Type 2 Diabetes Mellitus (T2D) accounts for approximately 96% of all diabetes
cases, making it one of the most prevalent noncommunicable chronic diseases and a major global public health concern[1]. T2D is characterized by a non-autoimmune, progressively heterogeneous decline in functional insulin secretion from pancreatic β-cells. The core pathophysiological mechanisms underlying T2D are insulin resistance (IR) and β-cell dysfunction[1]. |
| Therapeutic Targets in T2D |
| Established therapeutic targets for T2D include GLP-1, DPP-4, and SGLT2 — all of which play pivotal roles in regulating glucose homeostasis and enhancing insulin sensitivity. |
DPP-4 Inhibitors: Inhibit the proteolytic degradation of GLP-1, thereby
increasing endogenous GLP-1 levels[2]. |
| GLP-1 Receptor Agonists: Peptides structurally analogous to native GLP-1 that activate its receptor and exhibit prolonged in vivo activity following subcutaneous injection[2]. |
SGLT2 Inhibitors: Block glucose reabsorption in the renal proximal tubules,
promoting glycosuria and reducing blood glucose levels[2]. |
Recent cardiovascular outcome trials have shown that some SGLT2 inhibitors and GLP-1 receptor agonists significantly reduce the risk of cardiovascular and
renal events[1]. |
| Experimental Models for T2D |
Numerous compounds have diabetogenic properties, such as Alloxan (ALX),
Streptozotocin (STZ), Ferric nitrilotriacetate, and Dithizone. Among these, ALX
and STZ are the most commonly used agents for inducing diabetes in experimental models[4].
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| References: |
| [1] Lu X, et al. Signal Transduct Target Ther. 2024 Oct 2;9(1):262. |
| [2] Meier JJ. Nat Rev Endocrinol. 2012 Dec;8(12):728-42. |
| [3] Hattersley AT, et al. N Engl J Med. 2015 Sep 3;373(10):974-6. |
| [4] Dhuria RS, et al. Adv Biomed Res. 2015 May 29;4:117. |
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