Inflammation May Explain Why Glycemic Control Alone May Not Prevent Diabetic Heart Disease

Carlos F. Sánchez-Ferrer, M.D., Ph.D. Professor of Pharmacology Universidad Autónoma de Madrid, Interview with:
Carlos F. Sánchez-Ferrer, M.D., Ph.D.
Professor of Pharmacology
Universidad Autónoma de Madrid, Spain.

Medical Research: What are the main findings of the study?

Dr. Sánchez-Ferrer: We were studying the possible ways of interaction between high glucose levels, which are found in diabetes mellitus, with vascular damage,
which is the most common and devastating consequence of this disease.
An intriguing fact is that a very strict control of blood sugar in
diabetic patients is not sufficient to avoid the development of such
diabetes-induced cardiovascular diseases. We think our results can
explain why this is happening.

Using cultured smooth muscle cells from the main human artery (aorta)
in the presence of high concentrations of extracellular glucose, we
1. In the absence of inflammation, excess glucose in the culture fluid
didn’t enter the cells.
2. When extra glucose was forced into the cells, no harm was done in
the absence of inflammation.
3. When the inflammation-stimulating protein interleukin-1 (IL-1) was
introduced, more glucose entered the cells.
4. With IL-1, the glucose entering the cells was metabolized via
chemical pathways that spur escalating inflammation, overwhelming the
cells’ ability to counteract it.
5. In the presence of the anti-inflammatory drug anakinra, which blocks
the activity of IL-1, the deleterious changes didn’t occur.

Medical Research: Were any of the findings unexpected?

Dr. Sánchez-Ferrer: These results were rather consistent with previous work from our laboratory. Perhaps we had some surprise after observing how “healthy” non-inflamed cells could metabolize excess glucose without developing any damage.

Medical Research: What should clinicians and patients take away from your report?

Dr. Sánchez-Ferrer: An important message for the clinicians and patients is to explain why glycemic control, which is of course very important, can be not enough to prevent diabetic-induced cardiovascular diseases.

We should look for other therapeutic targets, aimed to reduce
inflammatory environment associated to diabetes. Therefore, changes in
life style, physical exercise, and weight reduction, can be important
not only because reduce blood glucose but because reduce inflammation.

Medical Research: What recommendations do you have for future research as a result of this study?

Dr. Sánchez-Ferrer: Our data indicates that, in addition to glycemic control, we likely
need to find new pharmacological targets focused to reduce diabetic
inflammatory environment. We think this will be a very important
future therapeutic approach.

For example, there are some preliminary data indicating that IL 1
receptor antagonist can reduce the development of diabetic vascular
complications. Antagonists for other inflammatory cytokines could be
also be useful. This is only the beginning of a research line and more
research is needed to obtain conclusive results.


Study presented at the American Heart Association’s High Blood Pressure Research Scientific Sessions 2014.

American Heart Association Meeting Report Abstract 560
Concepción Peiró, Ph.D.; Tania Romacho, Ph.D.; Verónica Azcutia, Ph.D.; Laura Villalobos, Ph.D.; Enrique Fernández, Ph.D.; Juan P. Bolaños, Ph.D.; and Salvador Moncada, M.D., Ph.D.


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