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. 2022 Sep 20;23(19):10988. doi: 10.3390/ijms231910988

Figure 2.

Figure 2

Schematic diagram showing the mechanisms of glycyrrhizic acid (GL) and its derivatives in improving insulin resistance in the liver and adipose tissue. GL and its derivatives act on the insulin receptor to regulate gluconeogenesis and enhance glycogen synthesis via PI3K/Akt signaling pathway, and increase glucose uptake via GLUT4, thus regulating glucose homeostasis. On the other hand, they increase lipolysis through PI3K/Akt/HSL pathway and reduce fatty acid synthesis through downregulating SREBP-1c/FAS/SCD1 pathway, thereby regulating lipid metabolism. Therefore, GL and its derivatives improve insulin resistance through improving glucose homeostasis and lipid metabolism. FAS: Fatty acid synthetase; G6Pase: Glucose-6-phosphatase; GLUT4: Glucose transporter 4; GSK-3β: Glycogen synthase kinase-3β; HSL: Hormone-sensitive lipase; IGF-1: Insulin-like growth factor 1; IL-6: Interleukin 6; IRS-1: Insulin receptor substrate 1; IRS-2: Insulin receptor substrate 2; PEPCK: Phosphoenolpyruvate carboxykinase; PI3K: Phosphoinositide 3-kinase; PTP1B: Protein tyrosine phosphatase 1B; SCD1: Stearoyl CoA desaturase 1; SREBP-1c: Sterol regulatory element-binding protein 1c; TNF-α: Tumor necrosis factor-α.