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Title: Liver-derived IGF1 enhances the androgenic response in prostate
Authors: Svensson, Johan
Kindblom, Jon
Shao, Ruijin
Moverare-Skrtic, Sofia
Lagerquist, Marie K
Andersson, Niklas
Sjogren, Mara
Venken, Katrien
Vanderschueren, Dirk
Jansson, John-Olov
Isaksson, Olle
Ohlsson, Claes # ×
Issue Date: Dec-2008
Publisher: Journal of Endocrinology
Series Title: Journal of Endocrinology vol:199 issue:3 pages:489-497
Abstract: Both IGF1 and androgens are major enhancers of prostate growth and ire implicated in the development of prostate hyperplasia and cancer. The aim of the present study was to investigate whether liver-derived endocrine IGF1 modulates the androgenic response in prostate. Mice with adult, liver-specific inactivation of IGF1 (LI-IGF1(-/-) mice) dispayed an similar to 80% reduction in serum IGF1 levels associated with decreased prostate weight compared with control mice (anterior prostate lobe -19%, P<0.05; dorsolateral prostate (DLP) lobe -35% P<0.01; ventral prostate (VP) lobe -47%, P<0.01). Reduced androgen receptor (Ar) mRNA and protein levels were observed in the VP lobe (-34% and -30% respectively, both P<0.05 versus control mice). Analysis of prostate morphology showed reductions in both the glandular and fibromuscular compartments of the VP and DLP lobes that were proportional to the reductions in the weights of these lobes. Immunohistochemistry revealed reduced intracellular AR immunoreactivity in the VP and DLP lobes. The non-aromatizable androgen dihydrotestosterone increased VP weight to a lesser extent in orchidectomized (ORX) LI-IGF1(-/-) mice than in ORX controls (-40%, P<0.05 versus control mice). In conclusion, deficiency of liver-derived IGF1 reduces both the glandular and fibromuscular compartments of the prostate, decreases AR expression in prostate, and reduces the stimulatory effect of androgens on VP weight. These findings may explain, at least in part, the well-known clinical association between serum IGF1 levels and conditions with abnormal prostate growth.
ISSN: 0022-0795
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical and Experimental Endocrinology
× corresponding author
# (joint) last author

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