From the present review it appears that
insulin-dependent diabetes is a common finding in
chronic pancreatitis, and impaired secretion of
insulin from beta-cells of the pancreatic islets is essential for the development of this form of secondary diabetes. Judged from a positive correlation between
insulin secretory capacity and stimulated pancreatic
enzyme output, beta-cell function may decrease in parallel with exocrine pancreatic function. However, in patients with
insulin-dependent diabetes secondary to
chronic pancreatitis beta-cell function was preserved to a greater extent and glucoregulation was better than in comparable Type 1 (
insulin-dependent) diabetic patients. Immunological phenomena and associations with certain HLA-alleles characterizing
Type 1 diabetes mellitus were not found in
insulin-dependent diabetes secondary to
chronic pancreatitis. This may contribute to the slower destruction of the beta-cells in
chronic pancreatitis than encountered in
Type 1 diabetes. The small number of
chronic pancreatitis patients who developed totally absence of endogenous
insulin production still have some alpha-cell function during i.v.
arginine and meal stimulation. However,
insulin-induced
hypoglycemia and
insulin withdrawal did not stimulate
glucagon secretion in the secondary diabetic patients in contrast to comparable Type 1 diabetics. Nevertheless,
blood glucose counterregulation is intact in the secondary diabetics due to preserved
catecholamine secretion. Furthermore,
ketonemia develops during dissipation of
insulin, in spite of absence of increased
glucagon secretion, emphasizing the role of
insulin dissipation for the development of
ketoacidosis in this form of diabetes. The suggested increased susceptibility to severe
hypoglycemia and less tendency to development of
ketonemia may further be influenced by altered
insulin sensitivity, nutritional factors and concomitant
hepatic failure in diabetes secondary to
chronic pancreatitis.
Pancreatic polypeptide secretion was absent in
chronic pancreatitis without endogenous
insulin production. Pancreatic polypeptide secreting cells thus seem to be at least as vulnerable as the beta-cells to the destructive processes characterizing
chronic pancreatitis, whereas
glucagon secreting alpha-cells preserve secretory capacity to a greater extent than PP-cells and beta-cells. No data, however, favour the view that absent
pancreatic polypeptide secretion has any major effect on the glucoregulation in diabetes secondary to
chronic pancreatitis. Increased plasma concentration of
somatostatin was found in patients with
insulin-dependent diabetes secondary to
chronic pancreatitis. The source of
somatostatin in the patients is unknown, but
somatostatin may contribute to a reduction in overall
blood glucose level in patients without endogenous insulin secretion due to inhibition of
glucagon secretion.(ABSTRACT TRUNCATED AT 400 WORDS)