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Bradykinin (BK), a peptide released during inflammatory response, has been investigated for its ability to regulate glucose metabolism in human fibroblasts. The peptide is able to significantly increase glycolytic flux in these cells. The strict relationship between the glycolytic rate and the levels of fructose 2,6-bisphosphate (Fru-2,6-P2) strongly suggests that the metabolite plays a key role in the regulation of glucose metabolism by bradykinin. The mechanism by which bradykinin increases Fru-2,6-P2 content involves the activation of 6-phosphofructo-2-kinase (PFK-2), the enzyme responsible for the synthesis of the metabolite. The study of the multiple signalling systems triggered by bradykinin demonstrates the involvement of the rise in intracellular Ca2+ concentration and of protein kinase C mediated pathway in the mechanism by which bradykinin increases Fru-2,6-P2 content and PFK-2 activity.
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