Subclinical exocrine pancreatic derangement in human diabetic patients evaluated from pure pancreatic juice

Abstract

To elucidate the mechanism responsible for histological derangement of pancreas in diabetic patients, pure pancreatic juice (PPJ) aspirated directly from pancreatic duct was analyzed before and after strict glycemic control on poorly controlled diabetic patients without clinical exocrine pancreatic dysfunction. PPJ obtained from 18 diabetics showed a significantly decreased amylase activity compared with ten healthy subjects (109 ± 4 versus 168 ± 9 U/mg protein, p < 0.005) in spite of negligible changes in lipase activity, protein concentration, bicarbonate concentration, and its volume. PPJ showed higher concentrations of prostanoids in diabetic patients than in healthy subjects (TXB 2, 259 ± 48 versus 118 ± 30 pg/mL, p < 0.05; 6-keto-PGF1α, 52.6 ± 11.5 versus 38.5 ± 7.5 pg/mL, p > 0.05). Ratio of 6-keto-PGF1α/TXB 2 of PPJ in diabetic patients was significantly lower than in healthy subjects (0.195 ±0.016 versus 0.422 ± 0.041, p < 0.005). After strict glycemic control for 1–3 months on nine of 18 diabetic patients, amylase activity of PPJ was significantly higher than that before the control (112 ± 4 versus 128 ± 7 U/mg protein, p < 0.01), but still significantly lower than that of healthy subjects ( p < 0.005). Lipase activity showed no significant difference between before and after the control. TXB 2 and 6-keto-PGF1α concentrations were decreased. Ratio of 6-keto-PFG1α/TXB 2 after the control (0.320 ± 0.038) significantly ( p < 0.005) increased from 0.168 ± 0.019 and reached a comparable level to that of healthy subjects. These data indicated that pure pancreatic juice in poorly controlled diabetics showed a significantly lower amylase activity and a decreased ratio of 6-keto-PGF1α/TXB 2, implying local derangement in exocrine pancreas by hyperglycemia. Strict glycemic control was proven to normalize the imbalance in prostanoids but not completely improve a decreased amylase activity.