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Liver-derived IGF1 enhances the androgenic response in prostate

Johan Svensson

Johan Svensson
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Jon Kindblom

Jon Kindblom Division of Endocrinology, Department of Oncology, Department of Physiology/Endocrinology, Laboratory for Experimental Medicine and Endocrinology, Department of Internal Medicine, Sahlgrenska Academy, Sahlgrenska University Hospital, Göteborg University, Gröna Stråket 8, SE-413 45 Göteborg, Sweden

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Ruijin Shao

Ruijin Shao Division of Endocrinology, Department of Oncology, Department of Physiology/Endocrinology, Laboratory for Experimental Medicine and Endocrinology, Department of Internal Medicine, Sahlgrenska Academy, Sahlgrenska University Hospital, Göteborg University, Gröna Stråket 8, SE-413 45 Göteborg, Sweden

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Sofia Movérare-Skrtic

Sofia Movérare-Skrtic
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Marie K Lagerquist

Marie K Lagerquist
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Niklas Andersson

Niklas Andersson
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Klara Sjögren

Klara Sjögren
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Katrien Venken

Katrien Venken Division of Endocrinology, Department of Oncology, Department of Physiology/Endocrinology, Laboratory for Experimental Medicine and Endocrinology, Department of Internal Medicine, Sahlgrenska Academy, Sahlgrenska University Hospital, Göteborg University, Gröna Stråket 8, SE-413 45 Göteborg, Sweden

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Dirk Vanderschueren

Dirk Vanderschueren Division of Endocrinology, Department of Oncology, Department of Physiology/Endocrinology, Laboratory for Experimental Medicine and Endocrinology, Department of Internal Medicine, Sahlgrenska Academy, Sahlgrenska University Hospital, Göteborg University, Gröna Stråket 8, SE-413 45 Göteborg, Sweden

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John-Olov Jansson

John-Olov Jansson
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Olle Isaksson

Olle Isaksson
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Claes Ohlsson

Claes Ohlsson
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Both IGF1 and androgens are major enhancers of prostate growth and are 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) displayed an ∼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.

Article Type:: Research Article

DOI:: https://doi.org/10.1677/JOE-08-0406

Volume/Issue:: Volume 199: Issue 3

Free access

Investigation of central versus peripheral effects of estradiol in ovariectomized mice

Niklas Andersson

Niklas Andersson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Ulrika Islander

Ulrika Islander Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Emil Egecioglu

Emil Egecioglu Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Elin Löf

Elin Löf Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Charlotte Swanson

Charlotte Swanson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Sofia Movérare-Skrtic

Sofia Movérare-Skrtic Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Klara Sjögren

Klara Sjögren Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Marie K Lindberg

Marie K Lindberg Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Hans Carlsten

Hans Carlsten Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Claes Ohlsson

Claes Ohlsson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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It is generally believed that estrogens exert their bone sparing effects directly on the cells within the bone compartment. The aim of the present study was to investigate if central mechanisms might be involved in the bone sparing effect of estrogens. The dose–response of central (i.c.v) 17β-estradiol (E2) administration was compared with that of peripheral (s.c.) administration in ovariectomized (ovx) mice. The dose–response curves for central and peripheral E2 administration did not differ for any of the studied estrogen-responsive tissues, indicating that these effects were mainly peripheral. In addition, ovx mice were treated with E2 and/or the peripheral estrogen receptor antagonist ICI 182,780. ICI 182,780 attenuated most of the estrogenic response regarding uterus weight, retroperitoneal fat weight, cortical BMC and trabecular bone mineral content (P<0.05). These findings support the notion that the primary target tissue that mediates the effect of E2 on bone is peripheral and not central.