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Table 6 Pharmacologic options for oral DM-2 treatment

From: Algorithm for the treatment of type 2 diabetes: a position statement of Brazilian Diabetes Society

Acarbose (Glucobay®) Slows down intestinal glucose absorption. Low potential of A1C reduction (0.5 - 0.8%). Gastrointestinal intolerance.
Metformin (Glifage®, others) Reduces primarily the hepatic glucose production and fights insulin resistance. High potential of A1C reduction (2%). Gastrointestinal intolerance. Does not cause hypoglycemia. May promote mild weight loss. Contraindicated in case of renal dysfunction.
- Rosiglitazone (Avandia®)
- Pioglitazone (Actos®)
Primarily fight insulin resistance and reduces hepatic glucose production. Increases muscle, fatty tissue and liver sensitivity to insulin. Intermediate A1C reduction potential (0.5 - 1.4%). Promote hydric retention and weight gain, increasing the risk of heart failure. Also increase the risk of fracture. Recent results of studies such as RECORD and BARI 2D indicate that rosiglitazone does not increase the risk of infarction and CVD.
- Glimepiride (Amaryl®)
- Glibenclamide (Daonil®)
- Gliclazide (Diamicron MR®)
- Others
Stimulate endogenous insulin production by pancreatic beta cells, with pharmacological action medium to long (8-24 hours). Useful to control fasting glycemia and 24-hour glycemia. High potential of A1C reduction (2%). May cause hypoglycemia. Glibenclamide has higher risk of hypoglycemia. An alleged deleterious action on human beta cells has not yet been confirmed.
- Repaglinide (Novonorm®, Prandin®)
- Nateglinide (Starlix®)
Stimulate endogenous insulin production by pancreatic beta cells, with short duration (1-3 hours). Useful to control post-prandial hyperglycemia. Intermediate potential of A1C reduction (1.0 - 1.5%). May promote weight gain and hypoglycemia. Repaglinide is more powerful than nateglinide.
Incretin mimetics and DPP-4 inhibitors
- Exenatide (Byetta®)
- Vildagliptin (Galvus®)
- Sitagliptin (Januvia®)
This is a new therapeutic class for treating diabetes, whose mechanism includes stimulating beta cells to increase insulin synthesis and action on pancreatic alpha cells, reducing glucagon production. Glucagon has the effect of increasing glycemic levels. Average potential of A1C reduction (0.5 - 0.8%, depending on the basal A1C value). Do not cause hypoglycemia but gastrointestinal intolerance and pancreatitis have been described (exenatide and sitaglipitn) [13, 14].
  1. This table represents only a partial relation of commercial medications of various drugs and does not represent a specific recommendation of any commercial brand.