BACKGROUND/AIMS Acute stimulation by cAMP of the sodium dependent glucose cotransporter SGLT1 has previously been shown. As prostaglandin E₂(PGE₂) increases intracellular cAMP concentrations via its receptor subtypes EP2R and EP4R, it was investigated whether PGE₂ could enhance intestinal glucose absorption.

RESULTS In the perfused small intestine, PGE₂ acutely increased absorption of glucose and galactose, but not fructose (which is not a substrate for SGLT1); in isolated enterocytes it stimulated 3-O-[¹⁴C]methylglucose uptake. The 3-O-[¹⁴C]methylglucose uptake could be inhibited by the cAMP antagonist RpcAMPS and the specific inhibitor of SGLT1, phlorizin. High levels of EP2R mRNA and EP4R mRNA were detected in villus tip enterocytes.

CONCLUSION PGE₂acutely increased glucose and galactose absorption by the small intestine via the SGLT1, with cAMP serving as the second messenger. PGE₂ acted directly on the enterocytes, as the stimulation was still observed in isolated enterocytes and RT-PCR detected mRNA for the cAMP-increasing PGE₂ receptors EP2R and EP4R.