Gut-brain signalling: Difference between revisions
imported>Graeme Daniel Logue |
imported>Andrew Critchley |
||
| Line 19: | Line 19: | ||
In here you could write about various informations linked to various references for example from journals. | In here you could write about various informations linked to various references for example from journals. | ||
<ref>First Author and Second Author, "The perfect reference for Subpart 1," ''Fake Journal of Neuroendocrinology'' 36:2 (2015) pp. 36-52.</ref> <ref>First Author and Second Author, "Another perfect reference for Subpart 1," ''Fake Journal of Neuroendocrinology'' 25:2 (2009) pp. 62-99.</ref> | <ref>First Author and Second Author, "The perfect reference for Subpart 1," ''Fake Journal of Neuroendocrinology'' 36:2 (2015) pp. 36-52.</ref> <ref>First Author and Second Author, "Another perfect reference for Subpart 1," ''Fake Journal of Neuroendocrinology'' 25:2 (2009) pp. 62-99.</ref> | ||
[['''Cholecystokinin''']] | |||
Cholecystokinin (CCK) is a peptide hormone synthesised and secreted by L-cells in the mucosal epithelium of the duodenum, it is released in response to the presence of partially digested lipids and proteins. It inhibits gastric emptying and stimulates the release of digestive enzymes from the pancreas and bile from the gall bladder by acting at the CCKA receptor (mainly found in the periphery but also found in some areas of the CNS). Because gastric emptying is inhibited, the partially digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion is reduced as there is no longer a stimulus. | |||
CCK is one of the most abundant neuropeptides in the CNS. It acts as a hunger suppressant by activating CCKB receptors found throughout the brain. It mediates satiety and can cause anxiety and nausea. | |||
CCK acts as a ‘gatekeeper’ for the response of other gut-brain signalling hormones on the afferent vagal neurons. At low levels (after fasting) CCK stimulates the expression of certain receptors associated with the stimulation of food intake (melanin concentrating hormone (MCH)-1 and cannabinoid CB1 receptors). At high levels (after food consumption) the MCH-1 and CB1 receptors are down regulated. Therefore CCK present at a high or low concentration can effect how the afferent vagal neurons respond to other neuro-hormones. | |||
In rats it has been found that CCK inhibits food intake in younger individuals more effectively than in older individuals. It also has a greater effect in males than in females. | |||
[['''Glucagon-like peptide-1''']] | |||
Glucagon-like peptide-1 (GLP-1) is a gut hormone secreted from L-cells in the mucosal epithelium of the duodenum and small intestine. It is derived from the pro-glucagon gene product and is released into the circulation in response to the presence of nutrients. It acts at the pancreas where it stimulates insulin release and suppresses glucagon release (because of these actions it is under investigation as a potential treatment for diabetes). It also increases insulin sensitivity. | |||
GLP-1 also acts on an inhibitory subset of neurons in the arcuate nucleus (part of the hypothalamus) via the brain stem (this eliminates the blood-brain barrier). Activation of these inhibitory neurons induces satiety and decreases food intake/hunger. It also decreases gastric emptying so adds to the feeling of being ‘full’. At higher concentrations GLP-1 causes nausea, and can induce Conditioned Taste Aversion (CTA) where the brain associates the taste of a certain food with being toxic (usually occurs when an individual consumes a food that had made them sick). | |||
In obese individuals, GLP-1 secretion is decreased. When weight is lost in obese individuals GLP-1 secretion returns to normal (so GLP-1 could contribute to the pathogenesis of obesity). GLP-1 receptor agonists have been targeted as a potential therapy for obesity. GLP-1 itself is not suitable as a clinical treatment for obesity as it has a very short half life (approximately 2 minutes) making storage impossible. | |||
===Title of Subpart 2=== | ===Title of Subpart 2=== | ||
Revision as of 08:18, 27 October 2009
This page was started in the framework of an Eduzendium course and needs to be assessed for quality. If this is done, this {{EZnotice}} can be removed.
