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There is mention on the Obestatin page that Obestatin be merged with Ghrelin. I strongly disagree. It is true that they are both coded on the same gene, but they are distinct in their action. I see nothing that justifies their being merged. —Preceding unsigned comment added by 71.15.92.103 ( talk) 17:22, 6 June 2008 (UTC)
it is my understanding the levels of ghrelin present in the plasma of obese individuals is low ccompared to the amount present in lean individuals.
That section absolutely needs to be improved, there's either something wrong or some complex mechanism is involved which needs to be explained better in the article.-- C39 13:34, 17 June 2007 (UTC)
Explanation: Ghrelin levels are low in obesity (except in Prader Willi snydrome). In fact most people with obesity don't get hungry (the growling stomach hunger caused by ghrelin). However the arcuate nucleus in obesity is oversensitive to ghrelin from chronically low levels of ghrelin and high levels of leptin. As a result the output from the NPY/AGRP cell is increased (more NPY and AGRP) and the output from the POMC cell (alpha MSH) is decreased. The result is increased cravings, decreased metabolic rate in the setting of low "hunger" levels. Ghrelin is also responsible for sleep progression which maybe why obese people have such a high rate of sleep disturbance.
Prader Willi is different. They have a genetic block of ghrelin stimulating the growth hormone releasing hormone receptor and as a result get very high ghrelin levels. These patients are obese because they overeat because they are always hungery ("the growling stomach hunger"). Todd Burstain, MD Associate Professor of Medicine, University of Iowa. todd-burstain@uiowa.edu —Preceding unsigned comment added by 129.255.246.56 ( talk) 18:49, 21 September 2007 (UTC)
"the novel stomach hormone ghrelin ... is an endogenous agonist at the growth hormone secretagogne [sic, s.b. secretagogue -dsws] receptor and is the motilin-related family of regulatory peptides"
Abstract
[1] full text
[2]
dsws 20:02, 29 July 2005 (UTC)
GHRELINWASORIGINALLY isolated from human and
rat stomach as a cognate endogenous ligand for the
GH secretagogue receptor. This 28-aminoacid
peptide has a posttranslational n-octanoyl modification
indispensable for its activity. Ghrelin stimulates GH release
when peripherally or centrally administered to rats and
when applied directly to rat primary pituitary cells. In
addition, ghrelin administration increases food intake and
body weight gain. Whereas ghrelin secretion is upregulated
under negative energy balance conditions, including
starvation, insulin-induced hypoglycemia, cachexia, and
anorexia nervosa, it is down-regulated under conditions of
positive energy balance, such as feeding, hyperglycemia, and
obesity. Gastric ghrelin enters the brain across the
blood-brain barrier . Recently, stomach-derived ghrelin’s
signals for starvation has been reported to be relayed to the
hindbrain via the vagus afferent nerve.Ateeq Muhammed Khaliq
Ghrelin, the endogenous ligand of the GH secretagogue receptor (GHS-R), is a newly identified, ubiquitously expressed molecule that has been involved in a wide array of endocrine and nonendocrine functions, including cell proliferation. In this context, the GHS-R type 1a, in the human ovary and testis as well as several testicular tumors. Ovarian malignancies, however, remain unexplored. Notably, a vast majority of ovarian tumors derive from the surface epithelium, which originates from the celomic epithelium. Considering the proven expression of ghrelin in the human ovary, and its reported effects in the proliferative activity of different cancer cell lines, we aimed at evaluating whether the ovarian surface epithelium as well as related reproductive structures and tumors are potential targets of ghrelin. To this end, expression of GHS-R1a was analyzed by immunohistochemistry in a panel of normal, metaplastic, and neoplastic tissues. Uniform GHS-R1a immunostaining was detected throughout the ovarian surface epithelium. Likewise, ciliated cells within the fallopian tube epithelium showed strong