In teleost fish, the progestin 17α, 20β-dihydroxy-4-pregnen-3-one (DHP) is an essential component of the spermatogenesis pathway. In a series of investigations on the mechanisms underlying progestin-stimulated spermatogenesis, we have found that DHP up-regulates the expression of cysteine dioxygenase1 (CDO1) in the Japanese eel testis. CDO1 is one of the enzymes involved in the taurine biosynthesis pathway. To evaluate whether taurine is synthesized in the eel testis, cysteine sulfinate decarboxylase (CSD), another enzyme involved in taurine synthesis, was isolated from this species. RT-PCR and in vitro eel testicular culture revealed that although CSD was also expressed in eel testis, neither DHP nor other sex steroids affect CSD mRNA expression in a similar manner to CDO1. Using an in vitro eel testicular culture system, we further investigated the effects of DHP on taurine synthesis in the eel testis. HPLC analysis showed that DHP treatment significantly increases the taurine levels in the eel testis. These results suggest that DHP promotes taurine synthesis via the up-regulation of CDO1 mRNA expression during eel spermatogenesis. Furthermore, we observed from our analysis that although taurine does not induce complete spermatogenesis, it promotes spermatogonial DNA synthesis and the expression of Spo11, a meiosis-specific marker. These data thus suggest that taurine augments the effects of sex steroids in the promotion of spermatogonial proliferation and/or meiosis and hence that taurine plays important roles in spermatogenesis.

The pyruvate metabolic response to the 1st exposure (exposure on the 1st day) to immobilization stress (IMO) were considerably altered by lesions of the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). The pyruvate metabolic responses to IMO were completely abolished by seven times repetition of exposure to IMO in the rabbits with lesions of ARC and VMH; they were similar to sham-operated groups. In rabbits with lesions of ST and FX, the pyruvate metabolic responses to the 7th exposure (exposure on the 7th day) to IMO were almost the same as those after the 1st exposure to IMO, but these metabolic responses were completely abolished by the seven times repetition of exposure to IMO in the sham-operated animals. These results suggest that firstly the ARC, VMH, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system are involved in the pyruvate metabolic responses to the 1st exposure to IMO, and secondly, that the AMYG-ST system and the HPC-FX system are involved in the disappearance process of pyruvate metabolic responses to IMO by the daily repetition of exposure to IMO.

Corticosterone was injected directly into the hippocampus of rabbits, and changes in hepatic acetate metabolism were studied. The microinjection of corticosterone with seasame oil into hippocampus decreased the rates of 14C transfer from 14C-1-acetate into CO2 and free cholesterol, and increased 14C transfer into glucose, ketone bodies, triglyceride, free fatty acids and phospholipids. But after microinjection of corticosterone into the hippocampus of rabbits with lesions of dorsal fornix, hepatic acetate metabolism did not differ from that of control rabbits, which received injection of seasame oil into the same brain region. From these results it might be suggested that the hippocampus is a part of corticosterone-sensitive brain regulator system in the hepatic acetate metabolism.

Glucagon was injected directly into the medial amygdala (AMYG) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the AMYG of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, cholesterol ester, free fatty acids and phospholipids but decreased those of 14C transfer into triglyceride. However, the glucagon injection into the AMYG of rabbits with lesions of stria terminals or into the parietal cortex of intact rabbits had no effects on the hepatic acetate metabolism. These observations support the hypothesis that the AMYG is a part of the glucagon-sensitive brain regulator system in the hepatic acetate metabolism.