Figure 1.

Schematic illustration of how Resveratrol (RSV) may affect intestinal glucose transport. 1. The activation of adenylate cyclase (AC) [22,23] and inhibition of phosphodiesterases (PDE) [21] and the subsequent increased in intracellular cyclic adenosine monophosphate (cAMP) levels are likely to activate protein kinase A (PKA) that is able to phosphorylate sodium–glucose-linked transporter 1 (SGLT1) at Ser418 with species-dependent effects [9,10]. PKA is also able to modulate the activity of the AMP-activated protein kinase (AMPK) via changing the activities of AMPK activating upstream kinases (liver kinase B1 (LKB1) activation [25,26], calcium/calmodulin-dependent protein kinase kinase (CaMKK) inhibition [29]) or by direct phosphorylation of AMPK (inhibition) [28]. 2. Resveratrol may (cAMP-mediated) exert effects on the Na⁺/K⁺-ATPase activity [30,31] and therefore change the driving force for Na⁺-coupled transport processes as the absorption of glucose and alanine. 3. Since Resveratrol is known to affect membrane properties and influences the formation of detergent resistant membrane fractions (DRM) [32,35], the association of nutrient transport proteins with DRMS and therefore their activity may be changed by Resveratrol.