Obesity and diabetes mellitus are the most common health problems with mass pathologies and microvascular complications, the alteration of trace elements could have deleterious effect on the health of the diabetic patients. Hypomgnesemia have been reported to occur at an increased frequency among patients with type2DM compared with non diabetic counter parts, hypomagnesemia occurs at an incidence of 13.5 to 47.7%ammong patients with type2DM .Magnesium is an important factor for enzyme involved in carbohydrate metabolism and a strong relation between insulin action and Mg has been reported, several evidences suggested that Mg play a key role in insulin resistance and type2DM. Aim of the study: to find out any correlation between hypomagnesemia and insulin resistance in obese and diabetic subjects, with special reference to the effect of albuminuria. Patients and methods:This study included 65 patients with type 2 diabetes aged (19-53) year who were attending the National Center Of Diabetes / ALMustansiria
University ; from the period Jun .to September.2008. Patients were on oral hypoglycemic drugs (i.e. metformin and /or glibenclamide). Patients with no insulin therapy and prolonged duration(more than 2 years) of disease were excluded from this study, the study patients were divided according to their BMI to three groups ;obese (BMI>30)without proteinuria, non obese (BMI<25),and obese (BMI>30) with proteinuria.
Venous blood samples were aspirated and divided in to two parts EDTA blood used for measurement of HbA1c by A1c variant reader and a second part in plain tube for immediate measurement of glucose, urea, creatinine ,protein by routine enzymatic kits , the rest was frozen at -20C°Until the time of assay for insulin by ELISA methods and magnesium by atomicabsorption spectrophotometry. Quicki test was conducted which means that decrement in Quicki test reflects increment in insulin resistance. As a cutoff point 0.33 or less is consistent with insulin resistance. Results: In this study QUICKI test revealed marked reduction (increased insulin resistance ) in obese type2 diabetic subjects, with or without proteinuria and non obese type2 diabetic (0.31±0.038, 0.30±0.033and 0.33±0.047respectivly) while in the control groups obese and non obese were normal values (0.382±0.029, 0.343±0.009. respectively). Serum total Magnesium was found to be low in obese type2 diabetics without proteinuria (0.56±0.106mmol/L), ( p<0.05) versus obese non diabetic age and sex matched control without proteinuria (0.79±0.093mmo/L). Serum Magnesium was found to be low in type2 diabetic subjects with proteinuria when compared with obese non diabetic counter parts and the difference was found to be highly significant (0.5±0.106mmol/L ), (p<0.001) comparing non
obese type2 diabetics with non diabetic lean counterparts (0.9±0.092mmo/L) revealed marked reduction in serum magnesium in diabetics (0.666±0.112mmol/L)(p<0.05). The correlation between serum magnesium and QUICKI test was found to be positive thus reduction of magnesium means an increment in insulin resistance in all enrolled diabetics and non diabetic control (r= 0.58, 0.58, 0.8) . The above mentioned correlation was found to be true for both total and ionized magnesium. Ionized magnesium was found to be low in type2 diabetics with proteinuria (0.312±0.08mmo/L), and without proteinuria (0.37±0.065mmol/L)
and non obese diabetics (0.44±0.076mmol/L), the correlation of ionized magnesium is positive with QUICKI test in the above mentioned groups of diabetics (r = 0.52, 0.76, 0.84). Glycated hemoglobin(HbA1c) as a marker of glycemic control was found to have a negative correlation with total serum magnesium in obese type2 diabetics with or without proteinuria and the non obese diabetics (r= -0.65, - 0.59, -0.55 respectively).
Conclusion: In the enrolled type2 diabetics it was found that insulin resistance is an evident observation, low serum magnesium had a significant.