Effects of sex steroid hormones on gastric emptying and gastrointestinal transit in rats

1995 ◽  
Vol 268 (1) ◽  
pp. G171-G176 ◽  
Author(s):  
T. S. Chen ◽  
M. L. Doong ◽  
F. Y. Chang ◽  
S. D. Lee ◽  
P. S. Wang

In vitro studies have shown that estrogen and progesterone can affect the contractile response and myoelectric activity of the gastrointestinal smooth muscle. The present study was designed to investigate the effect of sex steroid hormones on gastric emptying and gastrointestinal transit were assessed in rats 15 min after intragastric instillation of a test meal containing charcoal and 51Cr. Gastric emptying was determined by measuring the amount of labeled chromium contained in the small intestine as a percentage of the initial amount received. Gastrointestinal transit was evaluated by calculating both the geometric center of distribution of the radiolabeled marker and the charcoal transit in the intestine. The experimental animals included diestrus rats; ovariectomized rats treated with vehicle, estradiol, and/or progesterone; and normal male and orchiectomized rats treated with vehicle or testosterone. Female rats in diestrus had a slower gastric emptying and a lesser geometric center value than ovariectomized rats. Estradiol inhibited gastric emptying but did not affect gastrointestinal transit. Progesterone increased gastric emptying. Progesterone at lower dose (10 mg/kg) decreased the geometric center compared with higher doses (20 or 40 mg/kg) or vehicle controls. A mixture of estradiol (10 micrograms/kg) and progesterone (20 mg/kg) inhibited gastric emptying to a similar degree as estradiol (10 micrograms/kg) did. Testosterone had no influence on gastric emptying or gastrointestinal transit. These results suggest that estradiol and a mixture of estradiol and progesterone inhibit, whereas progesterone enhances, gastric emptying. Testosterone did not play a role in gastrointestinal motility.

1986 ◽  
Vol 251 (1) ◽  
pp. G46-G50 ◽  
Author(s):  
J. P. Ryan ◽  
A. Bhojwani

In vitro studies suggest that the female sex steroid hormones [estrogen (E) and progesterone (P)] can affect the myoelectric and mechanical activity of colonic smooth muscle. The present study was designed to examine the influence of the hormones on colonic transit in vivo. Transit was assessed by quantifying the distribution within the colon of a radiolabeled marker (0.5 microCi Na251CrO4), using the geometric center method of analysis. Studies were performed with adult male rats and the following groups of female rats: nonpregnant, ovariectomized, ovariectomy plus hormone pretreatment (100 micrograms X kg-1 X day-1 E + 2.5 mg X kg-1 X day-1 P for 4 days), and pregnant (day 18). Hormone-pretreated animals were studied 24 h following the fourth injection. The data can be summarized as follows. 1) Colonic transit was affected by the timing of the estrus cycle. Rats determined to be in proestrus-estrus had a geometric center value (1.97 +/- 0.50) significantly less than that of metestrus-diestrus animals (4.25 +/- 0.57). 2) Ovariectomy eliminated the biphasic transit pattern observed in estrus-cycling females and resulted in a geometric center value (4.19 +/- 0.17) comparable with that of the metestrus-diestrus animals. 3) E + P pretreatment of ovariectomized rats resulted in a significant decrease in the geometric center (1.94 +/- 0.19) compared with the untreated ovariectomized rats. 4) The geometric center value in pregnant animals (2.22 +/- 0.20) closely resembled the transit data for proestrus-estrus animals and hormone-pretreated animals.(ABSTRACT TRUNCATED AT 250 WORDS)


2010 ◽  
Vol 88 (4) ◽  
pp. 414-421 ◽  
Author(s):  
Nader Shahrokhi ◽  
Mohammad Khaksari ◽  
Zahra Soltani ◽  
Mehdi Mahmoodi ◽  
Nouzar Nakhaee

Recent studies have reported that estrogen and progesterone have a neuroprotective effect after traumatic brain injury (TBI); however, the mechanism(s) for this effect have not yet been elucidated. The aim of the present study was to investigate the role of sex steroid hormones on changes in brain edema, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) after TBI in ovariectomized (OVX) rats. In this study, 50 female rats were divided into 5 groups: control (intact), sham, and 3 TBI groups consisting of vehicle, estrogen (1 mg/kg), and progesterone (8 mg/kg). TBI was induced by the Marmarou method, and the hormones were injected i.p. 30 min after TBI. ICP was measured in the spinal cord, and CPP was calculated by subtracting the mean arterial pressure (MAP) from ICP. The results revealed that brain water content after TBI was lower (p < 0.001) in the estrogen and progesterone groups than in the vehicle group. After trauma, ICP was significantly higher in TBI rats (p < 0.001). The ICP in the estrogen and progesterone groups decreased at 4 and 24 h after TBI compared with vehicle (p < 0.001 and p < 0.05, respectively). The CPP in the estrogen and progesterone groups increased after 24 h compared with vehicle (p < 0.001). Also after TBI, the neurological score (veterinary coma scale) was significantly higher than vehicle at 1 h (p < 0.01) and 24 h (p < 0.001) in the group treated with estrogen. In conclusion, pharmacological doses of estrogen and progesterone improved ICP, CPP, and neurological scores after TBI in OVX rats, which implies that these hormones play a neuroprotective role in TBI.


