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

Abstract

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 ,

<p>Resveratrol attenuates hydrogen peroxide-induced aging through upregulation of autophagy in human umbilical vein endothelial cells</p>

“…Our previous study confirmed that estrogen protects endothelial cells and delays cellular senescence, and subsequent studies confirmed the role of estrogen in protecting cardiac function 33,34. However, the long-term usage of estrogen can lead to serious side effects such as increasing the risk of stroke, breast cancer, ovarian cancer, and others 13,14,35.…”

Chlorpyrifos Induces Metabolic Disruption by Altering Levels of Reproductive Hormones

“…Animal studies suggest that hyperglycemia can cause the release of RHs decrease. Similar with the relationship between RHs and hyperglycemia, some researchers concluded that the decreased testosterone level means the increase of the serum TC level for testosterone is synthesized from cholesterol. , The CPF may induce the metabolism syndrome by reducing the testosterone concentration, for testosterone can regulate lipid and glucose metabolism in adipose tissues, muscle, and liver, may reduce E 2 , and leads to obesity or T2DM in mammals for E 2 can change VLDL and TG levels, which are greatly related to obesity and T2DM, may alter FSH and LH levels, and then increase the LDL level and retard the LDL-C circulating level, subsequently resulting in obesity or T2DM. ,− …”

Reduction of oxidative stress improves insulin signaling in cardiac tissue of obese mice

“…Zafirovic et al, (24) showed that obesity, in addition to hindering glucose uptake and insulin signaling in the heart, elevates the production of NO in the heart through the increase in the expression of inducible nitric oxide synthase (iNOS). (24) Nitric oxide is an important vasodilator and directly influences cardiac contractility.…”

“…Zafirovic et al, (24) showed that obesity, in addition to hindering glucose uptake and insulin signaling in the heart, elevates the production of NO in the heart through the increase in the expression of inducible nitric oxide synthase (iNOS). (24) Nitric oxide is an important vasodilator and directly influences cardiac contractility. (25) However, from a biochemical point of view, NO can react with the superoxide anion, preventing it from being dismuted by superoxide dismutase (SOD) in H 2 O 2 .…”