Effect of Hyperglycemia on Fructose Biosynthesis in Mouse Seminal Vesicles. ∗

Summary

Male C57BL/6J mice were castrated and their sex accessory organs were allowed to regress for 30 to 35 days. At this time one-half of the castrate animals were made diabetic with alloxan. Both the diabetic and non-diabetic mice were given daily injections of 100 μg of testosterone propionate and sacrificed after 0, 2, 4, 8 and 12 days of hormone therapy. The frozen-dried weights of the seminal vesicles of the castrate, non-diabetic, testosterone propionate-treated animals did not differ significantly from that of the castrate, diabetic, testosterone propionate-treated mice. By day 12 of hormone therapy the weight of the seminal vesicles from the experimental animals had returned to a mass approximating that of the intact control group. The concentration of fructose in the seminal vesicles was significantly higher in the diabetic than in the non-diabetic mice. The concentration of fructose in the non-diabetic groups was almost identical with that observed in the intact control group. A second group of mice were castrated for 4 months, then one-half of them were made diabetic with alloxan. No hormone therapy was administered. On day 12 after the establishment of diabetes they were killed along with the castrated but non-diabetic control group. In the absence of testosterone propionate therapy diabetic animals did not produce significantly greater amounts of fructose than did castrated control animals with normal blood sugar levels. It appears that the male sex hormone is in some manner necessary for in vivo formation of seminal fructose from blood glucose, even when the latter substrate is present in excessive amounts. These data do not elucidate the mechanism whereby testosterone controls this conversion.