GHS-R1a expression. In contrast, other celomic derivatives, such as endometrium and endocervix, were negative for GHS-R1a immunoreactivity. In keeping with data from normal tissues, inclusion cysts from the surface epithelium expressed GHS-R1a. Similarly, benign serous tumors resembling fallopian tube epithelium were also positive, whereas serous cystadenocarcinomas showed GHS-R1a expression only in highly differentiated specimens. In contrast, other neoplasms, such as mucinous cystadenomas and cystadenocarcinomas, endometrioid tumors, clear cell carcinomas, and Brenner tumors, did not express GHS-R1a. In conclusion, our results demonstrate that the ovarian surface epithelium and related tumors are potential targets for systemic or locally produced ghrelin because they express the functional type 1a GHS-R. Considering the relevant role of the ovarian surface epithelium in key physiological events (such as ovulation) and neoplastic transformation of the ovary, the potential actions of ghrelin in those phenomena merit further investigation.--
Ateeq 3:15, 23 of june 2006 (UTC)
"Ghrelin levels increase before meals and decrease after meals" I can understand that it decreases after meals but what specifically prompts the increase? Tremello22 ( talk) 21:13, 22 March 2008 (UTC)
I provided some clarification to the Clinical Significance section wrt bariatric surgeries and ghrelin levels. There are many conflicting studies as to the long term effects on plasma ghrelin from gastric bypass (though it does seem to reduce ghrelin initially during the dramatic weight loss), a fact which I noted. I also added that surgeries which include vertical sleeve gastrectomy result in a 60% reduction in plasma ghrelin the long term. I removed the sentence about cognitive impairments associated with gastric bypass because the referenced research did not note ghrelin as causative and because a number of studies have indicated an absence of long term ghrelin reduction in gastric bypass patients. (The referenced study on cognitive impairments was actually quite interesting. I just don't see how it belonged in this ghrelin article if the cognitive impairments are not specifically linked to ghrelin in a referenced study.) — Preceding unsigned comment added by Bdmwiki ( talk • contribs) 09:47, 3 November 2013 (UTC)
I'm going to remove the mention of ghrelin being expressed in the hypothalamus. I might change it to say something like molecules originating from the ghrelin gene, but not acylated ghrelin, are expressed in the hypothalamus. See http://www.sciencedirect.com/science/article/pii/S030645221100889X. The part in this wiki article where it mentions the ghrelin expressed in the Arc being the one that stimulates the NPY neurons was pretty sketchy even if acyl-ghrelin was expressed there. Also, that paper reports both acyl and desyacyl ghrelin are not expressed in the hypothalamus, so I'm wondering whether any speculated results should even be included in this article, and not wait until we know exactly what ghrelin-like molecules are expressed in the hypothalamus until we include them in this wiki article as it seems they're not ghrelin. -- Africantearoa ( talk) 23:29, 2 October 2011 (UTC)
The lead paragraph is rather too technical. As a mere mortal with normal English as his moher tongue I found this almost impossible to understand. By all means the technical explanation should be in the article, but not in the lead section. In lay language, what it is, and what its functions is/are in simple everyday language would be enough.--
Hauskalainen (
talk) 08:50, 20 June 2009 (UTC)
I agree with this. Scientific articles need a layman's introduction accessible by a non-expert (as in most of us).
Shatuga (
talk) 15:39, 28 February 2012 (UTC)
Yes, can somebody please write a "ghrelin for dummies" article? 09/14/2012 — Preceding unsigned comment added by 12.133.223.254 ( talk) 20:53, 14 September 2012 (UTC)
There's something wrong with the first sentence. It's hard to understand and clumsy. I can't tell what it is supposed to mean. 69.225.15.250 ( talk) 15:58, 23 March 2010 (UTC)
It should also say that it is a peptide hormone, not just hormone.
