Glucostatic theory of appetite control

All unapproved Citizendium articles may contain errors of fact, bias, grammar etc. A version of an article is unapproved unless it is marked as citable with a dedicated green template at the top of the page, as in this version of the 'Biology' article. Citable articles are intended to be of reasonably high quality. The participants in the Citizendium project make no representations about the reliability of Citizendium articles or, generally, their suitability for any purpose. This article is currently being developed as part of an Eduzendium student project in the framework of a course entitled Appetite and Obesity at University of Edinburgh. The course homepage can be found at CZ:(U00984) Appetite and Obesity, University of Edinburgh 2010. For the course duration, the article is closed to outside editing. Of course you can always leave comments on the discussion page. The anticipated date of course completion is 01 February 2011. One month after that date at the latest, this notice shall be removed. Besides, many other Citizendium articles welcome your collaboration!

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Introduction

Since the early twentieth century, there has thought to have been a link between blood glucose and appetite. In 1916, Carlson suggested that glucose could serve as a signal for meal initiation (low levels) and meal termination (high levels) (Mobbs, 2005). But it was not until the 1950s that Mayer put forward the glucostatic hypothesis. Originally it was thought that a rise in plasma glucose, for example after a meal, was sensed by neurons in the hypothalamus. These neurons which contained “glucoreceptors” then signalled for meal termination. Glucose, therefore, was thought of as a satiety factor (Flint, 2006).

However, this theory has been debated for many years. While numerous studies produce results which appear to support Mayer’s hypothesis, a large number also refute it and compelling evidence has yet to be found. The theory, which was popular in the 1950s, was losing support by the 1980s. At this time, scientists were beginning to think that the control of appetite was a more complex mechanism that would have to depend on the integration of a number of signalling pathways. The glucostatic theory was not abandoned all together though as it was still thought to be important for short term appetite control. However, discoveries of peptides such as leptin became more likely candidates for long term appetite control.

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Reference: Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431 PMID 17072591

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