Antidiabetic Mechanisms and Treatments in Rodent Models

Rodent models have long underpinned preclinical investigations into type 2 diabetes, offering insights into pancreatic β-cell dysfunction, insulin resistance and metabolic derangements. Common paradigms include streptozotocin-induced β-cell injury, high-fat diet feeding and genetically predisposed strains, each recapitulating key features of human disease. Antidiabetic interventions tested in these systems span synthetic agents, natural extracts and novel small molecules. Mechanistic studies reveal that many compounds exert their effects by enhancing insulin signalling through the phosphoinositide 3-kinase–Akt pathway, activating AMP-activated protein kinase to promote glucose uptake, upregulating glucose transporter type 4 on muscle and adipose membranes, or by modulating incretin hormones such as glucagon-like peptide 1. Complementary approaches target oxidative stress and inflammation in pancreatic and peripheral tissues, safeguarding β-cell mass and improving insulin sensitivity. Experimental therapies range from bile acid derivatives that alleviate lipotoxicity and endoplasmic reticulum stress, to polysaccharide fractions with antioxidant and anti-inflammatory properties, and phytochemicals that engage multiple metabolic nodes. Together, these studies advance our understanding of disease mechanisms and inform the rational design of novel glucose-lowering agents.

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Antidiabetic Mechanisms and Treatments in Rodent Models publication trend

The graph below shows the total number of articles in antidiabetic mechanisms and treatments in rodent models across all publications each year (not limited to Nature Index journals).

Technical terms

Streptozotocin (STZ): A compound selectively toxic to pancreatic β-cells, used to induce experimental diabetes in rodents.

AMP-activated protein kinase (AMPK): A cellular energy sensor that, when activated, enhances glucose uptake and fatty acid oxidation.

Phosphoinositide 3-kinase–Akt pathway (PI3K/Akt): A central insulin signalling cascade that regulates glucose transport, glycogen synthesis and cell survival.

Glucose transporter type 4 (GLUT4): An insulin-responsive membrane protein responsible for glucose uptake in skeletal muscle and adipose tissue.

Incretin: A class of gut hormones, such as glucagon-like peptide 1, that potentiate insulin secretion after nutrient ingestion.

References

1. Tauroursodeoxycholic Acid (TUDCA) Relieves Streptozotocin (STZ)-Induced Diabetic Rat Model via Modulation of Lipotoxicity, Oxidative Stress, Inflammation, and Apoptosis. International Journal of Molecular Sciences (2024).
2. Characterization, In Vitro Biological Activity and In Vivo Cardioprotective Properties of Trametes versicolor (L.:Fr.) Quél. Heteropolysaccharides in a Rat Model of Metabolic Syndrome. Pharmaceuticals (2023).
3. Antidiabetic Potential of Monoterpenes: A Case of Small Molecules Punching above Their Weight. International Journal of Molecular Sciences (2017).