AIMS: Urinary tract infection (UTI) is a common clinical problem in diabetic 
patients; however, the relationship between UTI and glucosuria remains 
uncertain. To investigate the relationship, we examined the effect of glucosuria 
induced by sodium glucose cotransporter 2 (SGLT2) inhibitors on the progression 
of UTI in mice.
METHODS: From 1 day before transurethral inoculation with Candida albicans, 
female mice were treated orally once a day with an SGLT2 inhibitor in different 
treatment regimens: (i) dapagliflozin at 10 mg/kg for 2, 3 or 7 days, (ii) 
dapagliflozin at 0.1, 1 or 10 mg/kg for 3 days and (iii) dapagliflozin, 
canagliflozin or tofogliflozin at 10 mg/kg for 3 days. To evaluate the ascending 
UTI, the kidneys were removed 6 days after the inoculation, and the number of 
viable C. albicans cells in kidney was measured as colony-forming units (CFU).
RESULTS: In mice treated with dapagliflozin, the number of C. albicans CFU in 
kidney increased in accordance with both treatment duration and dose. The number 
of CFU significantly increased when mice were treated with 10 mg/kg 
dapagliflozin or canagliflozin but not tofogliflozin. With dapagliflozin and 
canagliflozin, urine glucose concentration (UGC) significantly increased up to 
24 h after drug administration; with tofogliflozin, UGC significantly increased 
only up to 12 h after drug administration.
CONCLUSIONS: Our data indicate that increased susceptibility to UTI is 
associated with a persistent increase in UGC.