Summary
The hypothesis that male diabetes mutant mice (C57BI/KsJ-db/db) are suffering from impairment of testicular steroidogenic function and pituitary
LH release was tested. A smaller postpubertal increase of testicular weight and a
reduction of plasma testosterone and androstenedione levels by 65% at 17 weeks of
age were most obvious from the comparison to homozygous lean controls. The ability
of constant amounts of Leydig cells, either in crude interstitial cell or in purified
Leydig cell suspensions, to respond to maximal doses of hCG or cyclic AMP was reduced
by at least 40% in adult diabetes mice. This defect could be attributed to a 40% decrease
of steroid-17α-monooxygenase activity as compared to lean mice. No differences occurred,
however, if Leydig cells were submaximally stimulated. GnRH-stimulated pituitary LH
release was not significantly changed. The impairment of testicular steroidogenic
function in diabetes mutant mice may represent a further aspect of infertility of
these animals and of diabetes mellitus.
Key-Words:
Diabetes Mellitus
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Diabetes Mouse
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Leydig Cells
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LH
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Pituitary
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Testis
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Testosterone
