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Glucocorticoid Inhibition of Growth in Rats: Partial Reversal with Somatostatin Antibodies^*

Departments of Health Sciences and Biological Sciences, University of Wisconsin-Milwaukee Milwaukee, Wisconsin 53201
Cattedra di Clinica Medica, University of Brescia Brescia, Italy 25152

Address requests for reprints to: Dr. William B. Wehrenberg, Department of Health Sciences, University of Wisconsin-Milwaukee, P. O. Box 413, Milwaukee, Wisconsin 53201.

Abstract

Clinically, glucocorticoids are important immunosuppressive hormones. Yet, these steroids are also potent inhibitors of growth. We hypothesized that glucocorticoids may partially inhibit growth by increased somatostatin (SRIF) secretion. We tested this hypothesis using passive immunization techniques. Male rats (»50 g) were treated daily (ip) for 33 days with saline (SAL) or dexamethasone (DEX, 40 µg/kg) and every fourth day with normal sheep serum (NSS) or SRIF antiserum (SRIF-ab, 0.25 ml). Body wts were recorded daily. Groups (n = 6) were: 1)SAL + NSS, 2)SAL + SRIF-ab, 3)DEX + NSS, and 4)DEX +SRIF-ab. Regression analysis of the growth curves clearly demonstrated differences in body wt gain for the four treatment groups (P < 0.01). Final body wt of SAL + NSS treated rats was 285 ± 5 g and 285 ± 12 g in SAL + SRIF-ab treated rats. DEX + NSS treated rats weighed significantly less (227 ± 4 g, P < 0.01) than SAL-treated rats. This glucocorticoidinduced decrease in body wt was partially reversed by the concomitant treatment of rats with SRIF-ab (241 ± 6 g, P < 0.05). This observation leads to the conclusion that the inhibitory effect of glucocorticoids on growth may be mediated, in part, by increased SRIF secretion. (Endocrinology 127: 2705–2708,1990)

Footnotes

^* This work was supported by the University of Wisconsin Graduate School and NIH Grants R01-DK-38324 and K04-DK-01874.

Received May 29, 1990.

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