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Journal of Clinical Pathology logoLink to Journal of Clinical Pathology
. 1984 Mar;37(3):302–306. doi: 10.1136/jcp.37.3.302

Exocrine pancreatic function in diabetes mellitus.

P Dandona, D B Freedman, Y Foo, J Perkins, A Katrak, D P Mikhailidis, S B Rosalki, A G Beckett
PMCID: PMC498704  PMID: 6699193

Abstract

An investigation of serum immunoreactive trypsin concentration and pancreatic isoamylase activity in patients with diabetes mellitus has shown that exocrine pancreatic deficit is maximal in insulin dependent diabetics, intermediate in those controlled with sulphonylureas, and absent in patients controlled with biguanides or diet or both. A significant correlation between the serum concentrations of both these pancreatic enzymes and C peptide was found. Serum pancreatic enzyme concentrations were not related to glycosylated haemoglobin concentrations, the dosage of insulin, or the age of onset of diabetes. The concentration of immunoreactive trypsin was found to be low in most of the insulin dependent diabetics in whom this enzyme was measured at the time of the clinical onset of diabetes. Thus exocrine pancreatic deficit in diabetes closely parallels the endocrine beta cell deficit and occurs concurrently with, or antedates, the clinical presentation of type I diabetes. It is therefore possible that in type I diabetes similar mechanisms are entailed in the pathogenesis of impaired endocrine and exocrine pancreatic function.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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