Diabetes, Heart Disease / 13.09.2014
Inflammation May Explain Why Glycemic Control Alone May Not Prevent Diabetic Heart Disease
MedicalResearch.com 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
observed:
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.
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