Salivary peptide P-C modulates both insulin and glucagon release from isolated perfused rat pancreas.

Abstract

Abstract-The effect of salivary peptide P-C, saliva-derived peptide on glucose induced insulin release was studied using perfused rat pancreas. Salivary peptide P-C (194 nM) remarkably potentiated glucose (8.3 and 16.7 mM)-induced insulin release, whereas the same concentration suppressed arginine (10 mM)-induced glucagon release. Both effects of salivary peptide P-C occurred in a concentration dependent manner. These findings suggest that salivary peptide P-C may modulate both the levels of insulin and glucagon in vivo.

Salivary Peptide P-C Potentiates Insulin Release and Inhibits Glucagon Release from Isolated Perfused Pancreas of the Diabetic GK Rat

“…1). The increase in IRI level induced by P-C was not due to the priming effect by glucose stimulation because repeated stimulation with glucose (16.7 mM) for 10 min released a constant amount of IRI, and the same concentrations of P-C used alone had no effect on the IRI level (8). At 194 nM, P-C had the same potentiating effect on the glucose (8 .3 mM)-induced IRI level as the repeated 10-min exposures to glucose.…”

“…The above findings suggest that the decrease in the level of P-C may be a significant preliminary signal for the occurrence of diabetes. Furthermore, we have reported that P-C has an anti-hyperglycemic effect on alloxan-induced diabetic mice (7) and that only at high concentrations of glucose (8.3 mM and above) does P-C potentiate insulin release in the perfused pancreas of normal Wistar rats (8). We speculate that hyperglycemia may be caused partly by a deficiency of P-C.…”

“…Normal Wistar rats were purchased from Sankyo Labo Service (Tokyo). Perfusion of the isolated pancreas was carried out as described previously (8). The perfusate was a basal medium of Krebs-Ringer bicarbonate buffer solution (pH 7.4) containing 0.5010 bovine serum albumin (Fraction V; Sigma, St. Louis, MO, USA), 2% dextran (T-70; Pharmacia, Uppsala, Sweden) and 2.8 MM D-glucose (12) saturated with a gas mixture of 95010 02 and 5% CO2.…”

“…In a previous study, we reported that P-C has an antihyperglycemic effect on alloxan-induced diabetic mice (7) and that P-C remarkably potentiates glucose (8.3 and 16.7 mM)-induced insulin release and inhibits arginine (10 mM)-induced glucagon release in a concentration-dependent manner in the isolated perfused pancreas of normal Wistar rats (8).…”

The Essential Amino Acid Domains in Salivary Peptide P-C That Potentiate Glucose-Induced Insulin Release and Inhibit Arginine-Induced Glucagon Release from Perfused Rat Pancreas

“…From immunohistochemical studies, P-Clike immunoreactivity was found to be localized not only in the serous cells of the salivary gland, but also in human pancreatic B cells (2), namely in the insulin-secretory granules of pancreatic B cells (3). We have reported that P-C remarkably potentiates glucose (8.3 and 16.7 mM)-induced insulin release, whereas the same concentration inhibits arginine (10 mM)-induced glucagon release in a concentration-dependent manner (4). Glucagon-like peptide-1 (GLP-1) stimulates insulin release and decreases glucagon release (5) similar to P-C, but it is noteworthy that the constitutional amino acid sequences in GLP-1 are quite different from those in P-C.…”