Insulin, IGF-1, and GH receptors are altered in an adipose tissue depot-specific manner in male mice with modified GH action

Rikke Hjortebjerg*, Darlene E. Berryman, Ross Comisford, Stuart J. Frank, Edward O. List, Mette Bjerre, Jan Frystyk, John J. Kopchick

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Growth hormone (GH) is a determinant of glucose homeostasis and adipose tissue (AT) function. Using 7-month-old transgenic mice expressing the bovine growth hormone (bGH) gene and growth hormone receptor knockout (GHR-/-) mice, we examined whether changes in GH action affect glucose, insulin, and pyruvate tolerance and AT expression of proteins involved in the interrelated signaling pathways of GH, insulinlike growth factor 1 (IGF-1), and insulin. Furthermore, we searched for AT depot-specific differences in control mice. Glycated hemoglobin levels were reduced in bGH andGHR-/- mice, and bGHmice displayed impaired gluconeogenesis as judged by pyruvate tolerance testing. Serum IGF-1 was elevated by 90% in bGH mice, whereas IGF-1 and insulin were reduced by 97% and 61% in GHR-/- mice, respectively. Igf1 RNA was increased in subcutaneous, epididymal, retroperitoneal, and brown adipose tissue (BAT) depots in bGHmice (mean increase6standard error of the mean in all five depots, 153% ± 27%) and decreased in all depots in GHR-/- mice (mean decrease, 62% ± 4%). IGF-1 receptor expression was decreased in all AT depots of bGH mice (mean decrease, 49% ± 6%) and increased in all AT depots of GHR-/- mice (mean increase, 94% ± 8%). Insulin receptor expression was reduced in retroperitoneal, mesenteric, and BAT depots in bGH mice (mean decrease in all depots, 56% ± 4%) and augmented in subcutaneous, retroperitoneal, mesenteric, and BAT depots in GHR-/- mice (mean increase: 51% ± 1%). Collectively, our findings indicate a role for GH in influencing hormone signaling in AT in a depot-dependent manner.

Original languageEnglish
JournalEndocrinology
Volume158
Issue number5
Pages (from-to)1406-1418
Number of pages13
ISSN0013-7227
DOIs
Publication statusPublished - 1. May 2017
Externally publishedYes

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