Figure 2. Potential biological mechanisms of dandelion-derived compounds to modulate cAMP and insulin secretion.

The diagram specifies potential mechanisms of bioactive components from dandelion (CGA, CRA, TS, and SEL) on insulin secretion and cAMP pathway. T2D can arise from several defects, including low response in β-cells (at the level of GLUT2, SUR1, G-protein-coupled receptors, and gene expression), enzymatic action in digestion, glycolysis, and Krebs cycle. Bioactive compounds may act directly or indirectly in a series of processes, thereby modulating and regulating some T2D defects and responses. The steps of insulin secretion are shown by numbers 1-7, with steps 1 and 2 showing how ATP is produced, steps 2-5 indicating the mechanism of K_ATP closure and opening of the calcium ion channels, and 5-7 showing the influx of calcium ions into the β-cell triggering insulin granules to release insulin via exocytosis. A to G shows the potential mode of action of CGA, CRA, TS, and SEL at various levels of β-cell activity following the inhibition of α-glucosidase during digestion in the small intestines. A and B represent the upregulation in the release of GLP-1 secreted by intestinal L-cells, and the subsequent inhibition of glucose absorption induced by dandelion components CGA, CRA and TS. C and D indicate the stimulation of G-protein-coupled receptors and activation of adenyl cyclase, which further activates steps E and F, where cAMP activates PKA, PKC, and IDX-1, resulting in gene modulation of insulin and GLUT2, as well as an increase in calcium flow, which eventually facilitates the release of insulin. X represents the modulation of the insulin receptor by dandelion-derived compounds, which induces insulin secretion via regulation of IDX 1 factor, GLUT2, glucokinase, and endoplasmic reticulum Ca ions.