Abstract
Here, we provide a focused review of the evidence for the roles of the vagus nerve in mediating the regulatory effects of peripherally and centrally produced GLP‐1 on eating behaviour and energy balance. We particularly focus on recent studies which have used selective genetic, viral, and transcriptomic approaches to provide important insights into the anatomical and functional organisation of GLP‐1‐mediated gut‐brain signalling pathways. A number of these studies have challenged canonical ideas of how GLP‐1 acts in the periphery and the brain to regulate eating behaviour, with important implications for the development of pharmacological treatments for obesity.LINKED ARTICLESThis article is part of a themed issue on GLP1 receptor ligands (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.4/issuetoc
Highlights
The prevalence of obesity is increasing at an alarming rate
This chronic relapsing disease is associated with co-morbidities including type 2 diabetes, cardiovascular disease, stroke and cancer, resulting in higher mortality rates amongst individuals living with obesity (Abdelaal et al, 2017; Bray et al, 2017)
There is a consensus that increased energy intake, coupled with reduced energy expenditure, is the primary impetus for weight gain, lifestyle interventions aimed at reducing food intake and increasing exercise are largely ineffective in treating obesity (Grill, 2020)
Summary
We provide a focused review of the evidence for the roles of the vagus nerve in mediating the regulatory effects of peripherally and centrally produced GLP-1 on eating behaviour and energy balance. We focus on recent studies which have used selective genetic, viral, and transcriptomic approaches to provide important insights into the anatomical and functional organisation of GLP-1-mediated gutbrain signalling pathways. A number of these studies have challenged canonical ideas of how GLP-1 acts in the periphery and the brain to regulate eating behaviour, with important implications for the development of pharmacological treatments for obesity. KEYWORDS eating, feeding, glucagon-like peptide-1, neuropeptide, obesity, preproglucagon, vagus nerve
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