Significantly higher levels of erythrocyte membrane microviscosity (MV) [n-: 5.22 +/- 0.17 (4.70--5.92), mean +/- SD (range), poise, N = 67, P less than 0.005] measured by fluorescence depolarization using 1,6-diphenyl-1,3,5-hexatriene as a fluorescent probe were found in diabetic patients when compared with normal controls [5.05 +/- 0.15 (4.70--5.29), N = 22]. No significant differences in MV existed between males and females, nor was MV significantly correlated with diabetic age, duration of diabetes, plasma cholesterol, cholesterol/phsopholipid ratios, and plasma lecithin:cholesterol acyltransferase activities. No significant difference in MV was observed between groups with or without diabetic retinopathy. There was, however, significantly higher MV [5.29 +/- 0.19 (5.00--5.92), N = 20, P less than 0.05] in the group with fasting blood glucose (FBG) greater than or equal to 140 mg/dl than that [5.19 +/- 0.15 (4.70--5.46), N = 47] in the group with FBG less than 140 mg/dl. The changes in erythrocyte membrane MV presented in this study appear to be related to the current metabolic control of diabetic patients and are considered to be one of the factors responsible for the reduced erythrocyte deformability in diabetes.

The effects of dietary sardine oil rich in eicosapentaenoic acid, C20:5 (EPA), on erythrocyte membrane fluidity and membrane and plasma lipids were investigated in diabetic and control subjects. Before consumption of this oil, the levels of erythrocyte membrane fluidity were lower in the diabetic subjects, as noted in our previous work (Diabetes 1983; 32:585-91). Decreased membrane polyunsaturated fatty acid contents were evident. Daily consumption of 2700 mg of sardine oil for 8 wk increased erythrocyte membrane fluidity, as determined by electron spin resonance using the 12- or 16-stearic acid label. This increase was seen after 4 wk, and the level remained elevated for 8 wk. Membrane EPA of phospholipid acyl-chains significantly increased after 4 wk and was even more apparent after 8 wk. Membrane-free cholesterol to phospholipid molar ratios significantly decreased after 8 wk. Both the diabetic and normal subjects responded to the sardine oil in the same way. After feeding with sardine oil, there no longer were differences in erythrocyte membrane fluidity between the normal and diabetic subjects. We propose that improvement in membrane fluidity may contribute to the amelioration of altered cell membrane functions in diabetic patients.

This rapid, reliable equilibrium turbidimetric immunoassay for serum C-reactive protein involves a potent monospecific antibody. Polyethylene glycol-6000 to accelerate and enhance the immunoprecipitation reaction, and Tween-20 surfactant to lower and stabilize the sample blank values. Grossly lipemic, icteric, or hemolyzed sera can be assayed. Values up to about 220 mg/L, for which the standard curve is linear, can be measured without sample dilution. Results by the proposed method and by radial immunodiffusion (r 0.989) or laser nephelometry (r = 0.957) correlated well. Analytical recovery averaged 101.3%. Within-, between-, and day-to-day CVs ranged from 0.9% to 3.5%, 0.8% to 5.5%, and 1.9% to 4.8%, respectively. The method is demonstrably superior to radial immunodiffusion or nephelometry. Any spectrophotometer that can measure turbidimetrically at 340 nm can be used.

The dynamic properties of intact erythrocyte membrane in diabetic patients were investigated by means of electron spin resonance using three stearic acid spin labels (SAL): 5-, 12-, and 16-SAL. Significantly lower levels of erythrocyte membrane fluidity were revealed with 16-SAL as a probe in diabetic patients when compared with normal controls. However, there were no significant differences in fluidity values using 5- or 12-SAL between the two groups. Therefore, it became obvious that the decrease in fluidity was located in deeper sites (hydrophobic region) of the erythrocyte double membrane in diabetic patients. It was strongly suggested that changes in the membrane cholesterol to phospholipid molar ratios are not a principal factor contributing to the fluidity change. A significant increase of sphingomyelin and decrease of phosphatidylethanolamine were found in the erythrocyte membrane of diabetic patients and an alteration in membrane phospholipid classes and their acyl-chains could conceivably be related to the fluidity change. There were no significant correlations between change in membrane fluidity and most plasma lipids, plasma lecithin-cholesterol acyl-transferase activities, erythrocyte glycosylated hemoglobin, erythrocyte adenosine triphosphate, fasting blood glucose or duration of the disease. Plasma cholesterol of high-density lipoprotein showed a significant negative correlation with the membrane fluidity values. Some of the possible factors contributing to and the significance of the lower levels of erythrocyte membrane fluidity were discussed in conjunction with both metabolic and clinical aspects in diabetic patients.