristics of your 2 subtypes of Diabetes 2 are nor clearly presented and also because the consequences of your subtyping for the evolution of the disease and its treatment are aslo not evident.

Taking into account the remarks of the previous editors and reviewers, try to submit once more to the "Pancreatic Diseases & Treatment" an online journal with rather large horizons, accepting no conformist ideas in publications (but with excellent argumen,ts and proofs).

Good luck,

V.Coulic

Dear Véry: Thank you for your recommendation. I agree that my info with respect to our findings is not full, but the point is that HbA1c and FBG seem not represent the same pathophysiological mechanisms to diabetes. By my question I would like to only learn whether the same concern regarding them is already known and presented in literature, because it was no problem in scientific evidence of our findings, but in their novelty with respect to HbA1c and FBG for the editors. Best wishes, Dmitry

Dear Dmitri,

I don't really know, but I think that they reflect different situations in the organism and are linked: is it possible that HbA1c is high when FBG remains normal? Another question is FBG may be normal but after meal glycaemia is higher - it is a well known possibility (see classic books of Internal medicine and special Endocrinology, with are explaie-ned different types of normal and pathologic answer to food charge and glucose charge -" triangles"). In this case , if we consider that HbA level increase is linked with a higher glucose concentration in the organism - not only in blood - then FBG may be still normal and HbA1c already not. Don't forget that glycaemia in the result of many parameters action: glucose income (extra organism - food and drink-, intraorganism neoglycogenesis, and glucose utilization by brain, muscles, organs. So it is a global parameter. HbA1c is much more local and precise. So for conclusion about DM2 we need both but HbA1c is more liable because it testimony of an already established  pathological situation.  So you might be right. To find a correct answer to your question I think you have to come back to the authors who have defined the 2 concepts, that is to the classics. Nowadays, as far as I know,  there are no more discussions about the topic.

Nice to discuss with you

V.Coulic

Véry: In literature and in our study HbA1c and FBG are very weakly correlated in patients with diabetes and in health controls. In this case you can find persons with very high HbA1c, but low FBG and vise versa. Our study was a candidate gene study that was conducted to get a proof of concept that HbA1c and FBG are related to different inherited mechanisms leading to diabetes. One more it was no concerns with respect to statistical or methodological issues of our study, but to the novelty of the concept that HbA1c and FBG are not alternative indicators of type 2 diabetes and should be both assessed to determine a pathophysiological subtype of type 2 diabetes in particular person. That's why I appealed to the peers here to learn, whether I missed such information in diabetes literature and it is already known as the editors claimed. Our submission did not reach peers for external reviewing, but was stopped by the decision of editorial board. Thank you! Dmitry.

Dear Dmitri,

I understand why the editorial board of these journals have had such a reaction. They have not understood what you meant (or did not want to understand) because it seems evident and known that hte FBG and HbA1c are different things. Try to entitle you manuscript in another way, for instance insisting on the genetic aspect of the problem. And avoid endocrinologic journals... Re-read, nevertheless, the classics about diabetes to understand the opponents better and so to overcome them.

I wish you good luck

V.Coulic

Véry: Thank you! From my previous publication experience I've also felt that this is the matter of titles and cover letters. I have already played with them for these two diabetic journals, but the response was the same. Maybe you are right, I should try with more physiologically orienting journals. The big challenge is that expert committees in diabetes look forward to select one of them as the only best predictor in spite of evidence that the FBG and HbA1c are different things, as you said. In our case we showed that FBG and HbA1c are not only different things (it is a classics), but also predict different diabetes. I think this is the main difference between the classical viewpoint on these measures and our findings. Cordially, Dmitry.

Galactose in milk, and fructose in sucrose, high fructose corn syrup, fruits and fruit juice are more potent glycators than glucose. So HbA1C is presumably produced by galactose, fructose and glucose, while fasting glucose is only glucose. No wonder they are not well correlated. Those with high glycated haemoglobin may be heavy consumers of milk, orange juice, cake and chocolates, while those with high blood glucose may like their pasta, rice and bread, as well as obtaining glucose from milk and sucrose. HbA1C may well be the better predictor of damage, as glycation damages blood vessels. All carbohydrate is not equal. I advise patients to eat cheese not milk, vegetables not fruit, and starch not sugar. The glycaemic index suggests that only glucose matters, while galactose and fructose are much more of a problem.

Thank you Margaret, but you should pay attention on doses. For example, fructose at different doses has opposite effects on both HbA1с and blood glucose: lowering and increasing, but indirectly (possibly through insulin resistance/sensitivity).

The paper was accepted and is already on-line (the link below). I thank all people, who have replied.

http://www.endocrineconnections.com/cgi/content/long/EC-16-0009v1