INTRODUCTION: Magnesium is present in higher concentration within the cell and it is the second most abundant cation next to potassium. It plays an important role in manipulating important biological pyrophosphate compounds. The disturbance in magnesium level i.e., hypomagnesemia has been reported to occur in diabetic patients. Although diabetes can induce hypomagnesemia, magnesium deficiency has also been proposed as a risk factor for diabetes. Animal studies have shown that magnesium deficiency has a negative effect on post receptor signalling of insulin. Some short term metabolic studies suggested that magnesium supplementation has a beneficial effect on insulin action and glucose metabolism. Persistent hypomagnesemia leads to raised glucose level, insulin resistance and the degree of magnesium depletion positively correlates with serum glucose concentration and degree of glycosuria. The cause of hypomagnesemia was attributed to (1).Osmotic renal loss from glycosuria, (2). Decreased intestinal absorption of magnesium. Recently a specific tubular magnesium defect in patients with diabetes has been postulated. Hypermagnesuria results specifically from reduction in tubular absorption of magnesium. MATERIALS AND METHODS: This was a case control study conducted in 100 diabetic patients and 100 non- diabetic healthy controls who attended General Medicine OPD at Government Rajaji Hospital, Madurai during a period of 6 months (April 2014 to September 2014) .Patients aged between 30 to 70 years with positive history of diabetes were included in the study. Those patients with history of hypertension, gastrointestinal disorders, impaired renal function, alcoholic pancreatitis, therapy with diuretics, aminoglycosides, endocrine disorders, heart disease and those who were not willing to give consent were excluded from the study.100 diabetic patients and 100 non diabetic healthy controls in the age group of 31 to 70 years attending General Medicine OPD were included.A detailed history with detailed clinical examination was done. Blood samples were taken from each of the study groups and magnesium levels were assessed and compared between the case and control groups. Blood pressure was recorded. Cardiovascular disease was ruled out by history and ECG. Urine was examined for proteinuria.FBS valueswere assessed after 8 hours of fasting. PPBS values, Blood urea and serum creatinine values were measured. Serum magnesium was determined by using photometric method. Calmagite – a metallochromatic indicator when binds with magnesium in alkaline medium, it forms red colour complex and it is measured at 530 to 550 nm. To prevent interference by calcium, specific calcium chelating agent EDTA was added. To avoid the heavy metal complex formation, KCN was added. Polyvinylpyrrolidone and surfactant were also included to reduce the interference from lipemia and protein. Intensity of colour formed was directly proportional to the amount of magnesium present in the sample. RESULTS: In the present study, the mean age group of cases and controls were 50.39 ± 9.76 and 50.01 ± 10.15 respectively. The minimum age was 31 years and maximum age was 70 years. Maximum number of patients were in the age group of 41 to 50 i.e., 42%.Out of 100 cases, 70% were males and 30% were females. The mean FBS level among cases and control were 102.42mg/dl and 91.93 mg/dl respectively. The mean PPBS level among cases and control were 187.02 mg/dl and 123.83 mg/dl respectively
