Type 2 diabetes involves both insulin resistance and progressive beta-cell failure, so drugs can be grouped by the broken step they address. Metformin acts mainly on the liver, reducing hepatic glucose output and improving hepatic insulin sensitivity; it is usually the first oral agent because it targets a central defect without causing hypoglycemia. SGLT2 inhibitors block sodium-glucose cotransporter 2 in the proximal tubule, so more glucose is excreted in urine; this lowers glucose independently of insulin. GLP-1 receptor agonists mimic the incretin hormone GLP-1, increasing glucose-dependent insulin secretion, suppressing glucagon, slowing gastric emptying, and reducing appetite; DPP-4 inhibitors slow the breakdown of endogenous GLP-1 and GIP, producing a milder version of the same effect. Sulfonylureas close the beta-cell K-ATP channel directly, triggering insulin release even when glucose is not high, which is why they can cause hypoglycemia. Each class therefore maps onto a different node: hepatic glucose output, renal glucose reabsorption, incretin signaling, or direct beta-cell stimulation. Understanding the node explains both the benefit and the main risk of each drug.
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Where Type 2 Drugs Act
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Type 2 diabetes has two problems: tissues respond weakly to insulin, and beta cells eventually cannot keep up. Each drug class targets one of those problems. Metformin works mainly on the liver, reducing glucose release. SGLT2 inhibitors block glucose reabsorption in the kidney, so glucose leaves in the urine. GLP-1 receptor agonists and DPP-4 inhibitors strengthen incretin signaling, which boosts glucose-dependent insulin release and lowers glucagon. Sulfonylureas stimulate the beta cell directly by closing the K-ATP channel, which is effective but can cause hypoglycemia because secretion is no longer glucose-dependent. The diagram places each class at its node so you can predict both the benefit and the main risk.
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