Levels of tissue kallikrein, a component of the kallikrein??”kinin system (KKS), are elevated in people with Type 2 diabetes, Australian researchers have shown.

Interestingly, this relationship was unaffected by statin therapy, indicating that the KKS is not involved in the beneficial effects of statins on endothelial function.

David Campbell (St Vincent’s Institute of Medical Research, Fitzroy, Victoria) and co-workers tested the hypothesis that diabetes increases the activity of the KKS, a system with a broad spectrum of actions including inflammation and organ protection.

They obtained blood from 71 patients scheduled for coronary artery bypass (CABG) surgery, 16 of whom had diabetes. CABG patients were chosen because they routinely have arterial cannulae inserted before surgery, which allows rapid blood collection with minimal kallikrein activation.

Writing in the journal Diabetologia, Campbell et al report that circulating levels of tissue kallikrein were 62% higher in diabetic versus nondiabetic patients. Diabetic patients also had increased tissue kallikrein immunoreactivity in atrial myocytes and increased tissue kallikrein messenger RNA levels in atrial tissue.

By contrast, there were no differences in blood levels of angiotensin, bradykinin, and kallidin peptides, or in plasma levels of plasma kallikrein or kallistatin between diabetic and nondiabetic individuals.

Separate analyses showed that treatment with statins, aspirin, calcium antagonists, beta-blockers, or long-acting nitrates had no effect on circulating levels of any of the KKS components. However, statin therapy was associated with decreased plasma aldosterone levels, which the authors suggest may be due to an effect of statins on cholesterol supply for steroid-hormone synthesis.

Campbell et al say that the mechanism underlying the increase in tissue kallikrein in diabetes is uncertain, but it may be caused by hyperinsulinemia.

Noting that tissue kallikrein plays an essential role in protecting the heart from ischemic injury, they conclude: “[T]issue kallikrein may play a greater role in cardioprotection in Type 2 diabetic than in nondiabetic patients and may also contribute to the benefits that Type 2 diabetic patients derive from angiotensin-converting enzyme inhibitor and other therapies inhibiting kinin metabolism.”

They add: “Our findings do not support the idea that the KKS plays a role in the impaired endothelial function of Type 2 diabetes or in mediating the improvement of endothelial function by statin therapy in nondiabetic and diabetic patients.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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