1981EndocrinologyRequires access

SERUM LIPOPROTEINS INCREASE TESTOSTERONE PRODUCTION IN hCG-DESENSITIZED LEYDIG CELLS

Patrick G. Quinn, LORI J. DOMBRAUSKY, Yii‐Der I. Chen, Anita H. Payne

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Abstract

The effects of high density and low density lipoproteins (HDL and LDL) on testosterone synthesis by Leydig cells from rats treated three days earlier with 50 IU human chorionic gonadotropin (hCG) or from saline-injected control rats were investigated. HDL caused a significant, dose-dependent increase in both basal and hCG-stimulated testosterone production by Leydig cells from hCG-treated rats, but had no marked effect on Leydig cells from control rats. The serum testosterone concentration of hCG-treated rats was three times higher than in controls. Basal testosterone production by Leydig cells from hCG-treated rats was elevated two-fold in comparison to controls, while hCG-stimulated testosterone production was significantly lower than in controls. Both basal and hCG-stimulated testosterone production by Leydig cells from hCG-treated rats were significantly increased by the addition of HDL or LDL. Furthermore, HDL restored the hCG-stimulated testosterone production to the maximal amount produced by hCG-stimulated Leydig cells from control animals. When equivalent amounts of HDL or LDL cholesterol (140 microgram/ml) were added to the incubation, HDL caused a greater increase in testosterone production than did LDL. These results suggest that hCG-treatment, in vivo, caused a prolonged stimulation of the Leydig cells which resulted in depletion of the cholesterol available for steroidogenesis, since the addition of cholesterol in the form of HDL or LDL caused an increase in the testosterone production of these Leydig cells.

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What this paper is about

The effects of high density and low density lipoproteins (HDL and LDL) on testosterone synthesis by Leydig cells from rats treated three days earlier with 50 IU human chorionic gonadotropin (hCG) or from saline-injected control rats were investigated. HDL caused a significant, dose-dependent increase in both basal and hCG-stimulated testosterone production by Leydig cells from hCG-treated rats, but had no marked effect on Leydig cells from control rats. The serum testosterone concentration of hCG-treated rats was three times higher than in controls. Basal testosterone production by Leydig cells from hCG-treated rats was elevated two-fold in comparison to controls, while hCG-stimulated testosterone production was significantly lower than in controls. Both basal and hCG-stimulated testosterone production by Leydig cells from hCG-treated rats were significantly increased by the addition of HDL or LDL. Furthermore, HDL restored the hCG-stimulated testosterone production to the maximal amount produced by hCG-stimulated Leydig cells from control animals. When equivalent amounts of HDL or LDL cholesterol (140 microgram/ml) were added to the incubation, HDL caused a greater increase in testosterone production than did LDL. These results suggest that hCG-treatment, in vivo, caused a prolonged stimulation of the Leydig cells which resulted in depletion of the cholesterol available for steroidogenesis, since the addition of cholesterol in the form of HDL or LDL caused an increase in the testosterone production of these Leydig cells.

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Available abstract

The effects of high density and low density lipoproteins (HDL and LDL) on testosterone synthesis by Leydig cells from rats treated three days earlier with 50 IU human chorionic gonadotropin (hCG) or from saline-injected control rats were investigated. HDL caused a significant, dose-dependent increase in both basal and hCG-stimulated testosterone production by Leydig cells from hCG-treated rats, but had no marked effect on Leydig cells from control rats. The serum testosterone concentration of hCG-treated rats was three times higher than in controls. Basal testosterone production by Leydig cells from hCG-treated rats was elevated two-fold in comparison to controls, while hCG-stimulated testosterone production was significantly lower than in controls. Both basal and hCG-stimulated testosterone production by Leydig cells from hCG-treated rats were significantly increased by the addition of HDL or LDL. Furthermore, HDL restored the hCG-stimulated testosterone production to the maximal amount produced by hCG-stimulated Leydig cells from control animals. When equivalent amounts of HDL or LDL cholesterol (140 microgram/ml) were added to the incubation, HDL caused a greater increase in testosterone production than did LDL. These results suggest that hCG-treatment, in vivo, caused a prolonged stimulation of the Leydig cells which resulted in depletion of the cholesterol available for steroidogenesis, since the addition of cholesterol in the form of HDL or LDL caused an increase in the testosterone production of these Leydig cells.

Key concepts: Internal medicine, Endocrinology, Testosterone (patch), Leydig cell, Human chorionic gonadotropin, Basal (medicine), Cholesterol, Chemistry

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