-anon
"Evidence for a cardiovascular function of ghrelin has been found: expression of mRNA encoding both ghrelin and its receptor has been observed in the heart and aortas (89, 169), and intravenous injection of ghrelin into human volunteers induces a decrease in blood pressure (169). In addition, a radiolabeled ghrelin, [125I-His9]ghrelin, was shown to bind to heart and to peripheral vascular tissue." [3]
-- Dan Wylie-Sears 2 ( talk) 04:14, 4 September 2009 (UTC)
"Lack of sleep produces ghrelin, which stimulates appetite and creates less leptin, which, among its many other effects, suppresses appetite." Confusing. Isn't less leptin = increased appetite? —Preceding unsigned comment added by Settledownclown ( talk • contribs) 11:44, 10 November 2010 (UTC)
I guess they were meaning leptin's normal effects are to suppress appetite. Just awkwardly worded phrasing. -- Africantearoa ( talk) 05:21, 8 September 2011 (UTC)
The article says which organs produce it, and what it does, but it does not say what triggers production of the hormone. I'm guessing P/D1 cells produce it upon the stomach being empty and the pancreas produces it upon low blood glucose, but that's just a guess. If science doesn't know, it would make sense to mention it too. Whiterabbit fr31 ( talk) 22:25, 10 January 2012 (UTC)
First sentence:
"Ghrelin is a 28 amino acid hunger-stimulating peptide and hormone that is produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas."
Mechanism of action "It is produced mainly in the small and large intestines, but can also be secreted by the lungs, pancreatic islets, gonads, adrenal cortex, placenta, kidney and brain (Ariyasu, 2001). "
Though, hmm, the article I first find for Ariyasu et al. 2001 has the title "Stomach is a major source of circulating Ghrelin,...."
Also, high Leptin is not thought to cause satiety, even though low Leptin causes hunger. See Leptin article, etc. 172.5.154.148 ( talk) 20:28, 24 September 2013 (UTC)
I am responding to several appeals to have a simpler introduction. No references were deleted, and material I feel could be deleted or merged into the body of the site have been grouped into a last paragraph.
IiKkEe ( talk) 00:22, 2 May 2014 (UTC)
The WP:LEAD of an article should summarize the main points of the article. Furthermore an appropriate length of the lead for an article of this size is probably 2-3 paragraphs. Finally the scope of this article is wider than WP:MED, it also includes WP:MCB. Hence I think the following passage which conveys basic information about where the peptide comes from and what protein family it belongs to is very appropriate to include in the lead and should be restored:
Ghrelin together with obestatin is produced from cleavage of the ghrelin/obestatin prepropeptide (also known as the appetite-regulating hormone or growth hormone secretagogue or motilin-related peptide), which in turn is encoded by the GHRL gene. Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
Boghog ( talk) 09:18, 4 May 2014 (UTC)
IiKkEe ( talk) 07:47, 14 May 2014 (UTC)
Just found out this should be settled at WP:third party, NOT WP: dispute resolution. Will pursue.
IiKkEe ( talk) 19:46, 14 May 2014 (UTC)
To Seppi333 - Thank you for adding this sentence and reference to the lead: I think it's a great addition. Did you move it from the body of the article, or is it a new addition? If it was in there before, I missed it. I have separated it into its own paragraph to emphasize it. I would like to italicize "reward perception" to further emphasize it. Are you OK with that? Thanks.
