
<script type="text/javascript">
<!--
document.write('<div id="oa_widget"></div>');
document.write('<script type="text/javascript" src="https://www.openaire.eu/index.php?option=com_openaire&view=widget&format=raw&projectId=undefined&type=result"></script>');
-->
</script>pmid: 27697213
Ovarian steroids, such as estradiol (E2), control a vastness of physiological processes, such as puberty, reproduction, growth, development and metabolic rate. In fact, physiological, pathological, pharmacological or genetically-induced estrogen deficiency causes increased appetite and reduced energy expenditure, promoting weight gain and ultimately leading to obesity. Remarkably, estrogen replacement reverts those effects. Interestingly, although a wealth of evidence has shown that E2 can directly modulate peripheral tissues to exert their metabolic actions, novel data gathered in recent years have shown that those effects are mainly central and occur in the hypothalamus. Here, we will review what is known about the actions of E2 on energy homeostasis, with particular focus on brown adipose tissue (BAT) thermogenesis.
Adipose Tissue, Brown, Estradiol, ta1184, Animals, Homeostasis, Humans, Energy Metabolism
Adipose Tissue, Brown, Estradiol, ta1184, Animals, Homeostasis, Humans, Energy Metabolism
| citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 27 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Average | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
