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Updated: Nov 16, 2025

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Published on: November 16, 2011
Hypoglycemic Effects of Licochalcone A on the Streptozotocin-Induced Diabetic Mice and Its Mechanism Study
Zhonghua Luo1, Chaofan Fu1, Tao Li1
1Shenyang Pharmaceutical University, Shenyang 110016, China.
Abstract:
Type 2 diabetes mellitus (T2DM) is a type of metabolic illness based on relatively insufficient insulin secretion and insulin resistance (IR) as pathophysiological bases. Currently, it is the main type of diabetes. Hypoglycemic and hypolipidemic effects of licochalcone A (LicA) on high-fat diet and streptozocin-caused T2DM were studied. LicA can remarkably decline the IR index and blood glucose and serum lipid levels. Also, the treatment of LicA can improve the "three more and one less" phenomenon in T2DM mice, such as excessive drinking, eating, urine, and weight loss. In addition, LicA can improve oral glucose tolerance, pancreatic injury, and liver enlargement in T2DM mice. Network pharmacology analysis demonstrated that the observed pharmacological effects were mediated by regulating the insulin signal transduction pathway. Therefore, the PI3K/Akt-signaling pathway was selected for verification; it was demonstrated that LicA could improve the insulin-signaling pathway, protect islet cells, improve IR, reduce blood glucose levels, and alleviate lipid metabolism disorder. Its mechanism of influence may be closely related to LicA up-regulating the liver and pancreas IRS-2/PI3K/AKT-signaling pathway. Among them, the high-dose group of LicA had the best effect, which provided an idea for the use of LicA as a nutritional agent in the cure of T2DM.
Insights
Licochalcone A (LicA) effectively lowers blood glucose and improves insulin resistance in type 2 diabetes (T2DM) models. This natural compound shows promise as a nutritional agent for managing T2DM by enhancing the PI3K/Akt signaling pathway.
Area of Science:
- Metabolic disorders
- Pharmacology
- Natural product research
Background:
- Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disease characterized by insulin resistance and insufficient insulin secretion.
- Current management strategies for T2DM often require lifelong treatment and can have side effects.
Purpose of the Study:
- To investigate the hypoglycemic and hypolipidemic effects of licochalcone A (LicA) in a mouse model of T2DM.
- To elucidate the underlying molecular mechanisms of LicA's therapeutic action, focusing on insulin signaling pathways.
Main Methods:
- Induction of T2DM in mice using a high-fat diet and streptozocin.
- Administration of varying doses of LicA to T2DM mice.
- Assessment of metabolic parameters including blood glucose, serum lipids, and body weight.
- Oral glucose tolerance tests and histological examination of pancreatic and liver tissues.
- Network pharmacology analysis and verification of the PI3K/Akt signaling pathway.
Main Results:
- LicA significantly reduced insulin resistance index, blood glucose, and serum lipid levels in T2DM mice.
- LicA treatment ameliorated T2DM symptoms such as excessive thirst, appetite, urination, and weight loss.
- Improvements were observed in oral glucose tolerance, pancreatic islet cell damage, and liver enlargement.
- Network pharmacology identified the insulin signal transduction pathway as a key mediator, with PI3K/Akt pathway verification showing LicA up-regulates IRS-2/PI3K/AKT signaling in the liver and pancreas.
Conclusions:
- Licochalcone A demonstrates significant potential in improving insulin signaling, protecting islet cells, reducing blood glucose, and alleviating lipid disorders in T2DM.
- The therapeutic effects of LicA are closely linked to its ability to up-regulate the IRS-2/PI3K/AKT signaling pathway in the liver and pancreas.
- High-dose LicA exhibited the most pronounced effects, suggesting its potential as a nutritional agent for T2DM management.
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