Effects of 17β-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats

Obradović, Milan; Zafirović, Sonja; Jovanović, Aleksandra; Sudar-Milovanović, Emina; Mousa, Shaker A.; Labudović‐Borović, Milica; Isenović, Esma R.

doi:10.1016/j.mce.2015.08.020

Cited by 12 publications

(30 citation statements)

References 81 publications

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“…E 2 has a direct effect on the heart by influencing lipid metabolism and insulin sensitivity (Koricanac et al 2012). Furthermore, in the same rat model as used in this study we have previously reported that in vivo the administration of E 2 as a bolus injection reduced cardiac hypertrophy, decrease serum total cholesterol and high sensitivity C-reactive protein, and realigning of insulin signalling cascade (Obradovic et al 2015a, Obradovic et al 2015b). …”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 61%

“…Previous data has shown that leptin treatment reduces the expression of the FFA transporter protein CD36, and also reduces the level of CD36 located at the PM (Steinberg et al 2002). Our previous data revealed an increase in the level of serum leptin in obese, leptinresistant male rats (Obradovic et al 2015b) suggesting that the reduced expression of CD36 may be a result of increased levels of serum leptin. Although current data indicate that E 2 influences central leptin sensitivity by enhancing the expression of the leptin receptor (Clegg et al 2006), our leptin-resistant rats were treated with a single dose of E 2 which probably was not able to reduce long-term increased level of leptin and thus enables CD36 to be translocated to PM.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 63%

“…We chose this experimental rat model based on our previous results, and literature data (Barnard et al 1998, Obradovic et al 2015b). All metabolic parameters for these rats in response to the treatments administered in this study are detailed in our previous study (Obradovic et al 2015a).…”

Section: Animals and Experimental Treatmentmentioning

confidence: 99%

“…In this model the HF diet induces whole body IR/hyperinsulinemia, endothelial dysfunction and hypertension (Barnard et al 1998, Panchal et al 2011. Furthermore, we have previously demonstrated using the same male model rats, that a HF diet applied for 10 weeks induces obesity accompanied with abnormalities such as cardiac hypertrophy, increased serum insulin concentration, whole body IR, hyperlipidaemia, hyperleptinemia and inflammation (Obradovic et al 2015a, Obradovic et al 2015b). …”

Section: Introductionmentioning

confidence: 97%

“…Substantial evidence implies a direct causation between obesity and the increased risk of endothelial dysfunction, hypertension, coronary artery disease, heart failure and stroke (Lavie et al 2009, Lavie et al 2014. A high fat (HF) diet induces body fat accumulation, insulin resistance (IR) and metabolic disorders in animals (Buettner et al 2007, Obradovic et al 2015b). In our study, we used male rats fed a HF diet as a model of obesity-associated IR.…”

Section: Introductionmentioning

confidence: 99%

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17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović

Obradović

Sudar-Milovanović

et al. 2017

Molecular and Cellular Endocrinology

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Please cite this article as: Zafirovic, S., Obradovic, M., Sudar-Milovanovic, E., Jovanovic, A., Stanimirovic, J., Stewart, A.J., Pitt, S.J., Isenovic, E.R., 17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats, Molecular and Cellular Endocrinology (2017), doi: 10.1016/j.mce.2017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe aim of this study was to investigate the in vivo effects of estradiol (E 2 ) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. MaleWistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E 2 while the other half were placebo-treated. 24h after treatment animals were sacrificed. E 2 reduced cardiac free fatty acid (FFA Akt, protein kinase B; AS160, Akt substrate of 160 kDa; CD36, fatty acid transporters; E 2 ,

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 61%

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 63%

Section: Animals and Experimental Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović

Obradović

Sudar-Milovanović

et al. 2017

Molecular and Cellular Endocrinology

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Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221

Panic

Stanimirović

Obradović

et al. 2018

Biotech and App Biochem

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This study aimed to investigate in vivo effects of estradiol on the regulation of hepatic inducible nitric oxide synthase (iNOS) expression in the high fat (HF) diet-induced obesity. Also, we aimed to investigate whether activation of the extracellular signal-regulated kinase (ERK1/2), adenosine monophosphate-activated protein kinase (AMPK), Src kinase, and miR-221 is involved in estradiol-mediated regulation of iNOS in the liver of obese male Wistar rats. Male Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. Half of HF rats were treated with estradiol intraperitoneally (40 μg/kg), whereas the other half were placebo-treated 24 H before euthanasia. Results show that estradiol treatment of HF rats decreased hepatic iNOS mRNA (P < 0.05) and protein expression (P < 0.01), the protein levels of p65 subunit of nuclear factor κB (P < 0.05) and ERα (P < 0.05), ERK1/2 phosphorylation (P < 0.001), and ERα/Src kinase association (P < 0.05). By contrast, hepatic Src protein level (P < 0.05), AMPKα phosphorylation (P < 0.05), and miR-221 expression (P < 0.05) were increased in HF rats after estradiol treatment. Our results indicate that estradiol in vivo regulates hepatic iNOS expression in obese rats via molecular mechanisms involving ERK1/2, AMPK, Src, and miR-221 signaling.

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Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

et al. 2017

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Effects of 17β-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats

Cited by 12 publications

References 81 publications

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221

Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

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