Anti-Mullerian hormone (AMH) is
considered as a negative regulator of postnatal Leydig
cell (LC) differentiation, because AMH over expressing
mice (Mt-hAMH mice) testes are deficient in LC.
Therefore, in the present study Mt-hAMH mice was
used as a model to examine the process of postnatal LC
differentiation. Testis structure-function studies were
performed in age-matching Mt-hAMH and C57BL/6
(controls) mice; testicular components were quantified
and circulating testosterone and thyroid hormone levels
(thyroxine/T4 and triiodothyronine/T3; necessary for
postnatal LC differentiation) were determined. Results
revealed that Mt-hAMH mice were heavier and their
testis weights were smaller compared to controls. Mast
cells were present in Mt-AMH testis interstitium, but
absent in controls. The absolute volumes of seminiferous
tubules (ST), testis interstitium, LC and blood vessels
per testis were lower and lymphatic space was higher in
Mt-hAMH mice than in controls (p<0.05). The average
cell LC volume and their number per testis, ST length,
plasma testosterone, luteinizing hormone-stimulated
testosterone secretion per testis and per LC in vitro,
plasma T4 and T3 were significantly lower in Mt-hAMH
mice compared to controls (p<0.05). Increased body
weight in Mt-hAMH mice could be attributed to the
reduced T4 and T3. Reduced testis weight in Mt-AMH
mice is explained by the reduced ST volume in them.
Reduced plasma testosterone, testicular and LC
testosterone secretion in vitro in Mt-hAMH mice can be
explained by the reduced number, size and steroidogenic
potential of LC in Mt-hAMH mice. Study revealed
several structure-function deficiencies in Mt-AMH mouse compared to controls, which were not
documented in previous investigations. As
hypothyroidism causes arrest in postnatal LC
differentiation, it is suggested that the reduced LC
number in Mt-hAMH testes could be at least in part due
to their reduced thyroid hormone levels. However, latter
concept needs to be further tested in future
investigations