A brief overview of your interest group (be sure to put its name in bold in the first sentence) and the scope of the article goes here.[1]
The following list of sections should serve as a loose guideline for developing the body of your article. The works cited in references 2-5 are all fake; their purpose is to serve as a formatting model for your own citations. Andrew Critchley 10:54, 22 October 2009 (UTC)
Introduction
Obesity is becoming a growing problem throughout the world and for this reason significant research has been undertaken to increase in the knowledge of the physiological and molecular mechanisms which effect and control body mass. In order to regulate these mechanisms complex interactions between different systems take place. This article addresses the interaction between the gastrointestinal tract and the brain and how secretion of varying hormones from different areas of the body causes appetite enhancing and satiety signals to be sent to the brain. The main hormones which have been most intensely examined are: Ghrelin, obestatin, CCK, GLP-1, PYY and insulin which all play a major role in appetite regulation. The vagus nerve is also a key mediator of regulation and is highly involved signalling, and all of these inputs are processed by areas in the brain such as the hypothalamus and the nucleus tractus solitarius (NTS).
Title of Subpart 1
In here you could write about various informations linked to various references for example from journals. [2] [3]
Cholecystokinin (CCK) is a peptide hormone synthesised and secreted by L-cells in the mucosal epithelium of the duodenum, it is released in response to the presence of partially digested lipids and proteins. It inhibits gastric emptying and stimulates the release of digestive enzymes from the pancreas and bile from the gall bladder by acting at the CCKA receptor (mainly found in the periphery but also found in some areas of the CNS). Because gastric emptying is inhibited, the partially digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion is reduced as there is no longer a stimulus.
CCK is one of the most abundant neuropeptides in the CNS. It acts as a hunger suppressant by activating CCKB receptors found throughout the brain. It mediates satiety and can cause anxiety and nausea.
CCK acts as a ‘gatekeeper’ for the response of other gut-brain signalling hormones on the afferent vagal neurons. At low levels (after fasting) CCK stimulates the expression of certain receptors associated with the stimulation of food intake (melanin concentrating hormone (MCH)-1 and cannabinoid CB1 receptors). At high levels (after food consumption) the MCH-1 and CB1 receptors are down regulated. Therefore CCK present at a high or low concentration can effect how the afferent vagal neurons respond to other neuro-hormones.
In rats it has been found that CCK inhibits food intake in younger individuals more effectively than in older individuals. It also has a greater effect in males than in females.
Glucagon-like peptide-1 (GLP-1) is a gut hormone secreted from L-cells in the mucosal epithelium of the duodenum and small intestine. It is derived from the pro-glucagon gene product and is released into the circulation in response to the presence of nutrients. It acts at the pancreas where it stimulates insulin release and suppresses glucagon release (because of these actions it is under investigation as a potential treatment for diabetes). It also increases insulin sensitivity.
GLP-1 also acts on an inhibitory subset of neurons in the arcuate nucleus (part of the hypothalamus) via the brain stem (this eliminates the blood-brain barrier). Activation of these inhibitory neurons induces satiety and decreases food intake/hunger. It also decreases gastric emptying so adds to the feeling of being ‘full’. At higher concentrations GLP-1 causes nausea, and can induce Conditioned Taste Aversion (CTA) where the brain associates the taste of a certain food with being toxic (usually occurs when an individual consumes a food that had made them sick).
In obese individuals, GLP-1 secretion is decreased. When weight is lost in obese individuals GLP-1 secretion returns to normal (so GLP-1 could contribute to the pathogenesis of obesity). GLP-1 receptor agonists have been targeted as a potential therapy for obesity. GLP-1 itself is not suitable as a clinical treatment for obesity as it has a very short half life (approximately 2 minutes) making storage impossible.
Title of Subpart 2
You can also insert diagram.
Title of Part 2
You can also cite published work accessible online. [4]
Title of Part 3
You can also cite published work from books. [5]
References
- ↑ See the "Writing an Encyclopedia Article" handout for more details.
- ↑ First Author and Second Author, "The perfect reference for Subpart 1," Fake Journal of Neuroendocrinology 36:2 (2015) pp. 36-52.
- ↑ First Author and Second Author, "Another perfect reference for Subpart 1," Fake Journal of Neuroendocrinology 25:2 (2009) pp. 62-99.
- ↑ "Part 2," Appetite and obesity. 2006. Retrieved July 21, 2009 from http://www.appetiteandobesity.org/part2.html
- ↑ Authors names, "The perfect review for part 3," Publishers City (2009)