Blood flow-dependent prostaglandin F(2α) regulates intestinal glucose uptake from the blood

Abstract

Intestinal glucose uptake (GUi) from blood increased when blood flow (BF) was increased. The increase in BF could elevate shear stress. Therefore, we hypothesize that shear stress-induced release of autacoids mediates the increase in GU(i). A surgically separated segment of small intestine was perfused in situ with the use of an arterial circuit in anesthetized cats. Arterial and portal blood samples were taken simultaneously for assessment of GU(i). Adenosine was used to elevate intestinal BF. The GU(i) increased by 45.0 ± 18.3 from 25.3 ± 3.8 μmol · min-1 · 100 g tissue-1 when the BF increased about four times. It was not a direct effect of adenosine because GU(i) was not altered if the flow was held constant. This increase was blocked by a cyclooxygenase inhibitor, indomethacin, but not by nitric oxide synthase blocker N(G)-nitro-L-arginine methyl ester. Furthermore, prostaglandin F(2α) (PGF(2α)) but not PGE2 or PGI2 reversed the blockade of the increase in GU(i) after indomethacin during elevated blood flow, whereas they had no influence on basal uptake. The results suggest that shear stress-induced release of PGF(2α) mediated the increase in GU(i) when blood flow was elevated.