Search Results
You are looking at 1 - 2 of 2 items for
- Author: Akira Naito x
- Refine by access: All content x
Search for other papers by Hiroto Kobayashi in
Google Scholar
PubMed
Search for other papers by Saori Yoshida in
Google Scholar
PubMed
Search for other papers by Ying-Jie Sun in
Google Scholar
PubMed
Search for other papers by Nobuyuki Shirasawa in
Google Scholar
PubMed
Search for other papers by Akira Naito in
Google Scholar
PubMed
Cholestasis is associated with changes in hepatic cholesterol metabolism and serum estrogen levels. Ueyama and colleagues reported that the gastric estradiol-17β (E2) level in the portal vein is several times higher than that in the artery. This study aimed to clarify the relationships between gastric E2, hepatic estrogen receptor (ER) α and cholesterol metabolism in cholestatic male rats induced by bile duct ligation (BDL). After BDL, serum E2 levels in the portal vein and artery were measured by ELISA. The gene expression of gastric estrogen-synthesizing enzymes and various hepatic enzymes for cholesterol metabolism were measured by real-time RT-PCR, and gastric aromatase and hepatic ERα proteins were determined by immunohistochemistry and western blotting. Portal E2 levels increased by 4.9, 5.0, and 3.6 times that of controls at 2 days after BDL (BDL2d), BDL4d, and BDL7d respectively. The change in arterial E2 levels was positively correlated with that in the portal vein. Under these conditions, the expression of hepatic Ers1 (ERα) mRNA and protein was significantly reduced in a negative correlation with serum E2 levels in the portal vein after BDL. The expression of hepatic male-specific cytochrome P450 (CYP) genes Cyp2c55 and Cyp3a2 decreased and female-specific Cyp2c12 increased after BDL. It is postulated that the increase in gastric E2 levels, which occurs after BDL, results in the reduction of hepatic ERα, the elevation of arterial E2 level and leads to cholesterol metabolism becoming sex steroid dependent.
Search for other papers by Hiroto Kobayashi in
Google Scholar
PubMed
Search for other papers by Saori Yoshida in
Google Scholar
PubMed
Search for other papers by Ying-Jie Sun in
Google Scholar
PubMed
Search for other papers by Nobuyuki Shirasawa in
Google Scholar
PubMed
Search for other papers by Akira Naito in
Google Scholar
PubMed
Gastric parietal cells synthesize and secrete estradiol-17β (E2) into gastric veins joining the portal vein, and a large amount of gastric E2 first binds to its receptors in the liver. However, the role of the gastric E2 is not entirely clear during postnatal development. The objective of this study was to reveal the onset of aromatase and other steroid-synthesizing enzymes in the gastric mucosa; to determine the period of rising E2 levels in the portal vein; and to further understand the relationship between gastric E2 and liver estrogen receptor α (ERα). The immunoblot bands and the immunohistochemistry of gastric mucosa revealed that aromatase protein began to express itself at 20 days and then increased in the levels of aromatase protein from 20 days onward. Expression of mRNAs for gastric aromatase (Cyp19a1) and other steroid-synthesizing enzymes, 17α-Hydroxylase (Cyp17a1) and 17β-hydroxysteroid dehydrogenase (HSD17b3), also increased similar to the increment of aromatase protein. Portal venous E2 levels were elevated after 20 days and increased remarkably between 23 and 30 days, similar to gastric aromatase mRNA levels. The E2 level was approximately three times higher at 40 days than that at 20 days. The liver weight and Esr1 levels began to increase after 20 days and the increment was positively correlated with the change of portal venous E2 levels. These findings suggest that some changes may occur around 20 days to regulate the gastric E2 synthesis and secretion.
