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Table 1 – Clinical and biochemical characteristics of the study population: Comparison of control, obese and diabetic groups


Parameter Pr>F BMI (kg/m2


Fasting BGL (mg/dL)


HbA1c%


Control (mean ± SD), n = 20


) <0.0001* 24.91 ± 2.63 <0.0001* 84.25 ± 9.28


<0.0001* 5.16 ± 0.28


Obese (mean ± SD), n = 14


39.35 ± 3.61** 89.00 ± 7.69


5.45 ± 0.30


*Significant difference among three groups (P<0.001). **Significant difference between diabetic or obese group and control group (P<0.001).


††Significant difference between diabetic and obese groups (P<0.001).


BMI, body mass index; BGL, blood glucose level; HbA1c, hemoglobinA1c.


Diabetic (mean ± SD), n = 14


37.89 ± 6.58** 164.57 ± 62.00**†† 7.56 ± 1.41**††


The results of ANOVA (Pr>F) indicate that the mean values of BMI, BGL and HbA1c differed signifi- cantly among the three study groups (P<0.001). A pairwise comparison revealed that BMI levels were much higher in the diabetic group (37.89 ± 6.58 kg/m2 than in the control group (24.91 ± 2.63 kg/m2


) and obese group (39.35 ± 3.61 kg/m2


) ; P<0.001). In addition, there were statistically signifi-


cant elevations of BGL and HbA1c in the diabetic group compared to the control group (P<0.001). BGL and HbA1c were considerably higher in the diabetic group than in the obese group (P<0.001).


Incubations of adenosine (A) with D-glucose and D-ribose in separate experiments under physi- ological conditions of temperature (37 °C), pH 7.4, resulted in the formation of CMAd identified by LC/MS-ESI (Figure 1a and Figure 1b). The identity of CMAd was confirmed by its synthesis from adenosine and chloroacetic acid (Figure 1c).


Detection of CMAd in the urine samples of obese diabetic and nondiabetic subjects was done by HPLC and LC/MS analysis of the methanol extracts of the neutral pH adjusted, dried samples (Figures 2b and 3b). The ion M+H+


326 (CMAd) verified the presence of CMAd in the samples examined. The presence


of CMAd in diabetic and obese urine samples was confirmed by carrying out mixing experiments with synthesized CMAd (Figures 2c and 3c).


The boxplot charts in Figure 4 compare the three study groups for each clinical parameter (BMI, BGL and HbA1c). The first graph shows that the BMI values for all subjects in the control group were lower than those in the obese and diabetic groups. Though average BMI was slightly higher in the obese group than in the diabetic group, BMI values were elevated in the diabetic group (30 kg/m2


–53 kg/m2


HbA1c were much higher in the diabetic group than in the control and obese groups. The HbA1c values for all subjects in the control group were less than those in the diabetic group.


The reaction scheme for the detection of CMAd from glycoxidation reaction and fasting human urine sample is shown in Figure 5.


Discussion Important biomarkers of protein modification1,5,6 there is a sizeable body of work7-13


and lipid chemistry on DNA and RNA is limited. AMERICAN LABORATORY • 37 • AUGUST 2015 in diabetes have been widely used. Although on protein damage, information on the effects of carbohydrate


). The graphs of BGL and HbA1c show that the averages and variations in BGL and


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