Blood glucose activates protein kinase c (pkc) in human platelets

We investigate the alteration of PKC32 in human blood platetets during intravenous infusion of glucose (240 mg/mJ/min), insulin (25 mU/mJ/min) and octreotide (0.5 #g/min) over 180 min in 8 controls and 19 non-insulin dependent diabetes (NIDDM)patients using Western blot method. In all NIDDM patients glucose was elevated by 7.5-10 mmol/L during infusions. Insulin levels were around 40 #U/mL during the test which corresponds to normal postprandial levels. Significant increases (p0.05) of both membrane and cytosolic PKC32 occurred in 10 NIDDM patients suggesting that both translocation and increased synthesis of PKC 2 were stimulated by glucose elevation. Nine other patients showed no alteration of PKC32. These two group of NIDDM patients were similar regarding parameters of diabetes control, baseline glucose and glucose elevation during the test. However, the PKC32 -responsive group had lower levels of serum triglycerides (1.39+0.19 vs. 2.32+0.34 g/L; p=0.038). We conclude that 1. An acute blood glucose elevation by 5.5 mmol/L or more can activate PKC22 in platelets of NODDM patients in rive irrespective of parameters of metabolic control. 2. NIDDM patients differ in their PKC32 -responses to glucose elevation.