Fecal pancreatic elastase is a reproducible marker for severe exocrine pancreatic insufficiency. This test is valuable for longitudinal follow-up of exocrine pancreatic function.

Cellular mechanisms underlying the impairment of pancreatic fluid and electrolyte secretion in diabetes were examined using interlobular ducts isolated from rat pancreas. Fluid secretion was assessed by monitoring changes in luminal volume. HCO3(-) uptake across the basolateral membrane was estimated from the recovery of intracellular pH following an acid load. Exposure to high glucose concentrations inhibited fluid secretion and reduced the rate of basolateral HCO3(-) uptake in secretin-stimulated ducts isolated from normal rats. In ducts isolated from streptozotocin-treated diabetic rats, fluid secretion and basolateral HCO3(-) uptake were also severely impaired but could be largely reversed by incubation in normal-glucose solutions. Sodium-dependent glucose cotransporter 1 (SGLT1), glucose transporter (GLUT)1, GLUT2, and GLUT8 transcripts were detected by reverse transcriptase polymerase chain reaction in isolated ducts. Raising the luminal glucose concentration in microperfused ducts caused a depolarization of the membrane potential, consistent with the presence of SGLT1 at the apical membrane. Unstimulated ducts filled with high-glucose solutions lost luminal fluid by a phlorizin-sensitive mechanism, indicating that pancreatic ducts are capable of active glucose reabsorption from the lumen via SGLT1. In ducts exposed to high glucose concentrations, continuous glucose diffusion to the lumen and active reabsorption via SGLT1 would lead to elevation of intracellular Na+ concentration and sustained depolarization of the apical membrane. These two factors would tend to inhibit the basolateral uptake and apical efflux of Cl(-) and HCO3(-) and could therefore account for the impaired fluid and electrolyte secretion that is observed in diabetes.

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Exocrine pancreas is composed of acinar units and the duct system. Acinar cells secrete digestive enzymes and small amount of Cl --rich fluid, while ductal epithelium lining small (proximal) pancreatic ducts secretes large amount of HCO3 --rich isotonic fluid. Endocrine islets of Langerhans are dispersed throughout the exocrine tissue. A number of functional interrelations exist between exocrine and endocrine pancreas and most of them are mediated by the islet-acinar portal blood system that islet peptides directly regulate acinar cells (1). Exocrine dysfunction is frequently found in patients with type-I (insulin-dependent) and type-II (noninsulin-dependent) diabetes mellitus (DM). Fluid and HCO3-secretion, as well as enzyme secretion, are reduced in DM (2), suggesting that both acinar and ductal functions are impaired. It is generally accepted that PROCEEDINGS Glucose transport in interlobular ducts isolated from rat pancreas