摘要
Hyperglycemia impairs endothelium dependent relaxation by activating PKC in vitro. We determined in 11 patients with insulin resistance (IRS) and in 10 controls (CS) if :1) there is a reduced endothelium-mediated vascular vasomotion; 2) this alteration is associated with abnormal membrane (mPKC) and cytosol (cPKC) PKC activities in monocytes; 3) increased m and cPKC are associated with insulin resistance. Insulin sensitivity (by IVGTT), branchial artery endothelium mediated vasodilatation, mPKC and cPKC in monocytes were assessed. Patients with IRS had decreased insulin action. Monocytes from IRS patients showed higher both cPKC (111.53±15.03 vs. 73.6±9.12 pmol/min. mg protein, p = 0.0474) and mPKC (77.69±7.62 vs. 51.20±5.32, p=0.0117). Flow mediated vasodilation was significantly higher in CS than in IRS patients (8±3%vs. 3±1, p<0.01). Reciprocal correlations was observed between SI and mPKC (r2