Aim: To examine the effect of combination therapy with canagliflozin plus liraglutide versus each agent alone on beta cell function in type 2 diabetes mellitus (T2DM) patients.
Research Design And Methods: A total of 45 poorly controlled (HbA1c = 7%-11%) T2DM patients received an oral glucose tolerance test (OGTT) before and after 16 weeks of treatment with: (i) liraglutide (LIRA); (ii) canagliflozin (CANA); (iii) liraglutide plus canagliflozin (CANA/LIRA).
Results: Both liraglutide and canagliflozin significantly lowered HbA1c with no significant additive effect of the combination on HbA1c (0.
Objective: To examine the effect of combination therapy with canagliflozin plus liraglutide on HbA, endogenous glucose production (EGP), and body weight versus each therapy alone.
Research Design And Methods: Forty-five patients with poorly controlled (HbA 7-11%) type 2 diabetes mellitus (T2DM) on metformin with or without sulfonylurea received a 9-h measurement of EGP with [3-H]glucose infusion, after which they were randomized to receive ) liraglutide 1.2 mg/day (LIRA), ) canagliflozin 100 mg/day (CANA), or ) liraglutide 1.
Sodium-glucose cotransport 2 inhibitors (SGLT2i) lower plasma glucose but stimulate endogenous glucose production (EGP). The current study examined the effect of dapagliflozin on EGP while clamping plasma glucose, insulin, and glucagon concentrations at their fasting level. Thirty-eight patients with type 2 diabetes received an 8-h measurement of EGP ([3-H]-glucose) on three occasions.
View Article and Find Full Text PDFThe decrement in plasma glucose concentration with SGLT2 inhibitors (SGLT2i) is blunted by a rise in endogenous glucose production (EGP). We investigated the ability of incretin treatment to offset the EGP increase. Subjects with type 2 diabetes ( = 36) were randomized to ) canagliflozin (CANA), ) liraglutide (LIRA), or ) CANA plus LIRA (CANA/LIRA).
View Article and Find Full Text PDFObjective: To examine whether lowering plasma glucose concentration with the sodium-glucose transporter-2 inhibitor empagliflozin improves β-cell function in patients with type 2 diabetes mellitus (T2DM).
Methods: Patients with T2DM (N = 15) received empagliflozin (25 mg/d) for 2 weeks. β-Cell function was measured with a nine-step hyperglycemic clamp (each step, 40 mg/dL) before and at 48 hours and at 14 days after initiating empagliflozin.
The objective of this study was to examine the effect of renal sodium-glucose cotransporter inhibition with empagliflozin on the fasting plasma glucose (FPG) concentration and β-cell function in subjects with impaired fasting glucose (IFG). Eight subjects with normal fasting glucose (NFG) and eight subjects with IFG received empagliflozin (25 mg/day) for 2 weeks. FPG concentration and β-cell function was measured with a nine-step hyperglycemic clamp before and 48 h and 14 days after the start of empagliflozin.
View Article and Find Full Text PDFRenal glucose reabsorption was measured with the stepped hyperglycemic clamp in 15 subjects with type 2 diabetes mellitus (T2DM) and 15 without diabetes after 2 days and after more chronic (14 days) treatment with empagliflozin. Patients with T2DM had significantly greater maximal renal glucose transport (Tm) compared with subjects without diabetes at baseline (459 ± 53 vs. 337 ± 25 mg/min; < 0.
View Article and Find Full Text PDFAim: To examine metabolic factors that influence ketone production after sodium-glucose cotransport inhibitor (SGLT2) administration.
Research Design And Methods: Fasting plasma glucose (FPG), insulin, glucagon, free fatty acid and ketone concentrations were measured in 15 type 2 diabetes mellitus (T2DM) and 16 non-diabetic subjects before and at day 1 and day 14 after treatment with empagliflozin.
Results: Empagliflozin caused a 38 mg/dL reduction in FPG concentration in T2DM patients.