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Cell Biology Laboratory and the Department of Medicine Mount Zion Hospital
Medical Center and the Departments of Physiology and Medicine, University of California San Francisco San Francisco, California 94120
Address correspondence and requests for reprints to: Dr. Craig D. Logsdon, Cell Biology Laboratory, Mount Zion Hospital and Medical Center, P.O. Box 7921, San Francisco, California 94120.
Abstract
To examine the role of glucocorticoids in the regulation of the acinar pancreas, adult male rats were adrenalectomized (Adx) and replaced with no corticosterone (B), normal B, or high B. Plasma B concentration, body weight gain, and thymus weight were used as independent measures of treatment efficacy. Compared to controls, Adx animals had a 75 ± 0.5% (n = 30) reduction in pancreatic amylase content; a 50% decrease occurred within 1 day and the maximal 75% decrease was observed after 5 days. In Adx animals, amylase content was normalized by normal B replacement and was increased to 235 ± 39% (n = 30) of control by high B replacement. Furthermore, in all Adx rats, pancreatic content of amylase and plasma B concentration was significantly correlated (r = 0.81, n = 30). The effect of adrenalectomy was selective for amylase; contents of ribonuclease, chymotrypsin, and elastase were not altered. However, the effects of high B replacement were not selective, and increased the content of all digestive enzymes.
To determine whether the changes in enzyme content were associated with changes in messenger RNA (mRNA), pancreatic RNA was probed with 32P-labeled complementary DNAs for amylase, ribonuclease, and chymotrypsin. After adrenalectomy and B replacement there was a significant correlation only between amylase mRNA (r = 0.87, n = 13) and plasma B concentration. These data indicate that physiological levels of B have a selective effect on pancreatic amylase gene expression. In contrast, high levels of B have the separate, nonselective effect of increasing the content of all digestive enzymes without increasing corresponding mRNA levels. (Endocrinology 121: 1242–1250,1987)
Footnotes
* Portions of this work have been previously reported at the 1986 meeting of the Laurentian Hormone Conference [Rec Prog Horm Res 43:113, 1987 (Abstract)] and the 1986 meeting of the American Pancreatic Society [Dig Dis Sci 31:1139, 1986 (Abstract)]. This research was supported by NIH Grants AM-28172, HL-2974, DK-35912, and DK-32994, and by Mount Zion Hospital and Medical Center.
Received February 10, 1987.
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