Pine bark extract inhibits glucose transport in enterocytes via mitogen-activated kinase and phosphoinositol 3-kinase
2011
El-Zein, Ola | Kreydiyyeh, Sawsan Ibrahim
OBJECTIVE: Pine bark extract (PBE) has been reported to have hypoglycemic effects but its mode of action is still unclear. This work studied the effect of PBE on glucose uptake by Caco-2 cells in isolation of its effect on insulin, which may appear if ingested by the animal. METHODS: Caco-2 cells were incubated in the presence of PBE and [¹⁴C] 3-O-methyl-D-glucose as a tracer and the change in radioactivity of the incubation medium was taken as a measurement of glucose uptake. To determine the mechanism of action of the extract and type of transporters involved, Na⁺-coupled glucose transporter-1 (SGLT1) and glucose transporter-2 (GLUT2) and different signaling mediators known to be involved in glucose transport were inactivated by specific inhibitors. Changes in the protein expression of glucose transporters were studied by western blotting. RESULTS: The extract significantly decreased glucose transport but did not affect the activity or expression of Na⁺/K⁺ adenosine triphosphatase. It was concluded that PBE affects the number of glucose transporters in the brush-border membrane. This conclusion was confirmed by western blot analysis. The results showed that the extract acts by activating p38 mitogen-activated kinase, which in turn activates SGLT1 transporters and two different pathways that target GLUT2: an inhibitory pathway involving phosphoinositol 3-kinase and a stimulatory pathway involving mitogen activated protein kinase/extracellular signal-regulated kinase kinase. The activity of the two pathways is orchestrated by SGLT1. CONCLUSION: Pine bark extract inhibits glucose absorption by p38 mitogen-activated kinase and constitutes a potential complementary therapeutic or prophylactic agent for diabetes and its complications.
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