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Assessing Endogenous Insulin Production by Repaglinide Stimulation of C-Peptides

Jun 14, 2005
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C-peptide stimulation test a practical diagnostic method to determine the presence of endogenous insulin production, and eliminating guesswork about when insulin therapy should be initiate. After a basal fasting C-peptide blood specimen is obtained, repaglinide (2 mg) is given before breakfast. A second stimulated C-peptide blood sample is obtained 2 hours after taking the repaglinide. To introduce a C-peptide stimulation test as a method to assess endogenous insulin production and to determine the proper therapeutic management of diabetes mellitus (DM)

Insulin resistance induces hyperinsulinemia in metabolic syndrome. Prolonged overwork of pancreatic beta cells leads to type 2 DM when 50% of the beta cells become nonfunctional. Total beta-cell dysfunction necessitates use of insulin. The clinical challenge in the management of DM is to determine when insulin therapy should be initiated. A practical objective diagnostic test is needed to assess endogenous insulin production, so the clinician does not need to rely on the conventional trialand-
error method of trying insulin after maximal oral hypoglycemic therapy fails to control blood glucose levels.

 

Homeostasis model assessment is a complicated and clinically impractical method. Using serum C peptide as a marker of endogenous insulin, we have performed this test to determine precisely when to begin use of basal or bolus insulin (or both). We have stopped the unnecessary insulin use and resumed oral administration of antidiabetic agents if endogenous insulin production is still present. Thiazolidinedione and metformin use must be continued at all stages because insulin resistance persists, unless uncontrolled congestive heart failure or renal impairment occurs. This test also can rule out type 1 DM when endogenous insulin production is proved.

This C-peptide stimulation test is a simple and practical diagnostic method to determine the presence of endogenous insulin production, and it eliminates guesswork about when insulin therapy should be initiated in patients with type 2 DM.

Stanley Andrew Tan, MD, PhD, FACE, Marilyn Kay Wilson, RN, FNP-C, MS, CDE, John Stephan Pasztor, RD, MPH, CDE, and Linda Giles Tan, MD, FACC
AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS 14TH ANNUAL MEETING & CLINICAL CONGRESS
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