scholarly journals Postnatal development of gastric aromatase and portal venous estradiol-17β levels in male rats

2013 ◽  
Vol 218 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Hiroto Kobayashi ◽  
Saori Yoshida ◽  
Ying-Jie Sun ◽  
Nobuyuki Shirasawa ◽  
Akira Naito

Gastric parietal cells synthesize and secrete estradiol-17β (E2) into gastric veins joining the portal vein, and a large amount of gastric E2first binds to its receptors in the liver. However, the role of the gastric E2is 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 E2levels in the portal vein; and to further understand the relationship between gastric E2and 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 E2levels were elevated after 20 days and increased remarkably between 23 and 30 days, similar to gastric aromatase mRNA levels. The E2level was approximately three times higher at 40 days than that at 20 days. The liver weight andEsr1levels began to increase after 20 days and the increment was positively correlated with the change of portal venous E2levels. These findings suggest that some changes may occur around 20 days to regulate the gastric E2synthesis and secretion.

2017 ◽  
Vol 78 (4) ◽  
pp. 351-362 ◽  
Author(s):  
Rene Zempoalteca ◽  
Mercedes G. Porras ◽  
Suelem Moreno-Pérez ◽  
Gabriela Ramirez-Funez ◽  
Elsa L. Aguirre-Benítez ◽  
...  

Endocrinology ◽  
2002 ◽  
Vol 143 (8) ◽  
pp. 3162-3170 ◽  
Author(s):  
Takashi Ueyama ◽  
Nobuyuki Shirasawa ◽  
Mitsuteru Numazawa ◽  
Keiko Yamada ◽  
Momoko Shelangouski ◽  
...  

Abstract Estrogen, if it is produced in the gastrointestinal tract, may overflow into the systemic circulation in the case of increased portal-systemic shunting. This idea is in accord with a significant step-up in serum estradiol (E2) concentration in the portal vein of rats, compared with that in the artery. Gene expression of aromatase, estrogen synthetase, was demonstrated by RT-PCR in the gastric mucosa of male and female adult rats, equivalent to that in the ovary. Aromatase activity and production of E2 in the gastric mucosa were demonstrated by 3H2O assay and gas chromatography-mass spectrometry, and they were inhibited by aromatase inhibitor, 4-hydroxyandrostenedione. Conversion of 14C-androstenedione to 14C-E2 through 14C-testosterone in cultured gastric mucosa was also demonstrated. Parietal cells exhibited strong signals for aromatase mRNA and immunoreactive protein by in situ hybridization histochemistry and immunohistochemistry. Estrogen receptor α mRNA and immunoreactive protein were demonstrated in hepatocytes by RT-PCR, in situ hybridization histochemistry, and immunohistochemistry. Total gastrectomy reduced portal venous E2 concentration, without changing systemic E2 concentration, together with down-regulation of estrogen receptor α mRNA level in the liver. These findings indicate that gastric parietal cells play a potent endocrine role in secreting estrogen that may function as a regulator of the gastro-hepatic axis.


2013 ◽  
Vol 219 (1) ◽  
pp. 39-49 ◽  
Author(s):  
Hiroto Kobayashi ◽  
Saori Yoshida ◽  
Ying-Jie Sun ◽  
Nobuyuki Shirasawa ◽  
Akira Naito

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.


1995 ◽  
Vol 269 (5) ◽  
pp. E827-E833 ◽  
Author(s):  
V. Colomb ◽  
A. Leturque ◽  
G. Guihot ◽  
M. Loizeau ◽  
S. Lavie ◽  
...  

To optimize artificial nutrition (AN) techniques for patients suffering from malnutrition or reduced intestinal absorption, utilization of energy fuels, especially glucose, requires better understanding. Because the liver plays a key role in glucose homeostasis, the aim of this study was to assess the effects of continuous intragastric and intravenous nutrition on insulin secretion and several markers of liver glucose metabolism, especially glucose transporter GLUT-2. Wistar male rats underwent catheterization of either stomach (intragastric) or vena cava (intravenous) and received 24 h/day the same all-in-one formula over 7 to 14 days. The metabolic parameters from intragastrically fed rats did not differ significantly from those from orally fed control rats. Intravenous nutrition induced insulin resistance (marked hyperinsulinemia and/or mild hyperglycemia) and reduced liver GLUT-2 protein and mRNA levels. The decrease in liver GLUT-2 gene expression might be mediated either by an inhibitory role of hyperinsulinemia or by the decrease in gut or portal factors. These results suggest that the route of nutrient delivery influences their utilization by the liver.


2003 ◽  
Vol 17 (2) ◽  
pp. 203-208 ◽  
Author(s):  
Marie K. Lindberg ◽  
Sofia Movérare ◽  
Stanko Skrtic ◽  
Hui Gao ◽  
Karin Dahlman-Wright ◽  
...  

