Effects of elevated serum insulinlike growth factor-II on growth hormone and insulinlike growth factor-I mRNA and secretion

Derrell M. Wilson, Susan N. Perkins, James A. Thomas, Steven Seelig, Susan A Berry, Thomas E. Hamm, Andrew R. Hoffman, Raymond L. Hintz, Ron G. Rosenfeld

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8 Scopus citations


The insulinlike growth factors (IGF) appear to exert feedback control over their own production. In an effort to determine the physiologic mechanisms for this feedback modulation, we utilized a previously developed in vivo model in which rIGF-II secreting tumor cells are transplanted into immunodeficient rats to form IGF-II secreting tumors. The tumor-bearing rat have serum IGF-II concentrations sevenfold greater than those in controls (119 ± 16 ng/mL [mean ± SE] v 17 ± 2 ng/mL, P < .0001). Serum IGF-I concentrations were reduced among the tumor-bearing rats (438 ± 42 ng/mL v 606 ± 32 ng/mL, P = .002) and were negatively correlated with IGF-II concentrations (r = -.47, P = .025), suggesting that IGF-II suppressed the secretion of IGF-I. Increased serum IGF-II concentrations, however, did not affect basal growth hormone concentrations (tumor-bearing, 44 ± 12 ng/mL; control 33 ± 6 ng/mL, P = 0.96). The GH response to GH releasing factor was likewise similar in both groups. Moveover, pituitary GH mRNA level were not different in the two groups, suggesting that IGF-II does not have a significant effect on GH secretion in this in vivo model. There was no association between serum glucose and serum IGF-I or IGF-II concentrations. To examine the effect of IGF-II on IGF-I production from the liver, we measured IGF-I mRNA levels in a subset of animals. Despite these differences in serum IGF-I concentrations, the tumor-bearing rats did not have significantly lower liver IGF-I mRNA levels. These data suggest that IGF-II may act at sites other than the pituitary or liver to alter serum IGF-I concentrations.

Original languageEnglish (US)
Pages (from-to)57-62
Number of pages6
Issue number1
StatePublished - Jan 1989

Bibliographical note

Funding Information:
From the Department of Pediatrics, Medicine, and Laboratory Animal Medicine, Stanford University. Stanford, CA. and the Department of Pediatrics, University of Minnesota, MN. Presented in part to the American Federation of Clinical Research. Western Section, Carmel. CA, February 1987. Supported in part by NIH grant Nos. DK32817. DK38480. lP40RRO3624-01, lR24RRO259601. DK28229, DK36054. AGO1312. and DK24085. and the American Institute for Cancer Research. Dr. Thomas is a recipient of a Science Research Program award of the March of Dimes Birth Defects Foundation. Dr. Rosenfeld is a recipient of a Research Career Development Award from the NIH (DKO1275). Dr. Perkins is a recipient of a NRSA (DKO7768). Address reprint requests to Dr. Darrell M. Wilson, S-322, Stanford University Medical Center, Stanford, CA 94305. o 1989 by Grune & Stratton, Inc. 0026-0495/89/3801-0009$03.00/O


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