According to in vitro experiments the serum- and glucocorticoid-inducible kinase SGK1 stimulates peptide transport. The present study explored the contribution of SGK1 to intestinal peptide transport regulation in vivo. Currents (Ip) induced by 5 mM of the dipeptide glycyl-glycine (gly-gly) were determined in Ussing chamber. Cytosolic pH (pHi) was determined by BCECF-fluorescence and Na⁺/H⁺-exchanger activity estimated from Na⁺-dependent pH recovery (DpHi) following an NH3 pulse. In part, mice were treated 4 days with 10mg/gBW/day glucocorticoid dexamethasone (DEX). Ip was without DEX virtually identical in SGK1-knockout mice (sgk1^-/-) and their wild type littermates (sgk1^+/+). DEX increased Ip in sgk1^+/+ but not in sgk1^-/-. pHi was similar in sgk1^-/- and sgk1^+/+ with or without DEX. Irrespective of DEX, addition of 5 mM gly-gly to perfusing solution led to similar decline in pHi in sgk1^-/- and sgk1^+/+ but sustained exposure to 5 mM gly-gly was followed by a decline of pHi in sgk1^-/- > sgk1^+/+. In both, presence and absence of gly-gly, DpHi was significantly enhanced by DEX in sgk1^+/+ > sgk1^-/-. Irrespective of DEX, during sustained exposure to gly-gly DpHi was in sgk1^+/+ > sgk1^-/-. In conclusion, glucocorticoids stimulate peptide transport and both, glucocorticoids and peptide transport stimulate Na⁺/H⁺-exchanger activity, effects partially dependent on SGK1.