Glucostatic theory of appetite control

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In the early 20th century, a link was made between blood glucose and appetite that led to the glucostatic theory of appetite control. In 1916, Carlson suggested that plasma concentrations of glucose could serve as a signal for both meal initiation (low levels) and meal termination (high levels) [1]. However, it was not until the 1950's that Mayer put forward the glucostatic theory. This theory proposed that the rise in plasma glucose concentration after a meal was sensed by "glucoreceptor" neurons in the hypothalamus, which then signalled for meal termination. Glucose was thus thought of as a likely satiety factor [2]. The theory, popular in the 1950s, was losing support by the 1980s, as scientists recognized that the control of appetite was a complex mechanism that depended on many signalling pathways. The glucostatic theory was not abandoned altogether, as it was still thought to be important for short-term appetite control, but newly discovered peptides such as leptin became more likely candidates for long-term control.

## Contents

* 1 Physiological background
* 2 Short-term control of appetite and satiety
* 3 Long-Term Control of Feeding and Energy Balance
* 4 References

## Physiological background[edit]

Glucose homeostasis must be finely regulated by the absorption of food and the flow of stored energy through different metabolic pathways. For the brain, glucose must be supplied continuously from the blood because the brain itself is unable to store sugar. Changes in glucose level thus elicit complex neuroendocrine responses that restore blood glucose levels to the optimum range [3]. The hypothalamus and the caudal brainstem contain important centres which are responsible for monitoring blood glucose and regulating appetite [4].

## Short-term control of appetite and satiety[edit]

The Glycaemic Index (GI) measures the effects of glycaemic carbohydrates on postprandial blood glucose levels. Foods that are digested rapidly and produce a sharp rise in blood glucose are high-GI, whereas foods that are digested and absorbed slowly have a low-GI.

Low GI diets prolong satiety and thereby reduce food intake; for example, in one study, children given low-GI breakfasts ate less lunch and showed less hunger than children who had high-GI breakfasts. [5] In obese adolescents, low-GI meals are associated with a lower insulin response than high-GI meals, and the time intervals between meals were longer in low-GI test meal group, indicating that low-GI meals increased satiety. [6] Another study investigated the effect of variations in postprandial glycaemia and insulinaemia on appetitive sensations in overweight and obese women. They modulated the rate of ingestion of a glucose beverage to examine the postprandial effects of high and low-GI meals. and reported a positive relationship between blood glucose concentrations and satiety [7]. On the other hand, Flint et al. found that in healthy young men, there was no association between glycaemic response and postprandial fullness whereas insulinaemic responses after a meal were positively correlated with postprandial satiety [2].

Thus, short-term studies suggest that glycaemic and insulinaemic responses may regulate hunger and satiety.

## Long-Term Control of Feeding and Energy Balance[edit]

The glucostatic hypothesis represents a physiological control system that fits the criteria for controlling short-term energy consumption. Alfenas and Mattes looked at the long-term effects on appetite of consuming high- or low-GI foods over days and weeks, and their findings suggested there were no significant differences in either glycaemic and insulinemic responses, or in hunger, fullness, and desire to eat [8]. The long-term control of feeding thus appears to involve other factors, such as the secretion of leptin from fat (adipose) tissue.

## References[edit]

1. ↑ Mobbs CV et al. (2005). "Impaired glucose signaling as a cause of obesity and the metabolic syndrome: the glucoadipostatic hypothesis". Physiol Behav 85: 3-23. DOI:10.1016/j.physbeh.2005.04.005. PMID 15924903. Research Blogging.
2. ↑ 2.0 2.1 Flint Aet al. (2006). "Glycemic and insulinemic responses as determinants of appetite in humans". Am J Clin Nutr 84: 1365-73. PMID 17158418.
3. ↑ Ritter S et al. (2006). "Hindbrain catecholamine neurons control multiple glucoregulatory responses". Physiol Behav 89: 490-500. PMID 16887153.
4. ↑ Mayer J (1955). "Regulation of energy intake and the body weight: the glucostatic theory and the lipostatic hypothesis". Ann N Y Acad Sci 63: 15-43. PMID 13249313.
5. ↑ Warren JM et al. (2003). "Low glycemic index breakfasts and reduced food intake in preadolescent children.". Pediatrics 112: e414. PMID 14595085.
6. ↑ Ball SD et al. (2003). "Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents.". Pediatrics 111: 488-94. PMID 12612226.
7. ↑ Arumugam V et al. (2008). "A high-glycemic meal pattern elicited increased subjective appetite sensations in overweight and obese women". Appetite 50: 215-22. PMID 17714828.
8. ↑ Alfenas RC, Mattes RD (2005). "Influence of glycemic index/load on glycemic response, appetite, and food intake in healthy humans". Diabetes Care 28: 2123-9. PMID 16123477.