Since (1) the His<sup>44</sup> residue is not present in CD59 from other animal species and (2) humans are particularly prone to develop complications of diabetes, our results indicate that the Lys<sup>41</sup> /His<sup>44</sup> glycation motif in human CD59 may confer humans a higher risk of developing vascular disease in response to hyperglycemia.
These results indicate that there may be some mutations of CD59 in diabetes population and the mutated CD59, which is more likely to be of glycation than the wild-type, may help to explain the distinct propensity of diabetes subjects to develop vascular proliferation complications.
The presence of this glycation motif in human CD59, but not in CD59 of other species, may help explain the distinct propensity of humans to develop vascular proliferative complications of diabetes.
To examine the possible role of reduced physical fitness in this condition 21 first degree relatives of NIDDM patients and 22 control subjects without any history of diabetes were examined employing a 150-min hyperinsulinaemic (0.6 mU insulin. kg-1.min-1) euglycaemic clamp combined with the isotope dilution technique (3-(3)H-glucose, Hot GINF), the forearm technique and indirect calorimetry.
The negative predictive value of a stimulated insulin (1-min + 3-min insulin - 2 X basal insulin) level greater than 24 microU/ml to be greater than 1.5 yr from diabetes was 90% (9 of 10 values) and 100% (10 of 10 values) at greater than 1 yr from overt diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)