Possible Interaction: Glucose and Dapagliflozin

“As expected, 24-h urinary glucose excretion significantly increased during dapagliflozin treatment and reversed during FU.”

“ Dapagliflozin increases urinary glucose excretion by selective inhibition of renal sodium-glucose cotransporter 2 (SGLT2).”

“ Dapagliflozin increases urinary glucose excretion by selective inhibition of renal sodium‐glucose cotransporter 2 (SGLT2).”

“ Dapagliflozin treatment increased glucose production in HK-2 cells and lowered blood glucose and induced gluconeogenesis in ob/ob mice.”

“By selectively and reversibly blocking the SGLT2 receptor, dapagliflozin prevents the reabsorption of glucose at the renal proximal tubule.”

“ Once-daily dapagliflozin treatment over 2 weeks significantly lowered fasting and fed glucose levels at doses ranging from 0.1 to 1.0 mg/kg and resulted in a significant increase in glucose utilization rate accompanied by a significant reduction in glucose production.”

“RESULTS Dapagliflozin potently and selectively inhibited human SGLT2 versus human SGLT1, the major cotransporter of glucose in the gut, and did not significantly inhibit facilitative glucose transport in human adipocytes.”

“When divided by BMI >27 and <27 kg/m2, basal glucose Ra, BOHB, and glycerol Ra AUC0–180 min were significantly higher in the low-BMI group with dapagliflozin treatment versus the low-BMI group with placebo.”

“ConclusionThese present results indicate that dapagliflozin can significantly reduce glucose , BMI, blood pressure and AHI, and improve hypoxemia during sleep and excessive daytime sleepiness, which thereby has potential as an effective treatment approach for OSAHS.”

“ Dapagliflozin lowers plasma glucose concentration by inhibiting the renal reuptake of glucose in the proximal renal tubules.”

“ Dapagliflozin reduced postprandial glucose and significantly decreased overall glucose variability.”

“Results: The 24-h MG decreased 18.2 mg/dL with dapagliflozin and increased 5.8 mg/dL with placebo (P < 0.001).”