An evaluation of the effects of some sulphonylureas on platelet function.

The effect of the sulphonylureas gliclazide (S 852) and glibenese on platelet function, blood lipid levels and the control of diabetes, was prospectively evaluated in 12 maturity-onset diabetic subjects by means of a double-blind crossover study. Including the pretrial period, platelet aggregation in response to collagen was uniformly lower than in matched normal controls, but neither drug produced any additional effect on platelet function. Control of blood glucose levels was no better than with comparable agents, and no measurable changes occurred in blood lipid levels.

The inexhaustible beta cell.

Repeated intensive pancreatic beta-cell stimulation was carried out in 42 subjects, comprising 22 normal controls, 10 mild to "severe" maturity-onset diabetics, and 10 chronic pancreatitis patients. Each subject received 75 gm. oral glucose twice and 1 mg.

Immunoreactive glucagon responses to intravenous tolbutamide in chronic pancreatitis.

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.

Insulin responses to crude cholecystokinin-pancreozymin in normal subjects, in patients with chronic pancreatitis and patients with mild maturity onset diabetes.

The effects of repeated injections of 75 U crude cholecystolinin-pancreozymin (CCK-PZ) at increasing plateau glucose concentrations achieved by glucose infusion were studied in 15 controls, 8 chronic pancreatitics and 8 mild maturity onset diabetics. In control subjects CCK-PZ alone caused minor insulin release but proportinally greater secretion with increasing blood glucose concentrations. Chronic pancreatitis patients who had normal responses to intravenous glucose responded normally to the CCK-PZ but at significantly higher plateau glucose levels.

Fasting blunts the TSH response to synthetic thyrotropin-releasing hormone (TRH).

Thyrotropin (TSH) responses to intravenous thyrotropin-releasing hormone (TRH) were studied in 9 men after 12 and 36-h fasts separated by more than a week and performed in random order. The TSH, basally and in response to TRH, was significantly lower after the 36-h fast compared to that after 12 h. The mechanism for this effect is not clear, but may be related to the altered hormonal or fuel status associated with prolonged fasting.

Stimuli for heptadecapeptide gastrin release: a comparison of oral and intravenous arginiine-monochloride and oxo in normal, vagotomized and antrectomized patients.

Arginine, administered intravenously, was a more potent stimulus to gastrin release than oral Oxo-feeding, while oral arginine failed to elicit a response in normal subjects. Intravenous arginine stimulated a rise in serum gastrin only in normal subjects but not in antrectomized or vagotomized patients. The gastric antrum appears to be the major site of production of heptadecapeptide gastrin and 'mini' gastrin, as measured by the anti-serum used in our radio-immunoassay.