Horm Metab Res 2005; 37(5): 326-330
DOI: 10.1055/s-2005-861478
Original Clinical
© Georg Thieme Verlag KG Stuttgart · New York

Secretin-stimulated Amylase Release into Blood is Impaired in Type 1 Diabetes Mellitus

A.  Swislocki1 , R.  Noth1 , A.  Hallstone1 , E.  Kyger1 , G.  Triadafilopoulos1
  • 1 Sections of Endocrinology and Gastroenterology, Medical Service, Veterans Affairs Medical Center, Martinez, California, and Department of Internal Medicine, School of Medicine, University of California, Davis, California
Further Information

Publication History

Received 1 June 2004

Accepted after revision 25 November 2004

Publication Date:
22 June 2005 (online)

Zoom Image

Abstract

Background: Prior studies have provided data indicating the existence of close interaction between pancreatic endocrine and exocrine function, but few clinical studies have explored this relationship in depth. We compared pancreatic exocrine function non-endoscopically in individuals with type 1 diabetes mellitus, type 2 diabetes mellitus, and normal glucose tolerant controls, to assess the importance of local insulin production to pancreatic exocrine function. Methods: The plasma amylase response to intravenous secretin challenge was measured in men with type 1 diabetes mellitus (n = 5), type 2 diabetes mellitus (n = 5), and normal controls (n = 3). Patients were characterized by their urinary excretion of c-peptide and albumin over 24 hours. Autonomic neuropathy was non-invasively assessed by measuring RR variation (with deep respiration on EKG). Results: Post-secretin amylase responses were generally absent with low baseline levels in the patients with type 1 diabetes mellitus. Patients with type 2 diabetes mellitus and controls showed similar twofold increases over baseline after secretin administration. When normal glucose tolerant and type 2 diabetic patients were pooled and compared against type 1 diabetes mellitus, the differences were statistically significant (p < 0.03). Total amylase response correlated positively, but weakly, with 24 h urinary C-peptide excretion (r = 0.507; p < 0.112), but not with glycemic control, duration of diabetes, or indices of autonomic neuropathy. Conclusions: Patients with type 1 diabetes mellitus, but not type 2 diabetes mellitus, have reduced pancreatic exocrine function, supporting the concept of a local paracrine effect of insulin on pancreatic acinar cells. Further studies are needed to determine the clinical impact of this deficiency, and whether such patients with type 1 diabetes mellitus would benefit from therapy with pancreatic enzyme supplementation.