Are high blood sugar level the cause of diabetes?

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Diabetes mellitus is a metabolic disorder which constitutes one of the leading diseases and with an increasing dominance worldwide.  This disease is characterized by severe health complications including heart diseases and stroke, severe blood flow problem in legs and damage to the eyes, nerve endings, and kidneys.The high blood glucose levels are directly related to the level of diabetic symptoms.  For diabetes when a patient is treated with medication for very high blood glucose levels, the rate of infarctions and strokes decreases significantly.

 

But this holds valid only till a certain point. According to Peter Nawroth, Medical Director of the Department of Endocrinology and Metabolism at Heidelberg University Hospital, “Large clinical trials in recent years have shown: Even when drugs could lower blood sugar below the diabetes threshold value, many patients nevertheless developed typical diabetic damage to nerves and kidneys.  This suggests that type 2 diabetes might, in fact, have molecular causes that are independent of insulin and glucose."

 

Aurelio Teleman leads the Division of Signal Transduction in Cancer and Metabolism at the German Cancer Research Center (DKFZ) in Heidelberg. According toher, in Type 2 diabetes, high levels of glucose metabolite called methylglyoxal (MG), are seen. Methylglyoxal is a glucose-dependent substance and might be the essential reactive aldehyde behind diabetes and its complications.

 

Diabetes was the first disease where evidence emerged for the increased formation of methylglyoxal in the cells and the serum. Methylglyoxal (MG) shows toxic effects on insulin secretion from pancreatic beta-cells, and on modifications of proteins and nucleic acids.  Earlier doctors thought that high levels of MG were the results of high blood glucose levels, but this new research shows that perhaps diabetes is a result of high MG and not the culprit behind it.

 

MG is a highly reactive compound derived from glucose and fructose metabolism and has been implicated in diabetic complications. MG promotes impaired functions of insulin signalling. Recently, a study also found higher concentrations of MG causes rapid acidification in pancreatic β-cells where insulin is produced.

 

Studies were conducted by Heidelberg researchers for investigating long-term elevated concentration on the organism. For this experiment, fruit fly model was chosen after the rat study. The energy metabolism developed very early during evolution; thus, the results are the same for all mammals and humans.

 

In the fruit flies using genetic engineering, the researchers turned off the enzyme breaking down MG. The glucose metabolite MG accumulated in the bodies and these flies developed insulin resistance instantly, they became obese, and as their age increased, the glucose levels changed.

 

Form the above experiments on rats and fruit flies, it was concluded that sufficient increase in the MG levels triggers insulin resistance and causes other diabetic disturbances. Thus, finding MG is not a consequence but a cause of type 2 diabetes. [1]

 

Several other factors like subsequent metabolic processes also play a role in developing insulin resistance like lifestyle, exercise and these should be taken care of too!

 

References :

1. Alexandra Moraru, Janica Wiederstein, Daniel Pfaff, Thomas Fleming, Aubry K. Miller, Peter Nawroth und Aurelio A. Teleman. Elevated Levels of the Reactive Metabolite Methylglyoxal Recapitulate Progression of Type 2 Diabetes. Cell Metabolism, 2018 DOI: 10.1016/j.cmet2018.02003

2. Kender Z, Torzsa P, Grolmusz K V, Patócs A, Lichthammer A, Veresné Bálint M, Rácz K, Reismann P. The role of methylglyoxal metabolism in type-2 diabetes and its complications.  2012 Apr 15;153(15):574-85. doi: 10.1556/OH.20129348.

3. Dornadula S, Elango B, Balashanmugam P, Palanisamy R, Kunka Mohanram RPathophysiological insights of methylglyoxal induced type-2 diabetes. Chem Res Toxicol. 2015 Sep 21;28(9):1666-74. doi: 10.1021/acs.chemrestox.5b00171. Epub 2015 Sep 11.

 

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