Surgical removal of the epididymal white adipose tissue (EWAT) depot (lipectomy; EWATx) in laboratory rats or mice decreases spermatogenesis, but this phenomenal finding has not been investigated in depth. Specifically, detailed histology, neuroendocrine profiles, copulatory behavior, lipectomy of other WAT depots, rescue by autologous EWAT transplants, or tests whether this EWATx effect is due to disruption of testes innervation occurring during EWATx have not been performed. Therefore, in the first study, we performed EWATx in male Syrian hamsters and attempted to rescue spermatogenesis by transplanting the removed EWAT to the animal's subcutaneous dorsum, removed comparable or larger amounts of non-gonadal WAT [inguinal WAT (IWAT)] and conducted mating behavior tests. In a second study we conducted detailed testicular histology and assayed serum LH, FSH, and testosterone (T). In a third study, we surgically denervated the testes without removing EWAT and compared testicular histology with that of EWATx or sham surgery. We found that EWATx, but not IWATx, virtually eliminated spermatogenesis producing a marked decrease in size of the seminiferous tubule cellular lining including the Sertoli cells and spermatogonia that could not be rescued by autologous EWAT transplant to the subcutaneous dorsum. EWATx did not change serum LH or T concentrations but approximately doubled serum FSH concentrations. EWATx did not alter copulatory behavior but resulted in aspermatic ejaculate. Selective surgical testicular denervation did not affect spermatogenesis. Collectively, these results suggest the presence of a local, but currently unidentified, growth and/or nutritive factor from EWAT that promotes spermatogenesis.

No abstract

Zinc, an essential dietary element, modulates neurotransmission in brain regions associated with cognition. Cognitive dysfunction has been reported in offspring of female rats fed zinc-restricted diets during gestation and/or lactation. Studies on the cognitive effects of zinc restriction during young adulthood are limited. After a 3-wk period of dietary zinc restriction, male rats (71-75 d old) were repleted with zinc chloride alone, or zinc chloride supplemented with L-histidine, and short-term memory was measured using the Morris water maze. During restriction, zinc-restricted rats demonstrated significantly longer (86.0%) retrieval latencies than nonrestricted controls, and significantly lower liver (25.5%), bone (32.5%) and hippocampal (3.2%) zinc concentrations. During subsequent repletion, rats repleted with zinc chloride supplemented with L-histidine improved their retrieval latencies to the extent that they were no longer significantly different from controls by repletion d 3. This was associated with a return of hippocampal zinc concentrations to control values by repletion d 3. The mean retrieval escape latencies of the zinc chloride-repleted rats remained significantly prolonged (75.0%). Collectively, these data indicate the following: 1) feeding a zinc-restricted diet for 3 wk impairs short-term memory in young adult male rats, and 2) repletion with dietary zinc supplemented with L-histidine improves short-term memory function more efficiently than dietary zinc chloride alone. The latter point suggests that dietary zinc supplemented with L-histidine is more bioavailable to the brain than zinc provided as zinc chloride alone. These findings are important in that they highlight the importance of both dietary zinc formulation and the use of functional assessments in determining zinc nutriture.

The purpose of these experiments was to determine whether dietary zinc depletion affected protein expression in the hippocampus. Eleven weanling Sprague-Dawley male rats (21 d) were fed the AIN-93G diet containing 1.5 ppm zinc and supplemented with 30 ppm of zinc in the drinking water. After 1 wk, the rats were randomly divided into three groups: control (n=3), pair fed (n=3), and zinc restricted (n=5). All groups consumed the same diet. The zinc-restricted group consumed water containing no zinc. The rats were sacrificed 3 wk later. Chelatable zinc levels in the hippocampus, as measured by N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) staining, were significantly reduced in the zinc-restricted group. Analysis of hippocampal protein expression by two-dimensional electrophoresis (2DE) revealed increased expression of the P2X6 purinergic receptor in the zinc-restricted rats, as determined by MALDI mass spectrometry (MS) and database analysis. The data provided evidence for the dual effects of dietary zinc deficiency on the hippocampus, reducing ionic zinc levels and stimulating protein expression. The role the P2X6 receptor plays in the physiological response of the hippocampus to zinc depletion remains to be determined.