Metabolism2016CohortMetabolic/DigestiveModerate Quality

Suprefort Improves Glycemic Control in Type 2 Diabetes: A Pilot Study

Dedov I.I., Shestakova M.V., Mayorov A.Y.

Endocrinology Research Center

Diabetes Research and Clinical Practice 118(1): 112-119

Study Type
Cohort
Sample Size
n = 96
Tx: 48 | Ctrl: 48
Duration
90 days treatment + 3 months follow-up
Citations
118(9 yrs)

Abstract

Type 2 diabetes (T2D) is characterized by progressive beta-cell dysfunction and insulin resistance. This pilot study evaluated Suprefort (pancreatic peptide complex) in T2D patients inadequately controlled on metformin alone. Ninety-six patients (HbA1c 7.5-9.5%) received either metformin plus Suprefort (20mg orally twice daily for 90 days, n=48) or metformin alone (n=48). Primary endpoint was change in HbA1c at 90 days. The Suprefort group showed significantly greater HbA1c reduction (from 8.3±0.7% to 7.1±0.8% vs. control reduction to 7.9±0.9%, p<0.01). Fasting plasma glucose decreased by 1.8±0.6 mmol/L vs. 0.7±0.5 mmol/L (p<0.001). HOMA-IR (insulin resistance index) improved by 32% in Suprefort group vs. 12% in controls. C-peptide levels (marker of beta-cell function) increased, suggesting preserved insulin secretion. Homeostatic model assessment of beta-cell function (HOMA-B) improved 28%. Lipid profiles showed reduced triglycerides and improved HDL cholesterol. Weight remained stable in both groups.

Study Population

Type 2 diabetes patients (age 45-68 years), HbA1c 7.5-9.5% on metformin monotherapy, BMI 27-35 kg/m², disease duration 3-8 years

Background

Type 2 diabetes progressively worsens as pancreatic beta-cells fail. Most medications eventually lose effectiveness. Preserving beta-cell function is a key therapeutic goal.

Study Design

Diabetic patients inadequately controlled on metformin alone received Suprefort as add-on therapy.

Results

Glycemic Control

HbA1c (the gold standard diabetes marker reflecting 3-month average glucose) improved dramatically:

  • Suprefort group: 8.3% → 7.1% (near target!)
  • Control group: 8.3% → 7.9% (minimal change)

This 3x greater reduction is clinically meaningful.

Insulin Sensitivity

HOMA-IR (insulin resistance index) improved by 32% with Suprefort vs. only 12% with metformin alone, indicating the peptide enhances insulin effectiveness.

Beta-Cell Preservation

The most exciting finding: C-peptide levels increased by 18%, suggesting Suprefort actually preserves or enhances pancreatic insulin production.

HOMA-B (beta-cell function index) improved 28% - this is rare with diabetes medications.

Metabolic Benefits

Beyond glucose:

  • Triglycerides decreased 21%
  • HDL ("good") cholesterol improved
  • No weight gain (common with many diabetes drugs)

Significance

Suprefort appears to address the root problem in T2D: beta-cell dysfunction. This offers hope for disease modification rather than just symptom management.

Future Directions

Larger randomized trials are needed to confirm these promising pilot results and explore long-term beta-cell preservation.


Statistical Results

HbA1c reduction: Suprefort to 7.1±0.8% vs. control to 7.9±0.9% (1.2% vs. 0.4% reduction, p<0.01). Fasting glucose: -1.8±0.6 vs. -0.7±0.5 mmol/L (p<0.001). HOMA-IR improvement: -32% vs. -12% (p<0.01). HOMA-B increase: +28% vs. +8% (p<0.05). C-peptide increase: +18% vs. +4% (p<0.05). Triglycerides: -21% vs. -8% (p<0.05).

Study Limitations

  • Pilot study - small sample size
  • Non-randomized design
  • Relatively short duration (90 days)
  • Limited to metformin monotherapy patients
  • Mechanism of beta-cell preservation unclear
  • No diabetes complications assessed

Adverse Events

  • Mild nausea (4.2%)
  • No hypoglycemic events
  • No serious adverse events
  • Weight-neutral

Key Findings

  • Significant HbA1c reduction
  • Improved insulin sensitivity
  • Preservation of beta-cell function
  • Better lipid profiles
  • Weight-neutral therapy

Mechanism of Action

Enhancement of pancreatic beta-cell protein synthesis, improvement of insulin secretion, reduction of beta-cell apoptosis, and anti-inflammatory effects on pancreatic tissue.

HomeResearchToolsVisualsLibraryContact