Oha classication
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"Hypoglycemic Agents"[MeSH Terms] AND "type 2 diabetes"
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I'm assuming "OHA" means oral hypoglycemic agents, the drugs used in type 2 diabetes. If you meant something else, tell me and I'll redo it.
Classification of oral hypoglycemic agents
| Class | Examples | Main mechanism | HbA1c fall (%) | Key points |
|---|---|---|---|---|
| Biguanides | Metformin | Lowers hepatic glucose output and raises insulin sensitivity | 1-2 | No hypoglycemia, weight neutral, cheap. Causes diarrhea and B12 deficiency, and carries a lactic acidosis risk. Avoid if GFR <30, in decompensated heart failure, and around contrast studies. |
| Sulfonylureas (insulin secretagogues) | Glimepiride, glipizide, glibenclamide (glyburide), gliclazide | Close the K-ATP channel on beta cells, which increases insulin secretion | 1-2 | Cheap. Cause hypoglycemia and weight gain. Use caution in renal or liver impairment. |
| Meglitinides (non-sulfonylurea secretagogues) | Repaglinide, nateglinide | Also close the K-ATP channel, with rapid, short action | 1-2 | Mainly lower postprandial glucose. Can still cause hypoglycemia. |
| Thiazolidinediones (glitazones) | Pioglitazone, rosiglitazone | PPAR-gamma agonists that reduce insulin resistance | 0.5-1.2 | Cause edema, heart failure, weight gain, and fractures in women. Contraindicated in heart failure. |
| Alpha-glucosidase inhibitors | Acarbose, miglitol, voglibose | Delay intestinal carbohydrate absorption | 0.5-0.8 | Lower postprandial glucose. Cause flatulence and GI upset. |
| DPP-4 inhibitors (gliptins) | Sitagliptin, vildagliptin, linagliptin, saxagliptin | Prolong endogenous GLP-1 and GIP action | 0.4-0.8 | Weight neutral, no hypoglycemia on their own. Most need a dose reduction in renal impairment (linagliptin does not). |
| SGLT2 inhibitors (gliflozins) | Empagliflozin, dapagliflozin, canagliflozin, ertugliflozin | Increase renal glucose excretion | 0.5-0.8 | Cause weight loss and lower BP. Benefit heart failure and CKD. Cause genital and urinary infections and risk euglycemic DKA. |
The HbA1c, mechanism, and adverse-effect details come from Goodman & Gilman's Table 51-6.
Another way to group them by action
- Increase insulin supply (secretagogues): sulfonylureas, meglitinides. DPP-4 inhibitors do this in a glucose-dependent way.
- Decrease insulin resistance (sensitizers): metformin, thiazolidinediones.
- Reduce glucose absorption or increase excretion: alpha-glucosidase inhibitors, SGLT2 inhibitors.
Rosen's Emergency Medicine uses the same split: agents that increase insulin supply, such as sulfonylureas and secretagogues, versus agents that decrease insulin resistance, such as biguanides and thiazolidinediones. Sulfonylureas can be combined with metformin, acarbose, thiazolidinediones, or meglitinides (Swanson's Family Medicine Review).
Sources
- Goodman & Gilman's The Pharmacological Basis of Therapeutics, Table 51-6 (Comparison of Agents Used for Treatment of Diabetes)
- ROSEN's Emergency Medicine, "Management of Diabetes Mellitus"
- Swanson's Family Medicine Review, Table 4.11 (Classes of Oral Agents and Insulins)
Recent evidence
A 2025 living systematic review and network meta-analysis in the BMJ (PMID 40813122) compared diabetes drugs. SGLT2 inhibitors and GLP-1 receptor agonists are generally favored for cardiorenal outcomes over older oral agents. This is consistent with the library content, but I did not read the full paper, so check it before relying on the details.
GLP-1 receptor agonists such as semaglutide and liraglutide are injectable and are not oral hypoglycemic agents in the classic sense. Oral semaglutide is the exception.
I can add mechanism diagrams, drug doses, or a version tailored to your exam (MBBS, NEET-PG, and so on) if you want.
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