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Peripheral satiety signals: view from the Chair

International Journal of Obesity volume 33, pages S3–S6 (2009)Cite this article

The discovery and characterization of peripheral signals that regulate food intake and energy balance dates back over 50 years. Beginning with the ‘glucostatic’ and ‘lipostatic’ hypotheses, nutrients were considered strong candidates that could ‘tell’ the brain the state of satiety (glucose) or overall energy stores (fat), so that food intake and energy expenditure could be regulated to maintain energy balance.1, 2 Both of these hypotheses endure to this day. The lipostatic hypothesis remains as a central concept in our understanding of the regulation of energy balance. This is based on the key observations that (a) insulin is secreted from the pancreas in direct proportion to fat stores and provides a signal to the brain to initiate long-term changes in energy expenditure and food intake3 and (b) the peptide hormone leptin is released from adipose tissue itself, and defects in either the production or the signalling of leptin lead to obesity.4 The glucostatic hypothesis received validation with the discovery of glucose-sensitive neurons in the hypothalamic regions involved in the control of energy balance.5, 6

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Acknowledgements

I thank Adam Chambers for valuable comments on the manuscript. KA Sharkey is an Alberta Heritage Foundation for Medical Research Medical Scientist and the Crohn's and Colitis Foundation of Canada Chair in Inflammatory Bowel Disease Research at the University of Calgary.

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Authors and Affiliations

  1. Department of Physiology & Biophysics, Hotchkiss Brain Institute and Snyder Institute of Infection, Inflammation and Immunity, University of Calgary, Calgary, Alberta, Canada

    K A Sharkey

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Correspondence to K A Sharkey.

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Sharkey, K. Peripheral satiety signals: view from the Chair. Int J Obes 33 (Suppl 1), S3–S6 (2009). https://doi.org/10.1038/ijo.2009.8

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