ArticleThe Journal of clinical investigation2015
Hypoactivity following perturbed estrogen signaling in the medial amygdala.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Beta 3 Adrenergic Receptor Activation Rescues Metabolic Dysfunction in Female Estrogen Receptor Alpha-Null Mice.Frontiers in physiology · 2019Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Activation of estrogen receptor α (ERα) in the brain prevents obesity as the result of increased energy expenditure and decreased food intake. While ERα is present on several neural populations, it is not clear how different regions of the brain mediate the weight-regulating effects of ERα activation. In this issue of the JCI, Xu and colleagues provide extensive evidence that ERα is abundant on neurons expressing single-minded-1 (SIM1) in the medial amygdala (MeA) and that loss of ERα in these cells enhances weight gain in both male and female mice, as the result of reduced physical activity. Moreover, focal deletion of ERα from the MeA recapitulated these alterations in energy homeostasis. Conversely, overexpression of ERα in the MeA partially prevented mice from diet-induced obesity, while chemogenetic activation of SIM1-expressing neurons in the MeA transiently promoted physical activity. The results of this study provide important insight into the regions of the brain that mediate ERα-dependent energy homeostasis.
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