Fig. 4.

Absence of Na⁺-glucose cotransporter SGLT1 reduced renal mRNA expression of markers of tubular injury, inflammation, and fibrosis during recovery from ischemia-reperfusion (IR). Kidneys were harvested on day 16 after IR for quantitative RT-PCR analyses of mRNA expression. mRNA expression was normalized to the housekeeping gene hypoxanthine-guanine phosphoribosyltransferase (Hprt). Absence of SGLT1 attenuated the increase in renal expression of markers of proximal tubular injury [kidney injury molecule-1 (Kim-1)], inflammation [chemokine (C-C motif) ligand 2 (Ccl2)], and fibrosis [fibronectin 1 (Fn1) and collagen type I-α₁ (Col1a1)] (A) and prevented the decrease in erythropoietin (Epo) expression (B), a marker of interstitial cells in the outer medulla and inner cortex. Absence of SGLT1 did not prevent the upregulation of hexokinase-2 (Hk2), a key glycolytic enzyme, but prevented the downregulation of peroxisome proliferator-activated receptor-γ coactivator-1α (Ppargc1a), a master regulator of mitochondrial biogenesis and function (C). Results are means ± SE; n = 6–8 mice/group. #P < 0.05 vs. sham and *P < 0.05 vs. WT mice using two-way ANOVA and Holm-Sidak post hoc analysis for multiple comparisons.