scholarly journals Activation of PPAR by Rosiglitazone Does Not Negatively Impact Male Sex Steroid Hormones in Diabetic Rats

PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Mahmoud Mansour ◽  
Elaine Coleman ◽  
John Dennis ◽  
Benson Akingbemi ◽  
Dean Schwartz ◽  
...  
Keyword(s):  
Steroid Hormones ◽  
Sex Hormones ◽  
Negative Impact ◽  
Polycystic Ovary ◽  
Elevated Serum ◽  
Sex Steroid Hormones ◽  
Female Rats ◽  
Sex Steroid ◽  
Peroxisome Proliferator ◽  
Zdf Rats

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.

Effect of sex steroid hormones on brain edema, intracranial pressure, and neurologic outcomes after traumatic brain injury

2010 ◽  
Vol 88 (4) ◽  
pp. 414-421 ◽  
Author(s):  
Nader Shahrokhi ◽  
Mohammad Khaksari ◽  
Zahra Soltani ◽  
Mehdi Mahmoodi ◽  
Nouzar Nakhaee
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Steroid Hormones ◽  
Brain Edema ◽  
Sex Steroid Hormones ◽  
Female Rats ◽  
Sex Steroid ◽  
Vehicle Group ◽  
Ovx Rats

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.

scholarly journals Selected Sex Related Differences in Pathophysiology of Cardiovascular System

2020 ◽  
pp. 21-31 ◽  
Author(s):  
O. KITTNAR
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Steroid Hormones ◽  
Sex Hormones ◽  
Peripheral Resistance ◽  
Sex Steroid Hormones ◽  
Sex Steroid ◽  
Plasma Norepinephrine ◽  
Arterial Blood

The annual incidence of cardiovascular diseases is age-dependently increasing both in men and women, however, the prevalence is higher in men until midlife. The higher incidence of cardiovascular disease in men than in women of similar age, and the menopause-associated increase in cardiovascular disease in women, has led to speculation that gender-related differences in sex hormones might have a key role in the development and evolution of cardiovascular disease. There are several suggested pathways in which gender and sex hormones can affect human cardiovascular system to produce original sexually different pathophysiology between women and men. Sex steroid hormones and their receptors are critical determinants of cardiovascular gender differences. Also arterial blood pressure is typically lower in women than in men what could be explained particularly by greater synthesis of nitric oxide (NO) in women. Female cardiomyocytes have a greater survival advantage when challenged with oxidative stress, suggesting that female hormones may play an important role in antioxidative protection of myocardium. It was also demonstrated in animal models that combination of XX chromosomes versus an XY chromosomes enhances sex differences in higher HDL cholesterol. Women were found to have reduced sympathetic activity (reflected by lower total peripheral resistance) and pulmonary artery pressure and enhanced parasympathetic activity relative to men. Similarly, men were found to have higher plasma norepinephrine levels than women. Regarding differences between the sexes in electrophysiology of the heart, two principle mechanisms have been proposed to explain them: hormonal effects on the expression or function of ion channels or, conversely, differences in autonomic tone. To improve diagnosis and treatment of cardiovascular diseases, greater focus on understanding the molecular and cellular physiology of the sex steroid hormones and their receptors in the cardiovascular system will be required.

186 DUODENAL AND RENAL TRANSIENT RECEPTOR POTENTIAL VANILLOID 6 APPEAR TO BE DISTINCTLY REGULATED BY SEX STEROID HORMONES, ESTROGEN AND PROGESTERONE, IN IMMATURE FEMALE RATS

2009 ◽  
Vol 21 (1) ◽  
pp. 192
Author(s):  
J.-H. Kim ◽  
K.-C. Choi ◽  
E.-B. Jeung
Keyword(s):  
Steroid Hormones ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Sex Steroid Hormones ◽  
Female Rats ◽  
Sex Steroid ◽  
Transient Receptor Potential Vanilloid ◽  
Immature Female ◽  
Immature Rats ◽  
Transient Receptor

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.

scholarly journals HORMONE-ASSOCIATED METABOLIC DISORDERS OF THE ORAL CAVITY ORGANS IN WOMEN OF REPRODUCTIVE AGE

2021 ◽  
Vol 78 (4) ◽  
pp. 127-134
Author(s):  
George Khodorovskyi ◽  
Lyubov Panina ◽  
Tetiana Shchurko
Keyword(s):  
Epithelial Cells ◽  
Oral Cavity ◽  
Steroid Hormones ◽  
Tight Junctions ◽  
Sex Hormones ◽  
Reproductive System ◽  
Periodontal Ligament ◽  
Sex Steroid Hormones ◽  
Sex Steroid ◽  
Periodontal Tissues

