Research Summary – Overeating and Alcohol Consumption
Very interesting Nature Communications article by our soon-to-be colleague, Craig Blomeley, and his collaborators, linking alcohol consumption with overeating in humans. Great timing on this topic for the festive season too! But a bit more about the research done for this publication:
The mechanisms are unclear, and have been proposed to involve intoxication-induced disregard of societal ideals of thinness. An exciting new paper published in Nature Communications (Cains, S. et al. Agrp neuron activity is required for alcohol induced overeating. Nat. Commun. 7, 14014 doi: 10.1038/ncomms14014 (2016)) elegantly shows that evolutionarily-conserved hunger modules are activated by dietary-relevant doses of alcohol, and form a critical link between alcohol and overeating.
The authors hypothesised that – since most genes associated with human obesity reside in the brain and conserved in lower animals – EtOH may stimulate appetite across mammals by interfering with brain energy signalling. This was tested by: 1) determining EtOH impact on natural eating of animals isolated from socialpressures, 2) examining EtOH action on genetically-defined hunger signals, 3) establishing a causal link between hunger cell activity and EtOH -induced overeating.
By genetically-targeted optical and electrical recordings, this research identifies core elements of the brain’s feeding circuits, the hunger-promoting Agrp cells that undergo rapid biochemical and electrical activation when exposed to dietary doses of ethanol. Furthermore, by circuit-specific chemogenetic interference, the paper also shows how Agrp cell activity is essential for ethanol-induced overeating.
Thus this data shows that ethanol creates hunger itself. Apart from the Agrp cells, other hunger regulators exist, for example eating-promoting Vgat neurons of the lateral hypothalamus, eating-suppressing oxytocin neurons of the paraventricular hypothalamus, and eating-suppressing cells of the parabrachial nucleus. These novel findings pinpoint a critical locus of alcohol-induced eating, by demonstrating that, in the absence of Agrp cell activity, alcohol action on other modules is insufficient to drive feeding.
These exciting findings also explain how a commonly-consumed nutrient generates a positive feedback on energy intake, offering new mechanistic and conceptual insight into pathological overeating behaviour linked to multiple morbid disorders. Finally, the authors propose that the alcohol-excitation of Agrp neurons – either direct as described in this paper, or via a yet unknown upstream element – is the critical step in the paradoxical overeating.
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