Composition:

Each Uncoated Bilayered tablet contains, Voglibose 0.2 mg, Metformin 500mg and Pioglitazone 7.5 mg. &
Each Uncoated Bilayered tablet contains, Voglibose 0.3 mg, Metformin 500mg and Pioglitazone 7.5 mg

Clinical Pharmacology:

Beta cell failure and peripheral insulin resistance are the basic pathophysiologic defects of type 2 diabetes mellitus.
An early and proactive approach to treating patients with type 2 diabetes mellitus using a triple combination of Metformin, Pioglitazone and Voglibose is presented here.
The UKPDS clearly demonstrated that sulfonylureas had no protective effect on progressive β- cell failure in newly-diagnosed type 2 diabetic patients over the 15-year study duration. Moreover, sulfonylureas were shown not to have a significant protective effect against atherosclerotic cardiovascular complications, and some studies even gave notion that sulfonylureas may accelerate the atherogenic process.
The relentless rise in hemoglobin A1c (HbA1c) levels observed with both sulfonylureas and metformin resulted from a progressive decline in β-cell function, and by 3 years, approximately 50% of diabetic patients required an additional pharmacological agent to maintain HbA1c levels below 7.0%. Although the add-on treatment improved glycemic control, after the initial decline in HbA1c concentrations, progressive β-cell failure continued and HbA1c values rose progressively. Thus, most clinical evidence shows that the glucose-lowering effect of sulfonylureas and metformin is not durable and that the loss of glycemic control is associated with progressive β-cell failure.
Metformin is traditionally known for its metabolic effects on the liver; and other metformin target tissues include skeletal muscle and adipose tissue. Metformin is a useful adjuvant to lifestyle modification in overweight and obese patients with type 2 diabetes mellitus, metabolic syndrome, or impaired glucose tolerance (IGT). AMP-activated protein kinase (AMPK), a serine-threonine kinase that functions as an intracellular energy sensor, has been involved in the molecular mechanisms of metformin's actions in the liver, muscle, endothelium, and the ovaries. Although metformin failure may occur rapidly in clinical practice, initiating treatment soon after diabetes diagnosis and while HbA1c levels are low might preserve β-cell function, prolonging the effectiveness of metformin.
The best evidence that retardation or arrest of β-cell loss can be achieved comes from interventions that reduce excess body adiposity or change its biology. Weight loss in the Diabetes Prevention Program and the Finnish Diabetes Prevention Study was associated with ongoing reductions in the rate of type 2 diabetes mellitus each year. This pattern would be expected if weight loss were slowing, or even stopping, the progression of β-cell deterioration. The same phenomenon has been observed repeatedly with Pioglitazone, which change lipid.
distribution and adipose-tissue biology to ameliorate some adverse metabolic effects of obesity, including insulin resistance.
There are five studies in subjects with IGT demonstrating that Pioglitazone prevent the progression of IGT to type 2 diabetes mellitus. The Actos Now for Prevention of Diabetes study showed an 81% reduction in the conversion of IGT to type 2 diabetes mellitus with pioglitazone. All five of these studies showed that, in addition to their insulin sensitizing effect, PIOGLITAZONEs have a major action to preserve β-cell function. Many in vivo and in vitro studies with human and rodent islets have shown that Pioglitazone exert a protective effect on β-cell function. Direct measurement of β-cell function in the Troglitazone in Prevention of Diabetes and Pioglitazone in Prevention of Diabetes studies proved that Pioglitazone can slow or even stop the loss of β-cell function. The mechanism appeared to be a reduction in the secretory demand for insulin that occurs when insulin resistance is treated.
The stepped ADA algorithm of metformin/sulfonylurea therapy in type 2 diabetes mellitus has been proven ineffective in achieving durable glycemic control even in newly-diagnosed patients.
The stepped ADA algorithm of metformin/sulfonylurea therapy in type 2 diabetes mellitus has been proven ineffective in achieving durable glycemic control even in newly-diagnosed patients.
When used in combination, one would expect an even more durable effect on preservation of β-cell function and reduction in HbA1c levels, although this remains to be proven in a longer-term study.
A treatment paradigm shift is recommended in which combination therapy is initiated with diet/ exercise, metformin (which has antiatherogenic effects and improves hepatic insulin sensitivity), a PIOGLITAZONE (which improves insulin sensitivity and preserves β-cell function with proven durability), and Voglibose (which retards Carbohydrate absorption).

Presentation:

DBOSE MP 275 : A Strip of 10 Tablets, A Box of 10 Strips.
DBOSE MP 375 : A Strip of 10 Tablets, A Box of 10 Strips.