Pancreatic hormone secretion in chronic pancreatitis without residual beta-cell function

1988 ◽  
Vol 118 (3) ◽  
pp. 357-364 ◽  
Author(s):  
S. Larsen ◽  
J. Hilsted ◽  
B. Tronier ◽  
H. Worning

Abstract. Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. No significant differences were found between the two diabetic groups regarding glucagon responses to arginine and meal ingestion. In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal. Thus, pancreatic glucagon secretion was preserved in patients with insulin-dependent diabetes secondary to chronic pancreatitis, having no residual beta-cell function. These findings suggest that pancreatic glucagon deficiency is not absolute in insulin-dependent diabetes secondary to chronic pancreatitis. A high level of somatostatin may contribute to a lower blood glucose level in patients with chronic pancreatitis.

1987 ◽  
Vol 3 (1) ◽  
pp. 27-43 ◽  
Author(s):  
David K. McCulloch ◽  
Jerry P. Palmer ◽  
Edward A. Benson

Diabetes ◽  
1987 ◽  
Vol 36 (4) ◽  
pp. 510-517 ◽  
Author(s):  
T. Kobayashi ◽  
T. Itoh ◽  
K. Kosaka ◽  
K. Sato ◽  
K. Tsuji

1987 ◽  
Vol 29 (3) ◽  
pp. 408-413
Author(s):  
Shin Amemiya ◽  
Kohsuke Higashida ◽  
Masatoshi Fujimoto ◽  
Kohtaro Asayama ◽  
Kazuyoshi Ichimura ◽  
...  

1991 ◽  
Vol 124 (5) ◽  
pp. 510-515 ◽  
Author(s):  
Steen Larsen ◽  
Jannik Hilsted ◽  
Else K. Philipsen ◽  
Bente Tronier ◽  
Meta Damkjær Nielsen ◽  
...  

Abstract. Insulin was withdrawn from 7 patients with Type I (insulin-dependent) diabetes and 4 patients with insulin-dependent diabetes secondary to chronic pancreatitis, both groups without residual beta-cell function. Median plasma glucagon concentrations rose slightly, but significantly after withdrawal of insulin in Type I diabetic patients (from 14 (range: 11-16) to 19 (14-25) pmol/l by 6 h), but not in the patients with secondary diabetes. This was accompanied by a significantly higher increase in blood glucose concentration from 5.1 (4.9-5.7) to 15.2 (12.9-18.1) mmol/1 by 6 h in Type I diabetic patients compared with patients with secondary diabetes (from 4.9 (4.3-6.7) to 13.1 (10.9-13.5) mmol/l) (p<0.01). Beta-hydroxybutyrate increased to a similar extent in the two groups, whereas no significant increases were found in glycerol and lactate in any of the groups. Increased secretion of glucagon is not essential for the development of hyperglycemia and ketonemia in patients with diabetes secondary to chronic pancreatitis, but may augment the degree of hyperglycemia in Type I diabetic patients compared with patients having secondary diabetes.


1985 ◽  
Vol 110 (4_Suppl) ◽  
pp. S73-S77 ◽  
Author(s):  
Ole K. Faber

Abstract. Beta-cell function, as evaluated from plasma C-peptide measurements, is found in all insulin dependent diabetic patients the first months of disease and in about 15% of patients with more than 15 years of treatment. The beta-cells are capable of modulating their secretory activity in response to changes in blood glucose. Even a minimal residual insulin secretion is of metabolic significance. Key words: insulin dependent diabetes mellitus, beta-cell function, C-peptide metabolic control.


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