REGULATION OF TESTICULAR FUNCTION BY INSULIN AND TRANSFORMING GROWTH-FACTOR-BETA

被引：43

作者：

BEBAKAR, WMW ^{[1
]}

HONOUR, JW ^{[1
]}

FOSTER, D ^{[1
]}

LIU, YL ^{[1
]}

JACOBS, HS ^{[1
]}

机构：

[1] MIDDLESEX HOSP,UNIV COLL & MIDDLESEX SCH MED,ENDOCRINE UNIT,LONDON W1N 8AA,ENGLAND

来源：

STEROIDS | 1990年 / 55卷 / 06期

关键词：

IGF-1; insulin; Leydig cell; steroids; testosterone; TGF-β;

D O I：

10.1016/0039-128X(90)90043-B

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Hyperinsulinism is associated with disorders of androgen production in humans. We have studied the effects of insulin and insulin-like growth factor-1 on androgen production in vitro using a crude preparation of mouse Leydig cells incubated with luteinizing hormone in a serum-free medium. We found a positive correlation between testosterone production and the luteinizing hormone dose over 3 hours. Exposure of the cells for 1 hour to insulin (1 μg/ml) prior to the addition of luteinizing hormone significantly augmented the amount of testosterone produced in response to the gonadotropin when added after this preincubation. In contrast, prior exposure of the cells to proinsulin (30 μg/ml), insulin-like growth factor-1 (30 ng/ml), or epidermal growth factor-1 (1 μg/ml) did not influence the testosterone response to luteinizing hormone. Transforming growth factor-β reduced the testosterone response to luteinizing hormone. Transforming growth factor-β (1,000 pg/ml) blocked the insulin augmentation of luteinizing hormone-stimulated testosterone production. We conclude that insulin has an endocrine effect on testosterone production by mouse Leydig cells in vitro. Furthermore, the Leydig cell response to insulin is itself sensitive to interaction with transforming growth factor-β which may operate as part of the paracrine control of Leydig cell function. © 1990.

引用

页码：266 / 270

页数：5

共 33 条

[1]

Burghen, Givens, Kitabchi, Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease, The Journal of Clinical Endocrinology & Metabolism, 5, pp. 113-116, (1980)

[2]

Geffner, Kaplan, Bersch, Golde, Landaw, Chang, Persistence of insulin resistance in polycystic ovarian disease after inhibition of ovarian steroid secretion, Fertil Steril, 45, pp. 327-333, (1986)

[3]

Tesone, de-Souza-Valle, Foglia, Charreau, Endocrine function of the testis in streptozotocin diabetic rats, Acta Physiol Latinoam, 26, pp. 387-394, (1976)

[4]

Calvo, de-Souza-Valle, Baranao, Tesone, Charreau, NADPH generating enzyme in Leydig cells from diabetic rats, Horm Metab Res, 11, pp. 161-164, (1979)

[5]

Benitez, Perez Diaz, Effect of streptozotocin diabetes and insulin treatment of Leydig cell function in the rat, Horm Metab Res, 17, pp. 5-7, (1985)

[6]

Gluud, Madsbad, Krarup, Bennet, Plasma testosterone and androstenedione in insulin dependent patients at time of diagnosis and during the first year of insulin treatment, Acta Endocrinol (Copenh), 100, pp. 406-409, (1982)

[7]

Romani, Robertson, Diczfalusy, Biologically active luteinising hormone in plasma. 1. Validation of the in vitro bioassay when applied to plasma of women, Acta Endocrinol (Copenh), 83, pp. 454-465, (1976)

[8]

Dufau, Veldhuis, Pathological relationships between the biological and immunological activities of luteinising hormone, Baillieres Clin Endocrinol Metab, 1, pp. 153-176, (1987)

[9]

Adashi, Fabics, Hsueh, Insulin augmentation of testosterone production in a primary culture of rat testicular cells, Biol Reprod, 26, pp. 270-280, (1982)

[10]

Moyle, Ramachandran, Effect of LH on steroidogenesis and cyclic AMP accumulation in rat Leydig cell preparations and mouse tumour Leydig cells, Endocrinology, 93, pp. 127-134, (1973)

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