Effects of dietary zinc deficiency on the reproductive system of young male sheep: testicular growth and the secretion of inhibin and testosterone
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The effects of dietary zinc deficiency on testicular development in young Merino rams (initial live mass, 22 kg) were tested. Four groups of five rams were fed ad libitum with diets containing 4, 10, 17 or 27 μg Zn g−1. To control the effects of loss of appetite caused by zinc deficiency, a fifth group (pair-fed control) was fed the diet containing 27 μg Zn g−1, but the amount of feed offered was restricted to that eaten voluntarily by the zinc deficient (4 μg Zn g−1) rams they were paired with. After 96 days on the diets, epididymal and testicular masses did not differ significantly between the animals fed 10, 17 or 27 μg Zn g−1 ad libitum, but were significantly lower in pair-fed controls, and lowest in the zinc-deficient animals. Testicular responsiveness to LH, as measured by testosterone production, increased substantially in most rams as the experiment progressed, the only exception being the zinc-deficient group, in which the response to LH was lower than in any of the other groups. Testicular concentrations of zinc and testosterone were lower in the zinc-deficient animals than in all the other groups. Plasma inhibin concentrations fell as the experiment progressed in rams fed 17 and 27 μg Zn g−1 ad libitum, but not in the other groups. The pair-fed control rams had smaller seminiferous tubules and less lumen development than did the controls fed ad libitum (27 μg Zn g−1). which were similar to the animals fed 10 or 17 μg Zn g−1. In zinc-deficient rams, the tubule development was further retarded and the interstitial regions were more extensive than in the other groups. We conclude that the overall effect of zinc deficiency on testicular development is due to a combination of a non-specific effect (low gonadotrophin concentrations caused by the low feed intake) and a specific effect due to the lack of zinc. The zinc-specific effect is localized within the testis where it reduces the development of the capacity to produce testosterone, leading to low intratesticular concentrations of testosterone, a critical factor for the growth, development and function of the seminiferous tubules.
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