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Phase 3 N=20 Randomized Quadruple-blind Treatment

Sitagliptin Therapy and Kinetics of Inflammatory Markers

Type 2 Diabetes Mellitus

Enrolled (actual)
20
Serious AEs
0.0%
Results posted
May 2020
Primary outcome: Primary: Measurement of C-reactive Protein Production Rate With Stable Isotope During Postprandial Period

Study Design & Population

Study type
Interventional
Phase
Phase 3
Interventions
Sitagliptin (Drug); Placebo (Drug)
Age
Adult, Older Adult · 18+ yrs
Sex
All
Sponsor
Laval University
Primary completion
Sep 2017

Outcome Measures

OutcomeResultp-value
PRIMARY
Measurement of C-reactive Protein Production Rate With Stable Isotope During Postprandial Period
SECONDARY
Measurement of Serum Amyloid A Production Rate With Stable Isotope During Postprandial Period
0.039; 0.049
SECONDARY
Measurement of L-selectin Production Rate With Stable Isotope During Postprandial Period
SECONDARY
Measurement of ICAM-1 Production Rate With Stable Isotope During Postprandial Period

Summary

Inflammatory processes are increasingly being recognized as a critical step in the pathogenesis of both diabetes and heart disease and may constitute a biological link between the two diseases. Inflammatory cytokines increase vascular permeability, change vasoregulatory responses, increase leukocyte adhesion to endothelium, and facilitate thrombus formation by inducing procoagulant activity, inhibiting anticoagulant pathways, and impairing fibrinolysis. Leukocyte adhesion to arterial endothelial cells is thought to be an important step in the development of atherosclerosis, and adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and L-selectin, play key roles in this process. Therefore, identifying novel therapeutic approaches that would favorably affect inflammation, endothelial function, and glucose is of significant interest. Investigators have recently demonstrated that, relative to placebo, sitagliptin treatment resulted in a significant reduction in plasma levels of various inflammatory markers and cell adhesion molecules. The results also suggest that the beneficial effects of sitagliptin on both inflammation and endothelial function are most likely mediated by an elevation in plasma GLP-1 levels and global improvement of the glucose-insulin homeostasis. However, the mechanisms underlying the beneficial effects of sitagliptin on these markers remain to be fully elucidated. The proposed study will address this key issue.

Eligibility Criteria

Inclusion Criteria

  • Males 18 to 65 years of age.
  • Post-menopausal women under age 65 on stable medical therapy for 6 months before the study (the patient should have demonstrated stable lipid panels)
  • Women should not be on hormone replacement therapy (no recent starting or stopping)
  • Type 2 diabetes as defined by the American Diabetes Association.
  • Non-smoker.
  • Body mass index between 25.0 and 40.0 kg/m2.
  • Baseline glycated hemoglobin A1c (HbA1c) between 6.5 and 8.5%.
  • Baseline fasting plasma glucose 1.7 mg/dL for men), dysproteinemia, nephrotic syndrome, or other renal disease (24-hour urinary protein ≥3 ± 1 g).
  • Active or chronic hepatobiliary or hepatic disease. In addition, patients with aspartate aminotransferase or alanine aminotransferase >2 x upper limit of the laboratory reference range will be excluded.
  • Subjects with coagulopathy (prothrombin time or partial thromboplastin time at Visit 1 >1.5 times control).
  • Subjects with hemoglobin >2 x the lower limit of the laboratory reference range will be excluded.
  • Patients who are known to have tested positive for human immunodeficiency virus (HIV).
  • Patients who are currently enrolled in another clinical study.
  • Patients who have used any investigational drug within 30 days of the first clinic visit.
  • Congestive heart failure New York Heart Association (NYHA) Class III or IV. Uncontrolled cardiac arrhythmias within 3 months of study entry.
  • Uncontrolled diabetes mellitus (HbA1c>8.5%) or other endocrine or metabolic disease known to influence serum lipids or lipoproteins. Clinically euthyroid subjects on replacement doses of thyroid hormone are eligible for enrollment.
View full record on ClinicalTrials.gov →

Data sourced from ClinicalTrials.gov (NCT02536248). Outcome figures and adverse-event rates are extracted automatically from the registry's posted results and are provided for clinician reference, not as a substitute for the primary publication.

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