Agents Used for Treatment of Type 1 or Type 2 Diabetes
| Mechanism of Action | Examplesa | HbA1c Reduction (%)b | Agent-Specific Advantages | Agent-Specific Disadvantages | Contraindications | |
|---|---|---|---|---|---|---|
| Oral | ||||||
| Biguanidesc* | ↓Hepatic glucose production | Metformin | 1-2 | Weight neutral, do not cause hypoglycemia, inexpensive, extensive experience, ↓ CV events | Diarrhea, nausea, lactic acidosis | Serum creatinine >1.5 mg/dL (men) >1.4 mg/dL (women) (see text), CHF, radiographic contrast studies, hospitalized patients, acidosis |
| α-Glucosidase inhibitorsc** | ↓GI glucose absorption | Acarbose, miglitol, voglibose | 0.5-0.8 | Reduce postprandial glycemia | GI flatulence, liver function tests | Renal/liver disease |
| Dipeptidyl peptidase IV inhibitorsc*** | Prolong endogenous GLP-1 action | Alogliptin, Anagliptin, Gemigliptin, linagliptin, saxagliptin, sitagliptin, teneligliptin, vildagliptin | 0.5-0.8 | Well tolerated, do not cause hypoglycemia | Reduced dose with renal disease; one associated with increase heart failure risk; possible association with ACE inhibitor-induced angioedema | |
| Insulin secretagogues: Sulfonylureasc* | ↑Insulin secretion | Glibornuride, gliclazide, glimepiride, glipizide, gliquidone, glyburide, glyclopyramide | 1-2 | Short onset of action, lower postprandial glucose, inexpensive | Hypoglycemia, weight gain | Renal/liver disease |
| Insulin secretagogues: Nonsulfonylureasc*** | ↑Insulin secretion | Nateglinide, repaglinide, mitiglinide | 0.5-1.0 | Short onset of action, lower postprandial glucose | Hypoglycemia | Renal/liver disease |
| Sodium-glucose co-transporter 2 inhibitors*** | ↑Urinary glucose excretion | Canagliflozin, dapagliflozin, empagliflozin | 0.5-1.0 | Insulin secretion and action independent | Urinary and vaginal infections, dehydration, exacerbate tendency to hyperkalemia | Limited clinical experience; moderate renal insufficiency |
| Thiazolidinedionesc*** | ↓Insulin resistance, ↑ glucose utilization | Rosiglitazone, pioglitazone | 0.5-1.4 | Lower insulin requirements | Peripheral edema, CHF, weight gain, fractures, macular edema | CHF, liver disease |
| Parenteral | ||||||
| Amylin agonistsc,d*** | Slow gastric emptying, ↓ glucagon | Pramlintide | 0.25-0.5 | Reduce postprandial glycemia, weight loss | Injection, nausea, ↑ risk of hypoglycemia with insulin | Agents that also slow GI motility |
| GLP-1 receptor agonistsc*** | ↑Insulin, ↓ glucagon, slow gastric emptying, satiety | Exenatide, liraglutide, dulaglutide | 0.5-1.0 | Weight loss, do not cause hypoglycemia | Injection, nausea, ↑ risk of hypoglycemia with insulin secretagogues | Renal disease, agents that also slow GI motility; medullary carcinoma of thyroid |
| Insulinc,d**** | ↑Glucose utilization, ↓ hepatic glucose production, and other anabolic actions | See text and Table 418-4 in HPIM-19 | Not limited | Known safety profile | Injection, weight gain, hypoglycemia | |
| Mechanism of Action | Examplesa | HbA1c Reduction (%)b | Agent-Specific Advantages | Agent-Specific Disadvantages | Contraindications | |
| Medical nutrition therapy and physical activityc* | ↓Insulin resistance, ↑ insulin secretion | Low-calorie, low-fat diet, exercise | 1-3 | Other health benefits | Compliance difficult, long-term success low |
aExamples are approved for use in at least one country, but may not be available in the United States or all countries. Examples may not include all agents in the class.
bHbA1c reduction (absolute) depends partly on starting HbA1c.
cUsed for treatment of type 2 diabetes.
dUsed in conjunction with insulin for treatment of type 1 diabetes. Cost of agent: *low, **moderate, ***high, ****variable.
Note: Some agents used to treat type 2 DM are not included in table (see text).
Abbreviations: CV, cardiovascular; HbA1c, hemoglobin A1c.