Effect of adding sitagliptin, a dipeptidyl peptidase-4 inhibitor, to metformin on 24-h glycaemic control and ?-cell function in patients with type 2 diabetes

2007 ◽  
Vol 9 (2) ◽  
pp. 186-193 ◽  
Author(s):  
R. Brazg ◽  
L. Xu ◽  
C. Dalla Man ◽  
C. Cobelli ◽  
K. Thomas ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glycaemic Control ◽  
Cell Function ◽  
Dipeptidyl Peptidase ◽  
Dipeptidyl Peptidase 4 ◽  
Dipeptidyl Peptidase 4 Inhibitor

scholarly journals Review on Teneligliptin: A novel antihyperglycemic agent

2019 ◽  
Vol 9 (4-s) ◽  
pp. 742-747
Author(s):  
V. D. Gorde ◽  
Punit R. Rachh
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Cell Function ◽  
Dipeptidyl Peptidase ◽  
Minimal Risk ◽  
Binding Characteristics ◽  
Dipeptidyl Peptidase 4 ◽  
Dipeptidyl Peptidase 4 Inhibitor ◽  
Β Cell Function

Diabetes mellitus relates a metabolic disorder of collective aetiology which is characterized by chronic hyperglycaemia caused due to disturbances of carbohydrate, lipid and protein metabolism due to impaired β cell function of pancreas or insulin resistance or both. Dipeptidyl peptidase-4 (DPP-4) inhibitors have recently emerged as a new class of antidiabetic that show favorable results in improving glycemic control with a minimal risk of hypoglycemia and weight gain. Teneligliptin is a recently developed oral dipeptidyl peptidase 4 inhibitor indicated for the management of type 2 diabetes mellitus. Teneligliptin, characterized by a "J-shaped" structure formed by five consecutive rings which give unique binding characteristics, reflect in higher potency than other dipeptidyl peptidase 4 inhibitor. Teneligliptin is a novel antihyperglycemic agent with a preferable profile in terms of long-term efficacy and safety in patients with type 2 diabetes. Keywords: Diabetes Mellitus, Dipeptidyl Peptidase 4 Inhibitor, Teneligliptin, Hypoglycemia,

scholarly journals Risk of morbidity and mortality in patients with type 2 diabetes treated with sodium-glucose cotransporter-2 inhibitor and/or dipeptidyl peptidase-4 inhibitor: a nationwide study

2021 ◽  
Vol 9 (1) ◽  
pp. e001765
Author(s):  
Gábor Sütő ◽  
Gergő A Molnár ◽  
Gyorgy Rokszin ◽  
Ibolya Fábián ◽  
Zoltan Kiss ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Propensity Score ◽  
Propensity Score Matching ◽  
Dipeptidyl Peptidase ◽  
Dipeptidyl Peptidase 4 ◽  
Sodium Glucose Cotransporter ◽  
Dipeptidyl Peptidase 4 Inhibitor ◽  
All Cause Mortality

IntroductionMortality and disability in diabetes mellitus are determined mostly by cardiovascular complications and cancer. The impact of dipeptidyl peptidase-4 inhibitor (DPP-4i) and sodium-glucose cotransporter-2 inhibitor (SGLT2i) monotherapy or combination on long-term complications of type 2 diabetes mellitus was studied.Research design and methodsPatients with type 2 diabetes treated with DPP-4i or SGLT2i during a 3-year period were identified in the database of the National Institute of Health Insurance Fund in Hungary. All-cause mortality, acute myocardial infarction, stroke, hospitalization for heart failure (HHF), lower limb amputation (LLA) and cancer were assessed. Outcomes of add-on SGLT2i to DPP-4i treatment in comparison with switching DPP-4i therapy to SGLT2i were also evaluated. After propensity score matching, survival analysis was performed with a Cox proportional hazards model.ResultsAfter propensity score matching, both SGLT2i and DPP-4i groups included 18 583 patients. All-cause mortality (HR, 0.80; 95% CI 0.68 to 0.94; p=0.0057), HHF (HR, 0.81; 95% CI 0.71 to 0.92; p=0.0018), and risk of cancer (HR, 0.75; 95% CI 0.66 to 0.86; p<0.0001) were lower in the SGLT2i population compared with DPP-4i. Risk of LLA was higher in the SGLT2i group (HR, 1.35; 95% CI 1.03 to 1.77; p=0.0315). SGLT2i in combination with DPP-4i results in lower all-cause mortality (HR, 0.46; 95% CI 0.31 to 0.67; p=0.0001), with a lower trend in stroke, LLA, HHF and cancer, but without any statistical difference.ConclusionsSGLT2i treatment leads to a lower risk of overall mortality, HHF and cancer when compared with DPP-4i treatment. Adding SGLT2i to DPP-4i instead of switching from DPP-4i to SGLT2i further lowers the risk of all-cause mortality.

scholarly journals Treatment with the Dipeptidyl Peptidase-4 Inhibitor Vildagliptin Improves Fasting Islet-Cell Function in Subjects with Type 2 Diabetes

2009 ◽  
Vol 94 (1) ◽  
pp. 81-88 ◽  
Author(s):  
David A. D'Alessio ◽  
Amanda M. Denney ◽  
Linda M. Hermiller ◽  
Ronald L. Prigeon ◽  
Julie M. Martin ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Cell Function ◽  
Glycosylated Hemoglobin ◽  
Fasting Blood Glucose ◽  
Dipeptidyl Peptidase ◽  
Islet Function ◽  
C Peptide ◽  
Dipeptidyl Peptidase 4

Abstract Context: Dipeptidyl peptidase 4 (DPP-4) inhibitors are proposed to lower blood glucose in type 2 diabetes mellitus (T2DM) by prolonging the activity of the circulating incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). Consistent with this mechanism of action, DPP-4 inhibitors improve glucose tolerance after meals by increasing insulin and reducing glucagon levels in the plasma. However, DPP-4 inhibitors also reduce fasting blood glucose, an unexpected effect because circulating levels of active GIP and GLP-1 are low in the postabsorptive state. Objective: The objective of the study was to examine the effects of DPP-4 inhibition on fasting islet function. Design: We conducted a randomized, double-blind, placebo-controlled trial. Setting: The study was performed in General Clinical Research Centers at two University Hospitals. Subjects: Forty-one subjects with T2DM were treated with metformin or diet, having good glycemic control with glycosylated hemoglobin values of 6.2–7.5%. Intervention: Subjects were treated with vildagliptin (50 mg twice daily) or placebo for 3 months, followed by a 2-wk washout. Major Outcome Measure: We measured insulin secretion in response to iv glucose and arginine before and after treatment and after drug washout. Results: There were small and comparable reductions in glycosylated hemoglobin in both groups over 3 months. Vildagliptin increased fasting GLP-1 levels in subjects taking metformin, but not those managed with diet, and raised active GIP levels slightly. DPP-4 inhibitor treatment improved the acute insulin and C-peptide responses to glucose (50 and 100% respectively; P &lt; 0.05) and increased the slope of the C-peptide response to glucose (33%; P = 0.023). Conclusion: Vildagliptin improves islet function in T2DM under fasting conditions. This suggests that DPP-4 inhibition has metabolic benefits in addition to enhancing meal-induced GLP-1 and GIP activity.

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