Sodium-glucose co-transport 2 inhibitor decreases fasting plasma glucose level in impaired fasting glucose but not in normal glucose tolerance subjects

Abstract

Renal sodium-glucose co-transport 2 inhibitor (SGLT2i) can reduce fasting plasma glucose (FPG) in patients with type 2 diabetes mellitus, but its effect on FPG and β-cell function in impaired fasting glucose (IFG) is unclear. The current article is the Chinses translation of an article entitled as Inhibition of Renal Sodium-Glucose Co-Transport with Empagliflozin Lowers Fasting Plasma and Improves Beta Cell Function in Subjects With Impaired Fasting Glucose , which was published in Diabetes in September [Diabetes, 2017, 66: 2495-2502], with the consent of Diabetes . Eight subjects with IFG and eight subjects with normal FPG (NFG) were included in the study. 9-stage high glucose clamp test was done before and 48 hours, 14 days after taking empagliflozin to quantitatively evaluate the effect of FPG reduction on islet β-cell function. The results showed that FPG concentration decreased only in IFG subjects from (110±2) to (103±3) mg/dl (P<0.01) after taking empagliflozin for 14 days, but the FPG remained unchanged [(95±2) to (94±2) mg/dl] in NFG subjects. The incremental area under the plasma C-peptide concentration curve during the hyperglycemic clamp increased by 22%±4% and 23%±4% in IFG subjects after 48 hours and 14 days, respectively (P<0.01); the plasma C-peptide response remained unchanged in NFG subjects. The insulin secretion/insulin sensitivity (disposition) index increased significantly in IFG, but not in NFG subjects. In conclusion, empagliflozin only reduces the FPG concentration and improves β-cell function in IFG. (Chin J Endocrinol Metab, 2017, 33: 874-879) Key words: Sodium-glucose co-transport 2 inhibitor; Empagliflozin; Fasting plasma glucose; β-cell function; Impaired fasting glucose.