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It is well established that inhibition of dipeptidyl peptidase (DPP)-IV reduces glucose levels in both fasting and postprandial states and preserves pancreatic beta cell function in patients with type 2 diabetes. Their mechanism of action is derived from increased incretin (GLP-1) levels, which stimulate insulin secretion as well as insulin biosynthesis and inhibit glucagon secretion from pancreas. Recent studies reported that combination therapy with DPP-IV inhibitors and metformin have additive or synergistic effects in lowering glycose level, preserving beta-cell mass and function as well as enhancing insulin sensitivity. However, there have been few studies about the difference of glucose lowering effect of combination therapy of DPP-IV inhibitors and metformin according to the secretory capacity of pancreas.
The researchers hypothesized that combination therapy with DPP-IV inhibitor and metformin may have more favorable glucose lowering effect in type 2 diabetic patients who have preserved pancreatic secretory function. The researchers plan to investigate the difference of glucose lowering effect of 24 weeks treatment with sitagliptin (DPP-IV inhibitor) in combination with metformin according to basal c-peptide and glucagon level in type 2 diabetic patients.
Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment
Seoul National University Bundang Hospital
Korea, Republic of
Seoul National University Bundang Hospital
Published on BioPortfolio: 2014-08-27T03:19:37-0400
This study will demonstrate the bioequivalence of metformin after single dose administration of sitagliptin/metformin 50/500 mg and concomitant administration of single doses of sitaglipti...
A clinical study to determine the safety and efficacy of sitagliptin in patients with Type 2 Diabetes Mellitus who have inadequate glycemic (blood sugar) control on metformin therapy.
This trial is designed to evaluate, in adult participants with Type 2 diabetes mellitus (T2DM) and inadequate glycemic control on sub-maximal metformin mono-therapy (1000 mg/day), the effe...
This study will determine the effect of concomitant administration of sitagliptin and metformin on post-meal incretin hormone concentrations in healthy adults.
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Efficacy and safety of replacing sitagliptin with canagliflozin in real-world patients with type 2 diabetes uncontrolled with sitagliptin combined with metformin and/or gliclazide: The SITA-CANA Switch Study.
To analyze the efficacy and safety of replacing sitagliptin with canagliflozin in patients with type 2 diabetes (T2D) and poor metabolic control despite treatment with sitagliptin in combination with ...
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To assess the efficacy and safety profile of the dipeptidyl-peptidase-4 inhibitor sitagliptin in a population of self-identified Hispanic/Latino patients with type 2 diabetes.
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A pharmaceutical preparation of sitagliptin phosphate and metformin hydrochloride that is used in the treatment of TYPE 2 DIABETES.
A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)
A pyrazine-derived DIPEPTIDYL-PEPTIDASE IV INHIBITOR and HYPOGLYCEMIC AGENT that increases the levels of the INCRETIN hormones GLUCAGON-LIKE PEPTIDE-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). It is used in the treatment of TYPE 2 DIABETES.
An analog of GLUCAGON-LIKE PEPTIDE 1 and agonist of the GLUCAGON-LIKE PEPTIDE 1 RECEPTOR that is used as a HYPOGLYCEMIC AGENT and supplemental therapy in the treatment of DIABETES MELLITUS by patients who do not respond to METFORMIN.
Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes (DIABETES MELLITUS; DIABETES INSIPIDUS).
Pancreatitis Acute pancreatitis is inflammation of the pancreas caused by the release of activated pancreatic enzymes. Common triggers are biliary tract disease and chronic heavy alcohol intake. Diagnosis is based on clinical presentation...