Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aquaporins (AQPs) that transport glycerol in addition to water are classified as aquaglyceroporins (AQP3, 7, 9). AQP7 in the adipose tissue and AQP9 in the liver may coordinately contribute to the increase in hepatic gluconeogenesis in states of insulin resistance. Thiazolidinedione (TZD) has been shown to increase adipose AQP7 and induce glycerol kinase (GlyK) which is nearly absent in adipocytes. In the present study, we analyzed both GlyK and AQP gene expression in adipose and hepatic tissues, and AQP3 in kidneys from Long-Evans Tokushima Otsuka (LETO), Otsuka Long-Evans Tokushima Fatty (OLETF), and rosiglitazone (RSG)-treated OLETF (RSG-OLETF) rats. We also evaluated AQP9 protein expression in cultured human hepatoma cells treated with oleic acid, Wy14643, or RSG. A 2-week RSG treatment increased AQP7 mRNA levels in the mesenteric fat, but not in the epididymal fat of OLETF rats. Rosiglitazone treatment markedly increased GlyK expression in both fat depots, with a greater increase in the mesenteric fat. The magnitudes of GlyK induction by RSG were greater than that of AQP7 in both adipose tissues (P < .05, each). AQP9 and GlyK levels in the liver were not affected by RSG treatment in OLETF rats. Oleic acid and Wy14643 upregulated AQP9 protein expression in cultured human hepatoma cells in a dose-dependent manner. AQP3 mRNA levels tended to increase in the outer medulla of the RSG-OLETF rats. These results indicate that in the adipose tissue TZD has an important role in the glycerol metabolic pathway through the regulation of AQP and GlyK, especially by GlyK induction. Free fatty acids may directly enhance glycerol availability in the liver via the upregulation of AQP9 levels. Renal AQP3 may be related to the fluid retention caused by TZD.
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PMID:The effects of thiazolidinedione treatment on the regulations of aquaglyceroporins and glycerol kinase in OLETF rats. 1615 25

Aquaporins (AQP) have important solute transport functions in many tissues including the epididymal efferent ducts (ED) and in the liver. We investigated the effect of neonatal exposure to diethylstilbestrol (DES) on AQP9 expressions in the ED and in the liver of rats. DES was administered from day 2 to day 20 postnatally at a dose of 4,8 microg/day, and AQP9 protein and mRNA were measured by immunoblotting and real-time PCR, respectively, along with immunohistochemistry. DES caused hepatic downregulation of AQP9 at both the protein and mRNA level; however, decreased AQP9 labeling was only observed in the periportal zone. In the ED, AQP9 protein expression was increased in the DES-treated animals by 300% that could be ascribed to a widening of the ED lumen, whereas no difference was observed in AQP9 mRNA expression. Immunohistochemical findings revealed that AQP9 expression was confined to the epithelial cells of the ED. In conclusion, neonatal DES exposure appears to upregulate AQP9 channels in the ED in male rats, whereas a downregulation in the hepatic expression was observed, particularly in the periacinous area.
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PMID:Expression of aquaporin 9 in rat liver and efferent ducts of the male reproductive system after neonatal diethylstilbestrol exposure. 1815 84

Fluid and solute transport across the epithelium of the male excurrent duct is important for sperm maturation and storage. Aquaporin 9 (AQP9), which allows permeation of water and neutral solutes, is abundant throughout the male reproductive tract, where it is expressed at the apical membrane of rat epididymal principal cells as early as at 1 week of age. We evaluated the effect of neonatal exposure to: 1) a GNRH antagonist (GNRHa); 2) diethylstilbestrol (DES); 3) ethinyl estradiol (EE); 4) DES plus testosterone (DES+TE); and 5) the anti-androgen flutamide on AQP9 expression in the epididymis of peripubertal rats. Control groups received the vehicle alone. In 25-day-old rats, quantification of the mean pixel intensity of immunofluorescence-stained sections showed a significant decrease in AQP9 staining in the apical membrane of epididymal principal cells after treatments with GNRHa, DES, or flutamide, compared to controls. These results were confirmed by western blotting. While EE induced a marked decrease in AQP9 levels by western blotting, the decrease in AQP9-associated fluorescence was not significant compared to controls. DES+TE-treated rats showed levels of AQP9 protein similar to controls, indicating maintenance of AQP9 expression by testosterone treatment in the presence of DES. Our data show that expression of AQP9 in the developing rat epididymis is downregulated by neonatal DES, GNRHa, EE, and flutamide, and that the effects mediated by estrogens can be prevented by testosterone administration.
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PMID:Aquaporin 9 expression in the developing rat epididymis is modulated by steroid hormones. 1994 40