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  • Review Article
  • Published:

Hormonal and neural mechanisms of food reward, eating behaviour and obesity

Key Points

  • The rise in the prevalence of obesity has prompted numerous research efforts dedicated to better understanding the mechanisms underlying this trend

  • A major focus of such research is the contribution of overeating, which can produce a positive energy balance and result in body weight gain

  • More recently, select endocrine factors associated with food intake and body weight have been shown to interact with neural systems of reward

  • Preclinical and clinical studies suggest that food reward and alterations in reward pathways may progress to food addiction

Abstract

With rising rates of obesity, research continues to explore the contributions of homeostatic and hedonic mechanisms related to eating behaviour. In this Review, we synthesize the existing information on select biological mechanisms associated with reward-related food intake, dealing primarily with consumption of highly palatable foods. In addition to their established functions in normal feeding, three primary peripheral hormones (leptin, ghrelin and insulin) play important parts in food reward. Studies in laboratory animals and humans also show relationships between hyperphagia or obesity and neural pathways involved in reward. These findings have prompted questions regarding the possibility of addictive-like aspects in food consumption. Further exploration of this topic may help to explain aberrant eating patterns, such as binge eating, and provide insight into the current rates of overweight and obesity.

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Figure 1: Potential relationships between endocrine factors and chemical signalling pathways, and effects on feeding behaviour.

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S.M. and A.T. researched data for the Review. S.M., A.T. and N.M.A. were involved in the writing of the paper. All authors contributed to the review and editing of the manuscript.

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Murray, S., Tulloch, A., Gold, M. et al. Hormonal and neural mechanisms of food reward, eating behaviour and obesity. Nat Rev Endocrinol 10, 540–552 (2014). https://doi.org/10.1038/nrendo.2014.91

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