title: 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 (TXB2, 259 +/- 48 versus 118 +/- 30 pg/mL, p < 0.05; 6-keto-PGF1 alpha, 52.6 +/- 11.5 versus 38.5 +/- 7.5 pg/mL, p > 0.05). Ratio of 6-keto-PGF1 alpha/TXB2 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. TXB2 and 6-keto-PGF1 alpha concentrations were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: First Department of Medicine, Osaka University Medical School, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Kawamori
authors.forename: M
authors.initials: M
authors.lastname: Katsura
authors.forename: S
authors.initials: S
authors.lastname: Ishida
authors.forename: Y
authors.initials: Y
authors.lastname: Yamasaki
authors.forename: M
authors.initials: M
authors.lastname: Tujii
authors.forename: S
authors.initials: S
authors.lastname: Kawano
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000681:Amylases / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D003927:Diet, Diabetic; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D008049:Lipase / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000201:enzymology / Q000503:physiopathology*; D010189:Pancreatic Juice / Q000737:chemistry* / Q000201:enzymology; D012016:Reference Values; D013929:Thromboxane B2 / Q000032:analysis
chemical_list: D015121:6-Ketoprostaglandin F1 alpha; D000681:Amylases; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D008049:Lipase; D013929:Thromboxane B2