There is emerging evidence of a possible relationship between the oral cavity and reproductive organs. Recent studies suggest these functional relations. The aim of this review was to synthesize the available evidence on this relationship. Clinical observation established that sex hormones enhance gingival inflammation in periodontal healthy women during pregnancy and that periodontal condition is associated with variation of sex hormones in blood. Estrogen regulates DNA synthesis in human gingival epithelial cells and periodontal ligament, estrogen reduces down regulation of cytokines. Estrogen and progesterone affect the periodontium via appropriate receptors (estrogen receptor and progesterone receptor). They are localized in human periodontium, demonstrating that periodontal tissues are the target tissues for these hormones. Testosterone receptors are found in the periodontal tissues. It inhibits prostaglandin secretion and reduces interleukin production. At the same time testosterone stimulates osteoblast proliferation and differentiation, also enhances matrix synthesis by fibroblast, osteoblasts, and periodontal ligament. The role of testosterone in the formation of teeth is demonstrated in the paper. In females and males, in saliva there are sex steroid hormones. The study examined the entry mode of hormones into saliva. The results suggest that lipid soluble unconjugated steroids (estriol, testosterone, progesterone) enter saliva via intracellular route; the conjugated steroids (lipid insoluble (dehydroepiandrosterone, conjugated estrogens)) enter via the ‘tight junctions’ (infiltrations through the tight junctions between the acinar cells). Recent evidence indicates that organs of the oral cavity (salivary glands, periodontal tissues, oral epithelial cells mucus) produce ghrelin-hormone which affects organs of the reproductive system directly or indirectly via hypothalamic-pituitary-gonadal axis. In all these organs, there is an appropriate receptor. In conclusion, the organs of oral cavity and organs of reproductive system are functionally linked by sex steroid hormones and ghrelin, besides that periodont can influence ovaries by neuro-reflectory link.  

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
Keyword(s):  
Gastric Emptying ◽  
Steroid Hormones ◽  
Gastrointestinal Transit ◽  
Sex Steroid Hormones ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sex Steroid ◽  
Normal Male ◽  
Myoelectric Activity ◽  
Geometric Center

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.

scholarly journals Sex Steroid Hormones in Older Men: Longitudinal Associations with 4.5-Year Change in Hip Bone Mineral Density—The Osteoporotic Fractures in Men Study

2010 ◽  
Vol 95 (9) ◽  
pp. 4314-4323 ◽  
Author(s):  
Jane A. Cauley ◽  
Susan K. Ewing ◽  
Brent C. Taylor ◽  
Howard A. Fink ◽  
Kristine E. Ensrud ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Steroid Hormones ◽  
Sex Hormones ◽  
Bone Mineral ◽  
Older Men ◽  
Sex Steroid Hormones ◽  
Mass Action ◽  
Sex Steroid ◽  
Mineral Density ◽  
Hip Bmd

Context: There is limited information on the association between sex hormones and bone loss in older men. Objective: Our objective was to determine the longitudinal association between sex steroid hormones and bone mineral density (BMD). Design and Setting: We conducted a prospective study of 5995 men aged at least 65 yr old at six U.S. clinical centers. Participants: Sex steroid hormones were measured in a random sample of 1602 men. After exclusions, 1238 men were included in cross-sectional analyses and 969 in longitudinal analyses. Baseline sex hormones were measured using liquid chromatography-mass spectrometry. Bioavailable (Bio) estradiol (BioE2) and testosterone (BioT) were calculated from mass action equations. SHBG was measured using chemiluminescent substrate. Main Outcome Measures: BMD of the total hip, measured at baseline and once or twice afterward over 4.6 yr of follow-up, was evaluated. Results: The annualized percent change in hip BMD increased with decreasing BioE2 (P trend = 0.03). Men with the lowest BioE2 (&lt;39.7 pmol/liter) compared with the highest BioE2 (≥66.0 pmol/liter) experienced 38% faster rate of BMD loss (P &lt; 0.05). There was no association between BioT and hip BMD loss. Men with lowest BioE2, lowest BioT, and highest SHBG experienced a 3-fold faster rate of BMD loss compared with men with higher levels (P = 0.02). A threshold effect of SHBG was observed; the rate of hip BMD loss increased in men with SHBG of 49–60 nm. Conclusions: Low BioE2 and high SHBG levels were associated with lower BMD and faster hip BMD loss. The combination of low BioE2, low BioT, and high SHBG was associated with significantly faster rates of BMD loss.

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