Premium
SGLT 1 and 2 Co‐localize To NHE3 In The Renal Brush Border, Which Is Not Impaired By Phloridzin
Author(s) -
Pessoa Thaissa Dantas,
Malnic Gerhard
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1041.27
Subject(s) - brush , brush border , chemistry , medicine , biophysics , endocrinology , biochemistry , materials science , biology , composite material , membrane , vesicle
Previous microperfusion studies have shown that NHE3‐dependent bicarbonate reabsortion is reduced (53.15%) by Phloridzin, a SGLT inhibitor, and modulated by glucose concentrations. We have postulated a possible colocalization of SGLT 1 and/or 2 to NHE3, which could be responsible for the functional changes. Male Wistar rats were treated with a single intravenous shot of 100mg Phloridzin or vehicle, sacrificed 25 minutes later and perfused with paraformaldehyde to fix renal tissue. The kidney slices were incubated with SGLT 1 or 2 plus NHE3 antibodies. Proximal tubule NHE3 staining was seen to be restricted to apical brush border (BB) whereas SGLT1 and 2 staining was distributed between BB and cytoplasm vesicles (CV). By using Pearson's colocalization analyis to define if SGLT1 and 2 are colocalized to NHE3 in BB, we found that colocalization coefficients were extremely high for both SGLT1 (0,84 ±0,039 n=5) and 2 (0,87 ±0,039 n=5) and Phloridzin treatment did not change these parameters (0,79 ±0,0,028 n=5 and 0,85 ±0,119 n=5 to SGLT1 and 2 respectively). On the other hand, whereas NHE3 expression was not altered by Phloridzin treatment, our analysis has shown that the glucose transporter inhibitor increases SGLT2 BB staining. These results indicate that the NHE3‐dependent bicarbonate reabsortion decrease is not due to a reduction of apical NHE3 expression but may be due to changes of NHE3/SGLT interaction.