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This Article Full Text Full Text (PDF) All Versions of this Article: 584/2/613    most recent jphysiol.2007.138578v2 jphysiol.2007.138578v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wong, T. P. Articles by Leung, P. S. Search for Related Content PubMed PubMed Citation Articles by Wong, T. P. Articles by Leung, P. S. Related Collections Alimentary

¹ Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China ²Department of Physiology, University College London, Hampstead Campus, London NW3 2PF, UK

There is increasing evidence that locally produced angiotensin AII (AII) regulates the function of many tissues, but the involvement of enterocyte-derived AII in the control of intestinal transport is unknown. This study examined whether there is a local renin–angiotensin system (RAS) in rat villus enterocytes and assessed the effects of AII on SGLT1-dependent glucose transport across the brush border membrane (BBM). Gene and protein expression of angiotensinogen, ACE, and AT₁ and AT₂ receptors were studied in jejunal and ileal enterocytes using immunocytochemistry, Western blotting and RT-PCR. Mucosal uptake of D-[¹⁴C]glucose by everted intestinal sleeves before and after addition of AII (0–100 nM) to the mucosal buffer was measured in the presence or absence of the AT₁ receptor antagonist losartan (1 µM). Immunocytochemistry revealed the expression of angiotensinogen, ACE, and AT₁ and AT₂ receptors in enterocytes; immunoreactivity of AT₁ receptor and angiotensinogen proteins was especially pronounced at the BBM. Expression of angiotensinogen and AT₁ and AT₂ receptors, but not ACE, was greater in the ileum than the jejunum. Addition of AII to mucosal buffer inhibited phlorizin-sensitive (SGLT1-dependent) jejunal glucose uptake in a rapid and dose-dependent manner and reduced the expression of SGLT1 at the BBM. Losartan attenuated the inhibitory action of AII on glucose uptake. AII did not affect jejunal uptake of L-leucine. The detection of RAS components at the enterocyte BBM, and the rapid inhibition of SGLT1-dependent glucose uptake by luminal AII suggest that AII secretion exerts autocrine control of intestinal glucose transport.

(Received 13 June 2007; accepted after revision 9 August 2007; first published online 16 August 2007)
Corresponding author P. S. Leung: Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China. Email: psleung{at}cuhk.edu.hk