The effects of prostaglandins (PG) Ei, E2, and F2 upon the release of glucagon and insulin from the isolated perfused rat pancreas were investigated. In the presence of 5.6 mM glucose the release of both glucagon and insulin was stimulated by PGF2CX at several concentrations ranging from 2.8 x 10~8 M to 3.6 x 10~6 M. Ten-minute perfusions of 1.4 x 10" M PGEi or 2.8 x 10 7 M PGF2C* evoked biphasic release of both islet hormones, and they augmented their biphasic release induced by 10 mM L-arginine. The addition of 5 mM fumarate, glutamate, and pyruvate permitted PGE2 to stimulate insulin release at a concentration as low as 1.1 x 10' 9 M. The failure of 10" 6 M oleic acid to elicit hormone release suggested that these effects of PGs were not nonspecific effects of long-chain fatty acids. In the absence of glucose, in response to 2.8 x 10" 7 M PGEi or PGE2 or PGF 2 a, the magnitudes of glucagon release were similar to or slightly greater than those seen with 5.6 mM D-glucose, but the release of insulin failed to occur. In the presence of 16'.? mM glucose, in response to 1.4 x 10" 6 M PGE 2 and 2.8 x 10" 7 M PGF 2 a, the release of glucagon was blunted and that of insulin unchanged as compared with the secretory responses seen in the presence of 5.6 mM D-glucose.These data indicate that administered PGs can stimulate acutely the release of glucagon and insulin at pharmacologic concentrations as well as at concentrations similar to those found in pancreatic tissues and effluent.These observations are in keeping with the hypothesis that PGs of the E and F series may play a role in the regulation of secretion of glucagon and insulin. DIABETES 27:801-09, August, 1978.The prostaglandins (PG) are a group of biologically active lipids that influence the release of various hormones, including those of the ovary, 2 adrenal gland, 3 " 5 and the anterior pituitary. 6 " 13The possible role PGs play in regulating the release of pancreatic islet hormones has been studied in vitro and in vivo. Information about the effects of PGs on secretion of glucagon is limited. Employing the method of the isolated perfused rat pancreas we have

To ascertain whether prostaglandins (PG) may play a role in the secretion of glucagon and in an attempt to elucidate the conflicting observations on the effects of PG on insulin release, the isolated intact rat pancreas was perfused with solutions containing 1.1 x 10(-9) to 1.8 x 10(-5)m PGE2. In the presence of 5.6 mM glucose significant increments in portal venous effluent levels of glucagon and insulin were observed in response to minimal concentrations of 2.8 X 10(-8) and 1.4 X 10(-7) PGE2, respectively; a dose-response relationship was evident for both hormones at higher concentrations of PGE2. When administered over 60 seconds, 1.4 X 10(-6)M PGE2 resulted in a significant increase in glucagon levels within 24 seconds and in insulin within 48 seconds. Ten-minute perfusions of 1.4 X 10(-6)M PGE2 elicited biphasic release of both islet hormones; Phase I glucagon release preceded that of insulin. Both phases of the biphasic glucagon and insulin release which occurred in response to 15-minute perfusions of 10 mM arginine were augmented by PGE2. These observations indicate that PGE2 can evoke glucagon and insulin release at concentrations close to those observed by others in the extracts of rat pancreas. We conclude that PG may be involved in the regulation of secretion of glucagon and insulin and may mediate and/or modify the pancreatic islet hormone response to other secretagogues.

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Rabbits received heart-rate (HR) and corneo-retinal potential (CRP) differential conditioning and reversal training. Group T-T received one frequency tone as CS+ and another as CS-. Group L-L received increase or decrease of overall compartment illumination as CS+ and the other stimulus as CS-. Group L-T (T-L) received increase in illumination or tone as CS+ and the other stimulus as CS-. Increases in compartment illumination were effective as the CS+ for HR but not CRP conditioning in the L-T (T-L) group, and for both HR and CRP conditioning in the L-L group. The HR CRs were decelerative in the T-T group, but accelerative for L-L subjects.

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