2009 ◽  
Vol 21 (1) ◽  
pp. 192
Author(s):  
J.-H. Kim ◽  
K.-C. Choi ◽  
E.-B. Jeung

Calcium-related proteins include transient receptor potential vanilloid (TRPV) 5 and 6, plasma membrane calcium-ATPase 1b (PMCA1b), and calbindin-D9k and -D28k. The TRPV6 is a major calcium channel located in the apical and basolateral membranes of cell and distributed widely in many other organs, especially in the exocrine tissues such as intestine and uterus. TRPV6s are generally regulated by vitamin D, a dietary calcium ion and hormone. In particular, uterine TRPV6 appears to be affected by sex steroid hormones, which are altered according to estrous cycle and pregnancy. In order to discover the effect of sex steroid hormones on the regulation of TRPV6, we examined the expression of TRPV6 mRNA by using RT-PCR and real-time PCR, and protein expression of TRPV6 by immunohistochemistry (IHC) in the uterus, duodenum, and kidney. To evaluate the effect(s) of sex steroid hormones on its uterine, duodenal, and renal regulation, 17β-estradiol [E2; 40 μg kg–1 of body weight (bw)] and/or progesterone (P4; 4 mg kg–1 of bw) or vehicle (n = 6/each group) were subcutaneously injected into Sprague-Dawley immature female rats (14 days old, n = 24 in total) for 3 days. As a result, the treatments of immature rats with E2 or P4 increased TRPV6 mRNA for calcium function or regulation in the uterus of immature rats. To confirm the specificity of E2 or P4 through their receptors, we treated the immature rats (extra n = 24 in total) with an estrogen receptor-antagonist, ICI 182,780 (ICI; 30 μg kg–1 of bw), and/or progesterone receptor antagonist, RU 486 (10 mg kg–1 of bw), at 3 days prior to E2 or P4 injection. Consequently, an increase in TRPV6 mRNA was observed in the following 2 treatments; ICI plus E2/P4 and E2/P4 alone. In IHC, we further observed that the expression of duodenal TRPV6 was increased by E2 or P4 and E2 or P4 plus ICI, while no difference was observed in renal TRPV6 by the treatments of sex steroid hormones. In conclusion, these results indicate that the expressions of uterine and duodenal TRPV6 may be induced by E2 and P4, but its renal expression may not be controlled by these steroids.


PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Mahmoud Mansour ◽  
Elaine Coleman ◽  
John Dennis ◽  
Benson Akingbemi ◽  
Dean Schwartz ◽  
...  

Peroxisome proliferator-activated receptor gamma (PPAR) activation decreased serum testosterone (T) in women with hyperthecosis and/or polycystic ovary syndrome and reduced the conversion of androgens to estradiol (E2) in female rats. This implies modulation of female sex steroid hormones by PPAR. It is not clear if PPAR modulates sex steroid hormones in diabetic males. Because PPAR activation by thiazolidinedione increased insulin sensitivity in type 2 diabetes, understanding the long term impact of PPAR activation on steroid sex hormones in males is critical. Our objective was to determine the effect of PPAR activation on serum and intratesticular T, luteinizing hormone (LH), follicle stimulating hormone (FSH) and E2 concentrations in male Zucker diabetic fatty (ZDF) rats treated with the PPAR agonist rosiglitazone (a thiazolidinedione). Treatment for eight weeks increased PPAR mRNA and protein in the testis and elevated serum adiponectin, an adipokine marker for PPAR activation. PPAR activation did not alter serum or intratesticular T concentrations. In contrast, serum T level but not intratesticular T was reduced by diabetes. Neither diabetes nor PPAR activation altered serum E2 or gonadotropins FSH and LH concentrations. The results suggest that activation of PPAR by rosiglitazone has no negative impact on sex hormones in male ZDF rats.


2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Rengfei Shi ◽  
Xiangyang Tian ◽  
Quanguang Zhang ◽  
Zepeng Cheng ◽  
Yu Feng

Objective Age-related muscle wasting (sarcopenia) is accompanied by a decrease in estrogen levels which can compromise the health of aging women. Recent studies have shown that the key enzyme of estrogen synthesis (aromatase) is detected in the skeletal muscle. The purpose of this study was to investigate the effects of exercise on the expression of aromatase and the synthesis of sex steroid hormones in skeletal muscle following exercise training. Methods Fourteen female ovariectomized rats were divided into two groups, treadmill running (n=7) and sedentary (n=7) group. Exercise training on a treadmill (25 m/min, 60 min/day, 6 days/week) for 5 weeks. Immunofluorescence assay was used to detect estradiol and aromatase levels in soleus muscle and plantar muscle. Detected the expression of AKT, Aromatase, FoxO1, MyoD protein level by Western blotting. Results We found that in ovariectomized rats, exercise training significantly increased the soleus and plantar muscles mass. The level of aromatase expression and 17-b-estradiol (E2) were increased significantly in skeletal muscle following exercise training(P < 0.05). In addition, the down-stream Akt-FoxO1-MyoD signaling pathway was significantly regulated in both soleus and plantaris muscles following exercise(P< 0.05). Conclusions These results demonstrate that exercise training increased the expression of aromatase and local estrogen production in skeletal muscle, which potentially influences skeletal muscle in ovariectomized rats through activation of Akt-FoxO1-MyoD signaling pathway.


Steroids ◽  
2019 ◽  
Vol 143 ◽  
pp. 91-96 ◽  
Author(s):  
Rengfei Shi ◽  
Xiangyang Tian ◽  
Yu Feng ◽  
Zepeng Cheng ◽  
Jianqiang Lu ◽  
...  

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