C-peptide Reactivity Research Articles

Failure of exogenous insulin to inhibit C-peptide release from the perfused rat pancreas.

In order to ascertain whether insulin secretion is inhibited by insulin per se, the effect of exogenous rat insulin on basal and stimulated rat C-peptide reactivity (CPR) release was studied in the isolated perfused rat pancreas. The pancreas was perfused with a medium containing 20 or 200 ng/ml of rat insulin for a 20 min equilibration period and successively for a 25 to 30 min test period during which time glucose (300 mg/100 ml), tolbutamide (500 micrograms/ml), glucagon (500 ng/ml) or arginine (10 mM) was added as a secretagogue. The concentration of glucose in the basal medium was 60 mg/100 ml. Exogenous insulin did not significantly suppress the basal CPR secretion, nor did it cause a suppression of the peak value or incremental area of CPR while the pancreas was stimulated, but it rather augmented them. No inhibitory effect of exogenous insulin on the basal or stimulated CPR release was noticed in the present study.

Effect of tolbutamide on plasma catecholamine in insulin dependent diabetics.

In 4 cases of insulin dependent diabetics, blood levels of glucose, C-peptide reactivity (CPR), free fatty acid, and catecholamines were followed after the intravenous tolbutamide response test. Plasma CPR was low and did not respond to tolbutamide injection, and blood levels of glucose and free fatty acid did not change during the test. Fifteen min after the tolbutamide injection, plasma epinephrine plus norepinephrine and norepinephrine levels fell to 87.5% and 67.4% of the initial values, respectively. These results suggest that decrease in the blood glucose and free fatty acid levels usually observed after tolbutamide injection is not the direct action of drug, but is secondary to insulin secretion, and tolbutamide-induced decrease in catecholamines may contribute to the secretion of insulin from the pancreatic beta-cells.

Nonautonomous Function of a Pancreatic Insulinoma

A 56-year-old woman with symptoms of weakness, visual blurring, and sweating underwent diagnostic studies to evaluate the etiology of her hypoglycemia. Fasting hypoglycemia was never documented; in diagnostic studies performed during her two hospitalizations and several outpatient glucose tolerance tests, the lowest fasting plasma glucose recorded was 56 mg/dl. The patient displayed exaggerated plasma insulin responses following oral glucose (peak response: 447 muU/ml at 30 min) and following 1 gm of iv tolbutamide (peak response: 719 muU/ml at 5 min) with symptomatic profound hypoglyceria during both tests. Basal per cent proinsulin was elevated at 49% (normal range 5-22%). Throughout a 72 h fast, values for plasma glucose, insulin, and glucose/insulin ratios were all within the normal range. During the infusion of exogenous insulin (0.1 U/kg for 60 min) serum C-peptide reactivity suppressed to less than 1.3 ng/ml when the plasma glucose fell below 40 mg/dl representing normal suppression. At surgery, a pancreatic beta cell adenoma was found and removed. This patient represents the uncommon circumstances in which stimulation tests with tolbutamide and glucose were more helpful in establishing a preoperative diagnosis than were the suppression tests.

Hypoglycemia and endogenous hyperinsulinism complicating diabetes mellitus: Application of the C-peptide assay to diagnosis and therapy

Described here is a patient with insulin-requiring diabetes mellitus in whom spontaneous fasting hypoglycemia developed. Endogenous hyperinsulinism was considered after the systematic exclusion of other causes of hypoglycemia, and this possibility was confirmed by measurement of serum C-peptide reactivity (CPR), an indicator of beta cell secretory function. Subtotal pancreatectomy relieved the fasting hypoglycemia, and was associated with a marked decline in CPR levels. The pancreatic islets showed hyperplasia and the beta cells were degranulated.