Faculty Research 1980 - 1989


Testicular LH receptors and circulating hormone levels in three mouse models for inherited diseases (Tfm/y, lit/lit and hyt/hyt).

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Disease-Models-Animal, Dwarfism-Pituitary: me, FSH, Gonadotropins-Chorionic, Hormones, Hypothyroidism: me, LH, Male, Mice, Mice-Mutant-Strains: me, Prolactin, Receptors-LH: me, SUPPORT-U-S-GOVT-P-H-S, Testicular-Feminization, Testis: me, Testosterone

JAX Source

Endocrinol-Exp-(Bratisl). 1986 Dec; 20(4):349-58.


HD20001, HD20033, AM17937


In mice with testicular feminization (Tfm/y), the concentration of LH receptors (LH-R) in the testes was greatly elevated, when compared to their normal controls (Ta/y). The administration of hCG caused, 24 hours later, a much greater decrease in the number of testicular LH-R in Tfm/y than in Ta/y mice. However, whereas in Ta/y mice, the decrease in LH-R was accompanied by a greater than 20 fold increase in plasma testosterone (T) levels, the same dose of hCG failed to alter plasma T levels in Tfm/y mice. Tfm/y mice were also characterized by significantly elevated circulating LH, FSH and PRL levels. Administration of hCG decreased testicular LH-R concentration in little (lit/lit) mice, whereas it had no effect in hypothyroid (hyt/hyt) and normal mice. Treatment with hCG elevated plasma T levels in all animals, but this increase was smaller in lit/lit than in Lit/- mice, while being greater in hyt/hyt than in Hyt/- mice. The present results suggest that the Tfm locus in the mouse is involved in the regulation of testicular LH-R. The only effect of GH deficiency on the parameters studied is on hCG-stimulated testicular steroidogenesis. The lack of negative autoregulation of LH-R by hCG in hyt/hyt mice may indicate a more active testicular LH-R metabolism, perhaps as a consequence of the chronic elevation of plasma TSH levels.

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