Abstract Estrogen is of importance for the regulation of adult bone metabolism. The aim of the present study was to determine the role of estrogen receptor-β (ERβ) in vivo on global estrogen-regulated transcriptional activity in bone. The effect of estrogen in bone of ovariectomized mice was determined using microarray analysis including 9400 genes. Most of the genes (95% = 240 genes) that were increased by estrogen in wild-type (WT) mice were also increased by estrogen in ERβ-inactivated mice. Interestingly, the average stimulatory effect of estrogen on the mRNA levels of these genes was 85% higher in ERβ-inactivated than in WT mice, demonstrating that ERβ reduces estrogen receptor-α (ERα)-regulated gene transcription in bone. The average stimulatory effect of estrogen on estrogen-regulated bone genes in ERα-inactivated mice was intermediate between that seen in WT and ERαβ double-inactivated mice. Thus, ERβ inhibits ERα-mediated gene transcription in the presence of ERα, whereas, in the absence of ERα, it can partially replace ERα. In conclusion, our in vivo data indicate that an important physiological role of ERβ is to modulate ERα-mediated gene transcription supporting a “Ying Yang” relationship between ERα and ERβ in mice.


Author(s):  
Swarup Kumar Kundu ◽  
Md. Abu Hadi Noor Ali Khan ◽  
Shonkor Kumar Das

Mushrooms are considered as a valuable source of important nutrients having hepatoprotective and anti-hyperlipidemic actions. Present experimental research was done to explore the beneficial role of mushroom on health in hypercholesterolemia. Total thirty Swiss albino mice were taken and randomly divided into three groups: control A, group B and group C. Each group consisted of ten mice. The control A group was fed with normal mice pellet and fresh water. Group B was fed with hypercholesterolemic diet and group C was supplied hypercholesterolemic diet with mushroom powder (500g/kg/mice body weight) for 60 days. After the experimental tenure, mice of each group were sacrificed ethically and the samples (liver and blood) were collected for gross, histological study and lipid profile analysis.  Increased liver weight, pale and hemorrhagic liver in gross observation along with some histological changes including dilation and congestion of central and portal vein, fat accumulation in hepatocyte and marked lymphocytic infiltration were found in group B, while mushroom supplementation recovered this gross and histological changes and reduced liver weight in group C. Just mild congestion and dilation was in the portal vein of group C. In lipid profile analysis, total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL) level significantly reduced respectively by 10%, 38% and 17% in group C than group B. High density lipoprotein (HDL) level also significantly increased by 20% in group C compared to group B. Therefore, it can be concluded that mushrooms might have potentially beneficial actions in recovering of some complications in hypercholesterolemia.


1988 ◽  
Vol 16 (03n04) ◽  
pp. 93-105 ◽  
Author(s):  
Satoshi Usuki

The effect of Hachimijiogan (HZ) and Keishibukuryogan (KB) on the steroid production in rats was examined in vivo and in vitro. In an in vivo study, HZ stimulated the testes from ten-week old male rats to produce testoterone, whereas KB decreased the tissue testosterone concentrations. The Δ4-androstenedione and estradiol-17β (E2) showed no significant changes. In an incubation study, HZ also stimulated the testosterone production. The data suggested that HZ produces testosterone in rat testes. The role of KB is questionable.


2007 ◽  
Vol 39 (4) ◽  
pp. 289-304 ◽  
Author(s):  
Shaheen Khan ◽  
Fei Wu ◽  
Shengxi Liu ◽  
Qian Wu ◽  
Stephen Safe

AbstractDeletion analysis of several 17β-estradiol (E2)-responsive genes have identified GC-rich sites that are associated with hormone-induced transactivation in MCF-7 breast cancer cells. However, the role of individual specificity proteins (Sps) in mediating hormone-induced gene expression has not been unequivocally determined. In transient transfection studies using E2-responsive GC-rich promoters from the E2F1, carbamoylphosphate synthetase/aspartate transcarbamylase/dihydroorotase (CAD), and retinoic acid receptor α (RARα) genes, RNA interference using small inhibitory RNAs for Sp1 (iSp1), Sp3 (iSp3), and Sp4 (iSp4) decreased both basal and E2-induced transactivation. The contributions of individual Sp proteins to basal and E2-induced activity were promoter dependent. iSp1, iSp3, and iSp4 also significantly inhibited hormonal induction of E2F1, CAD, and RARα mRNA levels; however, the enhanced inhibitory effects of the latter two small inhibitory RNAs suggest that Sp3 and Sp4 play a major role in estrogen receptor α/Sp-mediated gene expression in MCF-7 cells.


2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Shingo Tanaka ◽  
Hiroyuki Nagashima ◽  
Modesto Cruz ◽  
Tomohisa Uchida ◽  
Takahiro Uotani ◽  
...  

ABSTRACT The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IκB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.


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