Correlation between pancreatic endocrine and exocrine function and characteristics of pancreatic endocrine function in patients with diabetes mellitus owing to chronic pancreatitis.
CONCLUSIONS
Pancreatic endocrine capacities are remarkably disturbed in patients with pancreatic diabetes owing to calcific pancreatitis as opposed to those owing to noncalcific pancreatitis. Insulin secretion in calcific pancreatitis resembled that in insulin-dependent diabetes mellitus (IDDM), whereas insulin secretion in noncalcific pancreatitis resembled that in non-IDDM (NIDDM). The involvements of acinar cell and ductal cell function closely correlate with endocrine function (insulin and glucagon secretions) in chronic pancreatitis (pancreatic diabetes).


BACKGROUND
We sought to clarify the differences of pancreatic endocrine function between pancreatic diabetes and primary diabetes, and to verify the correlations between pancreatic exocrine and endocrine dysfunction in patients with chronic pancreatitis.


METHODS
Urinary C-peptide (CPR) excretion and fasting plasma glucagon levels in patients with pancreatic diabetes owing to calcific pancreatitis (19 cases) and owing to noncalcific pancreatitis (14 cases) were studied in comparison with those in patients with insulin-dependent diabetes mellitus (IDDM, 23 cases), noninsulin-dependent diabetes (NIDDM, 18 cases), and in healthy controls (11 cases). In addition, pancreatic exocrine function was investigated in patients with chronic pancreatitis (calcific and noncalcific) and in healthy controls. The correlation between pancreatic exocrine and endocrine function was studied.


RESULTS
The urinary CPR excretion in controls was 94.9 +/- 20.5 micrograms/d. The urinary CPR excretion in calcific pancreatitis was 12.8 +/- 7.4 micrograms/d and it resembled that in IDDM (9.4 +/- 5.8 micrograms/d). The urinary CPR excretion in noncalcific pancreatitis was 41.5 +/- 30.1 micrograms/d, being similar to that in NIDDM (49.3 +/- 21.0 micrograms/d). The plasma glucagon level in calcific pancreatitis was 64.1 +/- 15.9 rho g/mL, which was significantly lower than the values in IDDM (111.2 +/- 50.2 rho g/mL) and NIDDM (96.7 +/- 21.9 rho g/mL). The plasma glucagon level in calcific and noncalcific pancreratitis (88.4 +/- 29.6 rho g/mL) were significantly lower than that in controls (129.8 +/- 21.6 rho g/mL). The residual capacities of acinar cells and ductal cells were strongly correlated with urinary CPR excretion and plasma glucagon concentration.
Nakamura
T
T
Third Department of Internal Medicine, Hirosaki University School of Medicine, Aomori, Japan.
Imamura
K
K
Takebe
K
K
Terada
A
A
Arai
Y
Y
Tandoh
Y
Y
Yamada
N
N
Ishii
M
M
Machida
K
K
Suda
T
T
D000328:Adult; D000368:Aged; D000681:Amylases / Q000032:analysis; D001639:Bicarbonates / Q000032:analysis; D002096:C-Peptide / Q000652:urine; D002908:Chronic Disease; D003920:Diabetes Mellitus / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D005934:Glucagon / Q000097:blood; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007515:Islets of Langerhans / Q000378:metabolism / Q000503:physiopathology*; D008875:Middle Aged; D010179:Pancreas / Q000378:metabolism / Q000503:physiopathology*; D010195:Pancreatitis / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*
D001639:Bicarbonates; D002096:C-Peptide; D007328:Insulin; D005934:Glucagon; D000681:Amylases