Immunoreactive Glucagon Responses to Intravenous Tolbutamide in Chronic Pancreatitis

Abstract

The effects of tolbutamide infusion (1 gm. over forty minutes) on plasma pancreatic glucagon-like immunoreactivity (PGLI), serum insulin, and blood glucose were studied in six patients with chronic pancreatitis and six matched controls.asal PGLI levels were significantly higher in the patients, despite higher fasting glucose concentrations. Tolbutamide infusion had no significant effect on mean PGLI levels in controls but was associated with significant elevation in pancreatitis patients, despite higher circulating glucose levels in the latter. The data suggest that chronic calcific pancreatitis patients hypersecrete immunoreactive glucagon, possibly from a nonpancreatic source and that this immunocreactive material may be stimulated by sulfonylureas.

A case with glucagonoma syndrome -endocrine and metabolic studies-.

“…The plasma IRG responses in tolbutamide tolerance test carried out in our laboratory on five normal subjects were decreasing during the initial ten minutes followed by elevation in concert with hypoglycemia . Kalk et al (1975) described how tolbutamide injection elevated the plasma pancreatic glucagon level in patients with chronic pancreatitis. Samols et al (1969) reported a suppressive response of plasma IRG to tolbutamide in a case with glucagonoma.…”

Pancreatic Glucagon-Like Immunoreactivity in a Pancreatectomized Patient

“…In patients with chronic pancreatitis, elevated levels of pancreatic (or true) glucagon-like immunoreactivity (GLI) have been reported both in the fasting state (Kalk, Vinik, Bank, Buchanan, Keller andJackson 1974, Kalk, Vinik, Paul, Keller andJackson 1975) and in response to various stimuli (Kalk et al 1974(Kalk et al , 1975, Other workers have reported the presence of pancreatic GLI in the circu1ation of depancreatized dogs (Vranic, Pek and Kawamori 1974, Matsuyama and Foa 1974, Mashiter, Harding, Chou, Mashiter, Stout, DilJmond and Field 1975 and pancreatectomized humans (Muller, Brennan, Tan and Aoki 1974) using a pancreatic glucagon 'specific' antiserum. This pancreatic GLI may arise from a nonpancreatic source and is released in response to arginine stimulation in dogs (Mashiter et al 1975), but not in man (Muller et al 1974).…”