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Phase 3 N=22 Randomized Quadruple-blind Treatment

Sitagliptin and Kinetics of Triglyceride-rich Lipoproteins Apolipoprotein B48 and B100 in Patients With Type 2 Diabetes

Type 2 Diabetes Mellitus

Enrolled (actual)
22
Serious AEs
0.0%
Results posted
Sep 2014
Primary outcome: Primary: Measurement of Apolipoprotein B48 and Apolipoprotein B100 Production Rates With Stable Isotope During Postprandial Period — 2.1; 2.5; 27.5; 30.3 mg/kg/day

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
Mar 2013

Outcome Measures

OutcomeResultp-value
PRIMARY
Measurement of Apolipoprotein B48 and Apolipoprotein B100 Production Rates With Stable Isotope During Postprandial Period
2.1; 2.5; 27.5; 30.3
SECONDARY
Measurement of Glucagon-like Peptide-1 by ELISA
5.6; 3.1
SECONDARY
Measurement of Glucose
7.7; 8.9
SECONDARY
Measurement of Insulin
161.1; 179.5
SECONDARY
Measurement of Apolipoprotein B48 and Apolipoprotein B100 Pool Sizes With Stable Isotope During Postprandial Period
38.4; 48.5; 488.0; 537.8
SECONDARY
Measurement of Apolipoprotein B48 and Apolipoprotein B100 Fractional Catabolic Rates With Stable Isotope During Postprandial Period
6.2; 6.3; 5.9; 5.9

Summary

Sitagliptin is a potent and selective inhibitor of dipeptidyl peptidase IV (DPP-IV), and has been shown to reduce fasting and postprandial glucose levels in patients with type 2 diabetes mainly through incretin hormone-mediated improvements in islet function [13]. Although clinical studies to date indicate that fasting lipid levels are minimally affected by DPP-IV inhibitor treatment [14-16], animal studies suggested that DPP-IV inhibition reduce intestinal triglycerides (TG) absorption and apolipoprotein (apo) production [17] and increased chylomicron catabolism [18]. Interestingly, a recent study supporting this hypothesis showed that vildagliptin therapy was able to reduce postprandial intestinal triglyceride-rich lipoproteins (TRL) particles in patients with type 2 diabetes [19]. Recently, our group has reported that sitagliptin treatment significantly reduced plasma apo B-48 and TG concentrations in the postprandial state. Moreover, animal studies showed that sitagliptin decreased intestinal secretion of intestinal apo B-48, mainly by increasing level of glucagon-like peptide (GLP)-1 [20]. Therefore, the present study was designed to examine the effects of sitagliptin on the kinetics of TRL apo B-48 and in patients with type 2 diabetes. A possible reduction in postprandial atherogenic TRL apo B-48-containing lipoprotein levels by sitagliptin would add to therapeutic utility of this DPP-4 inhibitor and suggest the potential to reduce cardiovascular risk in patients with type 2 diabetes.

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 (NCT01334229). 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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