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Endocrinology, Vol 104, 137-139, Copyright © 1979 by Endocrine Society
ARTICLES |
JE Morley, SR Levin, M Pehlevanian, R Adachi, AE Pekary and JM Hershman
TRH has been shown to be present in the pancreas. To examine a possible role for TRH in the control of endocrine pancreatic function, we have studied the effects of TRH on the isolated perfused rat pancreas preparation. Arginine caused release of TRH from the preparation. The mean maximum TRH peak was 85 +/- 12 pg/ml and occurred later than the first phase of glucagon release. Glucagon (2000 pg/ml) did not release TRH from the preparation. There was no detectable basal release of TRH. Glucose did not stimulate release of TRH from the pancreas preparation. TRH (10 ng/ml) by itself had no effect on insulin or glucagon release. TRH enhanced arginine-induced glucagon release; mean summated glucagon was 8228 +/- 1138 (SE) pg/ml compared to controls (4530 +/- 447 pg/ml; P less than 0.01). There was a tendency for TRH to enhance second phase glucose-induced insulin release. Pancreatic physiology is in part regulated by locally acting hormones and TRH may be one of these hormones.
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