The effect of metformin on glycemic control, serum lipids and lipoproteins in diet alone and sulfonylurea-treated type 2 diabetic patients with sub-optimal metabolic control.

OBJECTIVE: To see if Metformin Monotherapy affects glycemic control, serum lipid or lipoprotein levels in the treatment of type 2 diabetes who were poorly controlled with diet alone or despite maximal doses of (sulfonylurea) oral glucose lowering agents. DESIGN: A prospective, clinical intervention trial conducted between 1996-1997. SETTING: Two out patient diabetic clinics of Karachi. PATIENTS AND METHODS: A 12-week prospective clinical intervention trial. A total of 30 type 2 diabetic subjects were enrolled, of Whom 21 (12 men and 9 women) completed the study period. Their ages ranged between 35 and 70 years, (mean +/- SD 53.3 +/- 9.31) years, with a mean duration since diagnosis of diabetes was 4.5 +/- 2.3 years, body mass index (mean +/- SD) 26.8 +/- 3.53 kg/m2. They were previously treated with diet alone or had already been taking maximum doses of sulfonylurea monotherapy with suboptimal glycemic control, i.e., raised fasting blood glucose concentrations of 6-15 mmol/L or (108-270 mg/dL) on two occasions, with significant hyperglycemic symptoms. The patients were treated with metformin monotherapy with a follow up of 12 weeks. The initial dosage was 500 mg twice daily, and the dosage was increased to two or three tablets depending on the patient's metabolic changes. By comparing before and after 12 weeks therapy with metformin we assessed the importance of baseline parameters (glycemic control, serum lipid and lipoprotein concentrations, and measures of change in body weight and body mass index). RESULTS: Metformin therapy significantly decreased fasting blood glucose levels in all patients [(mean +/- SD) 227.2 +/- 37.5 to 168.6 +/- 20.5 mg/dl, p < 0.001)]. Serum total cholesterol decreased marginally [(mean +/- SD) 200.3 +/- 18.7 to 181.4 +/- 19.4 mg/dl, p < 0.01)]. Serum total triglycerides concentration also decreased [(mean +/- SD) 195.9 +/- 31.9 to 174.2 +/- 26.6 mg/dl, P < 0.01)]. Low-density lipoproteins declined [(mean +/- SD) 123.5 +/- 16.9 to 105.5 +/- 19.1 mg/dl, P < 0.01)], and very-low density lipoprotein cholesterol also decreased [(mean +/- SD) 39.2 +/- 6.4 to 34.8 +/- to 5.3 mg/dl, P < 0.01)]. Whereas, high-density lipoprotein cholesterol tended to increase [(mean +/- SD) 37.7 +/- 5.1 to 39.5 +/- 4.9 mg/dl, P < 0.01)], while no significant changes occurred in body weight and body mass index. CONCLUSION: Metformin treatment was effective, safe, and generally well tolerated.

The effects of glibenclamide on serum lipids and lipoproteins in type II non-insulin dependent diabetes mellitus.

OBJECTIVE: To examine the effects of glibenclamide treatment on plasma lipids and lipoprotein levels. SETTINGS: Out patients of Type II diabetics from department of Baqai Diabetes and Endocrine Centre and two other diabetic clinics of Karachi. METHODS: The effects of glibenclamide on blood glucose and various aspects of lipoproteins has been studied in 26 (14 male, 12 female) Type II Diapetes patients before and after 12 weeks of glibenclamide therapy. Treatment was initiated with 5 mg oral glibenclamide with diet control. The initial dosage of glibenclamide was 5 mg/day taken half an hour before meal; this was increased to 5 mg per week and was adjusted according to the patient's tolerance to the drug and their glycemic control. RESULTS: The results demonstrated that fasting blood glucose declined from 221.53 + 7.84 to 165.02 + 5.12 mg/dl, (P < 0.001). There was a statistically significant increase in the plasma high-density lipoprotein cholesterol from 33.60 + 1.00 to 37.07 + 1.05 mg/dl, (P << 0.05). Total cholesterol, triglycerides, low-density lipoprotein cholesterol and very-low-density lipoprotein cholesterol did not change significantly. CONCLUSION: Improved glycaemic control in patients treated with glibenclamide with Type II Diabetes was achieved which lead to changes in lipoprotein metabolism. There was no evidence of changes in lipoproteins in directions associated with an increased risk for atherosclerosis.