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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) <ref name="pmid15924903">{{cite journal|author=Mobbs CV ''et al.''|title=Impaired glucose signaling as a cause of obesity and the metabolic syndrome: the glucoadipostatic hypothesis |journal=Physiol Behav |year= 2005 |volume= 85 |pages= 3-23 | pmid=15924903 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15924903 | doi=10.1016/j.physbeh.2005.04.005 }}</ref>. 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 <ref name="pmid17158418">{{cite journal| author=Flint A''et al.''| title=Glycemic and insulinemic responses as determinants of appetite in humans|journal=Am J Clin Nutr |year= 2006 |volume= 84|pages= 1365-73 |pmid=17158418 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17158418}} </ref>. 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.


==Physiological background==
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 <ref name="pmid16887153">{{cite journal|author=Ritter S ''et al.''|title=Hindbrain catecholamine neurons control multiple glucoregulatory responses| journal=Physiol Behav|year= 2006 |volume= 89 |pages= 490-500 |pmid=16887153 }}</ref>.
The [[hypothalamus]] and the caudal brainstem contain important centres which are responsible for monitoring blood glucose and regulating appetite <ref name="pmid13249313">{{cite journal| author=Mayer J| title=Regulation of energy intake and the body weight:  the glucostatic theory and the lipostatic hypothesis| journal=Ann N Y Acad Sci| year= 1955 | volume= 63| pages= 15-43| pmid=13249313}}</ref>.


==Short-term control of appetite and satiety==
The [[Glycaemic Index]] (GI)  measures the effects of glycaemic [[carbohydrate]]s 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''.


Begin your article with a brief overview of the scope of the article on [[interest group]]. Include the article name in '''bold''' in the first sentence.<ref>See the "Writing an Encyclopedia Article" handout for more details.</ref>
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. <ref name="pmid14595085">{{cite journal| author=Warren JM ''et al.''| title=Low glycemic index breakfasts and reduced food intake in preadolescent children. | journal=Pediatrics| year= 2003| volume= 112| pages= e414| pmid=14595085}}</ref> 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. <ref name="pmid12612226">{{cite journal| author=Ball SD ''et al.''| title=Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents. | journal=Pediatrics | year= 2003 | volume= 111| pages= 488-94 | pmid=12612226}} </ref> 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 <ref name="pmid17714828">{{cite journal| author=Arumugam V ''et al.''| title=A high-glycemic meal pattern elicited increased subjective appetite sensations in overweight and obese women| journal=Appetite | year= 2008 | volume= 50| pages= 215-22| pmid=17714828}} </ref>.
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 <ref name="pmid17158418"/>.


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


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==Long-Term Control of Feeding and Energy Balance==
 
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 <ref name="pmid16123477">{{cite journal| author=Alfenas RC, Mattes RD| title=Influence of glycemic index/load on glycemic response, appetite, and food intake in healthy humans| journal=Diabetes Care| year= 2005 |volume= 28 |pages= 2123-9 |pmid=16123477 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16123477}} </ref>. The long-term control of feeding thus appears to involve other factors, such as the secretion of [[leptin]] from fat ([[adipocyte|adipose]]) tissue.
Construct your article in sections and subsections, with headings and subheadings like this:
 
 
In the early twentieth century, a link was made between blood glucose and appetite, that led to the current '''glucostatic theory of appetite control'''. 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)　
 
==The role of insulin and ghrelin in the glucostatic theory==
 
It has been proposed that both ghrelin and insulin play important roles in appetite, hunger and the glucostatic hypothesis. However, studies have produced conflicting results and how these peptides relate to the glucostatic theory still remains unclear.
 
===Insulin===
 
Insulin, a peptide hormone, is required by cells in order to take up and use glucose from the blood. Studies have shown that insulin is correlated with satiety and food intake. It was found that in the short-term insulin is involved in limiting postprandial appetite (Flint, 2006). However, glycaemic responses appear to be more important for this. Another study found that in obese and overweight women serum insulin levels were negatively correlated with subjects hunger ratings. They were also positively correlated to fullness. Again it was found that glucose had a bigger part to play in this than insulin. Both these studies suggest that, although other factors appear to be important, insulin may play a role in appetite control.
 
Conversely, other studies have found no relationship between insulin and appetite. Because of this, it is uncertain how important insulin is in the control of appetite.
 
===Ghrelin===
 
It is now commonly accepted that ghrelin, a peptide produced in the stomach, stimulates appetite. It has been proposed that this peptide is involved in glucostatic signalling. Ghrelin levels peak before a meal or when a meal is expected. In rats it has been found that insulin-induced hypoglycaemia up regulates ghrelin mRNA expression. Ghrelin secretion is also inhibited by high glucose levels. This suggests that the cells which secrete ghrelin may be sensitive to changes in plasma glucose. This mechanism may play an important role in regulating energy metabolism.
 
When ghrelin is deleted, blood glucose is reduced and insulin levels are increased. This loss of ghrelin increases the ability of insulin to suppress glucose production. These findings show that ghrelin is important for glucose homeostasis. However, in a study by Sun et al. it was found that these effects were not related to changes in food intake or weight. As with insulin, there is little conclusive evidence suggesting an important role for ghrelin in the glucostatic hypothesis. There are, however, some studies have shown links between the two.
 
 
==Title of part 2==
 
==The Long-Term Control of Feeding and Energy Balance==
 
The glucostatic hypothesis represents a physiological control system that fits the criteria for controlling short-term energy consumption. In contrast, the long-term control of feeding occurs via a different mechanism involving the secretion of a hormone Leptin, from fat (adipose) tissue, and its action on the central nervous system.  The effects of leptin were first discovered in the 1950’s, although leptin itself was not discovered until 1994.  The concentration of leptin in the circulation is proportional to the amount of fat in the body, and it alters body weight by either inhibiting the intake of food or by triggering hyperphagia.  Once secreted, Leptin crossed the blood-brain-barrier via a receptor-mediated transport system (Wayne ''et al'' 2005).  Its receptors are highly expressed in the hypothalamus and brain stem nuclei; these are both areas that are known to control feeding and energy balance.  The binding of Leptin to these receptors influences the peptide systems, Pro-opiodmelanocortin (POMC) and Neuropeptide Y (NPY).  POMC neurons in the arcuate nucleus produce the peptide alpha-MSH, an appetite suppressant.  NPY is a potent feeding stimulant.  An increase in leptin levels inhibits peptides, such as NYP, and causes an increase in alpha-MSH, therefore causing a decrease in feeding and regulating the long-term control of energy balance (Ahima & Osei 2004).
 
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==References==
==References==
<references/>
{{reflist | 2}}[[Category:Suggestion Bot Tag]]

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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.

Physiological background

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

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

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

  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.
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