Glucostatic theory of appetite control

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Introduction

In the early twentieth century, a link was made 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 the long term control of appetite.

Title of Subpart 1

Glucose homeostasis must be finely regulated by the absorption of food and the flow of recently stored energy substances through different metabolic pathways. Especially for brain glucose, it has to be supplied continuously from the blood stream since there is no storage for sugar available in the brain. It is known that changes in glucose level elicit complex neuroendocrine responses that restore blood sugar levels to the optimum range. (Ritter, S. et al. 2006) It is traditionally believed that different regions of the forebrain; particularly the hypothalamus and the brain stem have important centres which are responsible for monitoring blood glucose level and regulating feeding. (Mayer, J. 1955) However, Ritter R. G. et al. claimed that glucoreceptor cells are located in the hindbrain. This means that the glucose sensing cells have direct access to the central nervous system and could elicit immediate responses to retain the physiological norm. (Ritter, R. C. et al. 1981)　They also explained that the catecholamine neurons in the hindbrain help mediating responses to glucose deficiency by linking glucoreceptor cells to forebrain and spinal neurons. This enables us to stimulate behavioural and hormonal responses that elevate blood sugar level. These include increased food intake, adrenal medullary secretion, corticosterone secretion and suppression of estrous cycles. Complex behaviours involved in activities such as detection and identification of food are mainly regulated by the forebrain. Her studies suggest that the hind brain mediates the motivation for these activities via the neuronal circuit activated by some of the glucose sensing cells. They hypothesized that the signals detected by the glucoceptors are projected to the hypothalamus via norepinephrine and epinephrine neurons in the hind brain. This motivation circuit would have engaged the physical sign of energy deficiency with these behaviours. (Ritter, S. et al. 2006)　

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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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