Strong relationships exist between endocrine and exocrine pancreas via the islet-acinar portal system, which allows the modulation of pancreatic acinar cells by endopancreatic hormones. In particular, insulin stimulates pancreatic protein synthesis, increases amylase protein and mRNA content, and enhances both pancreatic secretory response to colecystokinin and colecystokinin receptors (1). In type 1 diabetic patients, a reduction of pancreas function correlating with residual β-cell secretion was described ∼25 years ago with invasive tests (2). An easier evaluation of pancreatic function is now made possible with pancreatic elastase-1 (PE-1) dosage in stools, which shows good correlation with the gold standard of the secretin-cerulein test, is simple to perform, and has an acceptable cost (3,4). In type 1 diabetes, low PE-1 concentrations in stools correlate to poor blood glucose control (5,6). It is not known whether PE-1 correlates to residual β-cell function, which deeply influences metabolic control. The aim of this study was to evaluate the relationship of PE-1 in stools with both residual β-cell function and glycemic control in type 1 diabetic patients. We studied 37 consecutive type 1 diabetic patients and performed follow-up at the outpatient clinic of our diabetes unit (16 men and 21 women, aged 34 ± 2 years [mean ± SE]). Diabetes duration was 10.4 ± 1.3 years, BMI 23.9 ± 0.6 kg/m2, caloric intake 2,047 ± 71 kcal/day, fasting plasma glucose 8.76 ± 0.40 mmol/l, C-peptide (radioimmunoassay kit; Adaltis Italia, Bologna, Italy) 0.30 ± 0.07 ng/ml, and HbA1c (high-performance liquid chromatography method, Variant II; BioRad, Milan, Italy) 8.1 ± 0.24%. A total of 20 healthy subjects, matched for age, sex, BMI, and daily caloric intake, were used as control subjects (Table 1). Patients were on steady metabolic control, presented a stable body weight in the previous 6 months, did …
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Cavalot et al. (2004) studied this question.
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