A Prospective Study to Analyse the Metabolic Effect of Metformin with Glimepiride on Type 2 Diabetic Patients of North India.

Background: Diabetes Mellitus is a leading disease of developing countries and its incidence is increasing day by day. Among Oral Hypoglycemic agents, Metformin is still the best treatment choice for type 2 diabetes mellitus. Metformin is associated with improvements in lipoprotein metabolism, including decreases in LDL-C, fasting and postprandial TGs, and free fatty acids. Methods: This prospective study was carried out on Type 2 Diabetic patients attending the Diabetic clinic at Teerthanker Mahaveer Medical College & Research Center, Moradabad. Only those patients were included who were not adequately controlled with a stable dose of metformin monotherapy. A total of 125 patients were enrolled in the study taking Glimepiride plus Metformin. The patients received therapy of metformin 500mg three times daily & glimepiride 5mg twice daily. Results: Out of the 125 patients enrolled in the study, only 82 patients completed the study. Out of 82 patients, 49 were males and 33 females. There was a significant reduction (p<0.05) of FPG as compared to baseline. The (PPBS) was reduced from 275.95 ±63.599 (mg/dl) to 167.04±27.084 (mg/dl) at 12 weeks and141.36±31.064(mg/dl) at 24 weeks (mg/dl). There was a significant reduction (p<0.05) of Hb1Ac, TC, TAG, LDL, VLDL, UA, SGOT as compared to baseline but no significant rise in HDL was seen as compared to baseline. Conclusion: Significant improvement in fasting blood sugar (FBS), Postprandial blood sugar (PPBS), Lipid profile and Glycosylated hemoglobin as compared to baseline.

Reactive oxygen species and oxidative DNA damage.

Reactive oxygen species (ROS) such as the superoxide anion radical (O2.-) hydrogen peroxide (H2O2) and hydroxyl radical (.OH) have been implicated in the pathophysiology of various states, including ischemia reperfusion injury, haemorrhagic shock, atherosclerosis, heart failure, acute hypertension and cancer. The free radicals, nitric oxide (NO) and O2.- react to form peroxynitrite (ONOO-), a potent cytotoxic oxidant. A potential mechanism of oxidative damage is the nitration of tyrosine residues of protein, peroxidation of lipids, degradation of DNA and oligonucleosomal fragments. Several mechanisms are responsible for the protection of the cells from potential cytotoxic damage caused by free radicals. Cells have developed various enzymatic and nonenzymatic defense systems to control excited oxygen species, however, a certain fraction escapes the cellular defense and may cause permanent or transient damage to nucleic acids within the cells, leading to such events as DNA strand breakage and disruption of Ca2+ metabolism. There is currently great interest in the possible role of ROS in causing DNA damage that leads to cancer and spontaneous mutations. A high rate of oxidative damage to mammalian DNA has been demonstrated by measuring oxidized DNA bases excreted in urine after DNA repair. The rate of oxidative DNA damage is directly related to the metabolic rate and inversely related to life span of the organism.