Diet, exercise, and weight loss can improve glycemic control, but most patients with type 2 diabetes eventually require glucose-lowering pharmacotherapy. An A1C goal of <7% (while minimizing hypoglycemia) is recommended for most patients to prevent or reduce the microvascular complications of diabetes (retinopathy, nephropathy, neuropathy). An A1C target of <8% may be appropriate for patients who are older, have comorbid conditions, or are at risk of serious hypoglycemia-associated adverse events.

Diet, exercise, and weight loss can improve glycemic control, but almost all patients with type 2 diabetes require antihyperglycemic drug therapy. Treating to a target A1C of <7% while minimizing hypoglycemia is recommended to prevent microvascular complications of diabetes (retinopathy, nephropathy, and neuropathy). An A1C target of <8% may be appropriate for some older patients.

Diet, exercise, and weight loss can improve glycemic control, but almost all patients with type 2 diabetes eventually require drug therapy. Treating to a glycated hemoglobin (A1C) concentration of <7% can prevent microvascular complications (retinopathy, nephropathy, and neuropathy), but whether it prevents macrovascular complications and death is unclear. An A1C target of <8% may be appropriate for older patients and those with underlying cardiovascular disease (CVD), a history of severe hypoglycemia, diabetes-related complications, a limited life expectancy, or a long duration of disease.

The goal of drug therapy for type 2 diabetes is to achieve and maintain a near-normal glycated hemoglobin (A1C) concentration without inducing hypoglycemia; the target is generally an A1C of ≤7%. Treating to this target has been shown to prevent microvascular complications (retinopathy, nephropathy, and neuropathy), but whether it prevents macrovascular outcomes is unclear. An A1C target of <8% may be appropriate for older patients and those with underlying cardiovascular disease, a history of severe hypoglycemia, diabetes-related complications or comorbidities, or a long duration of disease.

The goal of drug therapy for type 2 diabetes is to achieve and maintain a near-normal A1C concentration without inducing hypoglycemia; the target is generally an A1C of <7.0%. Treating to this target has been shown to prevent the microvascular complications of retinopathy and nephropathy, but whether it prevents macrovascular outcomes remains unclear. Three large trials found that intensive glucose control did not reduce the incidence of macrovascular events. One of these trials (ACCORD) in >10,000 patients with type 2 diabetes, with or at high-risk for cardiovascular disease, found that treating patients intensively with antihyperglycemic drugs to an A1C target of 6.0% for a mean of 3.7 years did not significantly reduce the incidence of major cardiovascular events (the primary endpoint) and was associated with increased all-cause mortality compared to patients treated to an A1C target of 7.0-7.9%. An A1C target of 7-8% may be prudent in older patients and in those with underlying cardiovascular disease, severe hypoglycemia, or multiple diabetes-related complications or co-morbidities.

The development of hyperglycemia in type 2 diabetes results from a combination of metabolic abnormalities that includes insulin resistance, diminished insulin secretion and excess hepatic glucose production. Diet, exercise and weight loss are helpful in improving glucose control, but most patients ultimately require drug therapy.

The development of hyperglycemia in type 2 diabetes results from a combination of metabolic abnormalities including insulin resistance, diminished insulin secretion and excess hepatic glucose production. Diet, exercise and weight loss are helpful in improving glucose control, but most patients ultimately require drug therapy.

The development of hyperglycemia in type 2 diabetes results from a combination of metabolic abnormalities including insulin resistance, excess hepatic glucose production and diminished insulin secretion. In many patients, diet and regular exercise can improve glucose control. Most drugs currently available for management of type 2 diabetes increase insulin supply (sulfonylureas, other secretagogues and insulin itself), decrease insulin resistance (thiazolidinediones) or improve the effectiveness of insulin (biguanides). Alpha-glucosidase inhibitors reduce the rate of glucose absorption. Newer agents such as pramlintide (Symlin) and exenatide (Byetta) have multiple effects to increase satiety and reduce postprandial hyperglycemia.

Pramlintide acetate (Symlin - Amylin Pharmaceuticals), a synthetic analog of human amylin, has been approved by the FDA as adjunctive treatment for patients with type 1 or type 2 diabetes who inject insulin at mealtimes and have failed to achieve glucose control. Pramlintide is injected subcutaneously before meals.

The development of hyperglycemia in type 2 diabetes results from a combination of metabolic abnormalities including insulin resistance, excess hepatic glucose production and diminished insulin secretion. Most drugs currently available for management of type 2 diabetes fall into 2 categories: those that increase insulin supply (sulfonylureas, other secretagogues and insulin itself) and those that decrease insulin resistance or improve its effectiveness (biguanides, thiazolidinediones). Alpha-glucosidase inhibitors reduce the rate of glucose absorption.

Nateglinide (Starlix), a new meglitinide oral glucose-lowering agent, has been approved by the FDA.

Rosiglitazone, the second thiazolidinedione derivative to be marketed in the USA for treatment of type 2 diabetes, has been approved by the FDA for use either alone or combined with meformin.

Miglitol, an oral alpha-glucosidase inhibitor similar to acarbase, is now available for treatment of type 2 diabetes.