SFEBES2023 Poster Presentations Metabolism, Obesity and Diabetes (70 abstracts)
An unexpected food-aversion in mice lacking functional leptin signalling
Anna Curtis 1,2 , Yashoda Jayal 1 , Zijing Zhou 1 , Elina Akalestou 1 , Waljit S Dhillo 1 , Kevin G Murphy 1 & Bryn M Owen 1
1Imperial College London, London, United Kingdom. 2St George’s, University of London, London, United Kingdom
Defending body weight is a fundamental homeostatic process. Indeed, countless studies have demonstrated weight-maintaining hyperphagia in response to either increased energy expenditure or a reduction in the caloric density of available food. The principal effector of this adaptive food intake is thought to be the adipose tissue-derived hormone, leptin. According to the classical ’adipostat’ model, the hypoleptinemia resulting from weight loss drives food intake to restore body weight. In line with this hypothesis, animals and humans lacking functional leptin signalling display profound hyperphagia and obesity. However, during our recent studies on adaptive feeding behaviour in mice, we unexpectedly made two observations concerning leptin physiology. First, we found that hypoleptinemia is not responsible for the normal hyperphagia observed in response to a reduction in the caloric density of food. Second, mice lacking leptin signalling appear to display a profound aversion to food with low caloric density. Therefore, we propose herein that explaining these observations may require a fundamental re-evaluation of the classical ’adipostat’ model of leptin action.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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