English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Brain serotonin (5-HT) systems have a critical role in the regulation of appetite and body weight. Central serotonin 5-HT2C receptors contribute to the leptin-independent regulation of appetite [1]. On the other hand, central 5-HT2B and 5-HT1A receptors have implicated in the leptin-dependent regulation of appetite [2]. The recent article by Anderberg et al. [3] suggested that brain-derived serotonin is a critical mediator of the weight loss induced by GLP-1 receptor activation, and that central 5-HT2A receptors mediate the chronic anorexic and weight loss effects of central injection of exedin-4 (EX4) or of intraperitoneal injection of liraglutide. We question their results and conclusions.

Does brainstem-derived serotonin mediate GLP-1 receptor agonist-induced suppression of appetite and body weight via 5-HT2A receptors?