IiKkEe ( talk) 17:48, 5 May 2014 (UTC)
I think more information should be included on its relationship with ptsd. A good source to include and bad further sourcing would be http://www.foxnews.com/health/2013/12/11/mit-researchers-discover-possible-vaccine-for-post-traumatic-stress-disorder/ Dmatteng ( talk) 15:28, 12 September 2014 (UTC)
Dear all,
Regarding the sentence: "Circulating ghrelin concentrations rise before eating and fall afterward, more strongly in response to protein and carbohydrate than to lipids". It must be taken with caution, the studies are not conclusive. I know one that says the opposite, that is so, ghrelin levels increase with protein-rich meals. This sentence must be revised, with more sources, even proving otherwise. Jorge Pires ( talk) 16:19, 5 June 2015 (UTC)
“Hunger Hormone” No More?: Ghrelin promotes fat storage not feeding, according to a study. by Ruth Williams | The New Scientist, April 20, 2016 MaynardClark ( talk) 14:38, 1 June 2016 (UTC)
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The first sentence of the second paragraph says "When the stomach is empty, ghrelin is absorbed." This seems to contradict the general gist of the rest of the article, that an empty stomach raises the ghrelin level, causing hunger. Maproom ( talk) 12:11, 9 January 2018 (UTC)
I second this. There was an "Undo" edit in November that changed it from "secreted" to "absorbed." I'm almost certain "secreted" is the correct word here. Pdavis68 ( talk)
This section was removed because
There are several sections of this article relying on early-stage lab studies, and are therefore too weak for an encyclopedia. That's why we rely on WP:MEDSCI and WP:MEDASSESS. -- Zefr ( talk) 00:47, 26 March 2019 (UTC)
With most of the article based on old (before 2014) primary literature, there is more that can be covered on evolving clinical uses, beyond the short section here. Emerging clinical topics and reviews (although still based mostly on primary lab research):
These topics and reviews - all published within the last 5 years ( WP:MEDDATE) - provide higher-quality content more relevant to current understanding about ghrelin in physiological mechanisms, diseases, and drug development. -- Zefr ( talk) 15:27, 26 March 2019 (UTC)
New editor Suzanne Dickson, who has a long, distinguished publishing record on ghrelin - PubMed list here - made two mass-change edits on Oct 1-2. The first - which extensively cites her own work - sourced both reviews and outdated lab research, changed lede content, and provided improved sections on history, ghrelin receptor theory, and effects. The second has text and refs in [square brackets] possibly indicating copy from a different source. These edits were reverted as undiscussed here on the talk page, having format errors, having potential for WP:COI, and potential for copyright violations. I indicated to the editor in edit comments and on her talk page that providing rationale for the changes by talk page discussion, and in segments rather than a mass change, would be preferred to allow other editors to comment. The user's talk page shows her responses (which would better be transferred here for all editors to review). -- Zefr ( talk) 16:23, 2 October 2019 (UTC)
I would like to mention that "extensively" is an over-statement. Outdated means that wikipedia only valued work published recently. The work undertaken by the people in the field is not valued because it is old. I do not agree. I doubt anyone agrees that knows anything about the ghrelin field. In my edits, I included work from the giants who established the field ... CY Bowers, Roy G Smith, Kangawa and Kogima, David Cummings, Tamas Horvath, Matthias Tschöp and Mark Heiman, Jeffrey Zigman, Alfonso Abizaid, Zane Andrews and many more. I DID NOT COPY ANYTHING FROM ANY SOUCE OTHER THAN THIS WEB PAGE ITSELF. Everything in both versions was either written by me de novo over the past 36 hours or was a direct edit on your web page of the text already existing. Some text was simply moved and combined. The same information was repeated over and over, sometimes better than others. It seems like too much work to improve wikipedia. It seems experts especially are not the people you want to edit. I will write to all ghrelin researchers that are senior informing them of what has happened and asking them to read this and other dialogues. I know they also are disappointed with the ghrelin web page. At least I tried.
From my perspective, our biggest problem is attracting and retaining good editors. I loved what MontanaBW wrote: "Wikipedia needs to improve the sometimes hostile and toxic environment for article creators and editors, both new and old." Amen. We routinely drive away potential good editors with unrestrained criticism, which often comes across as an arrogant attack. I frequently encourage friends and colleagues to contribute to Wikipedia. The few that do usually tell me later something like, "Why should I spend time writing on a topic I know in-depth, only to have some jerk delete it all and throw a bunch of rules with colons at me and treat me like I'm an ignoramus?" I try my best to encourage them to "hang tough" and "don't let the rule-bound editors suffering from a superiority complex get in your way." But most have made up their mind and moved on to "volunteer work where my contributions are appreciated."
Suzanne Dickson recommended this edit for the lede on her talk page.
References
The proposed revision contains sources all over 9 years old, several of which are primary lab studies. It also is unformatted for WP:REFPUNCT. Following WP:MEDLEDE, I suggest this paragraph below could be used with the Muller review as the main ref, using some of the current lede. -- Zefr ( talk) 03:38, 3 October 2019 (UTC)
References
Is it appropriate to include animal research? David notMD ( talk) 04:27, 3 October 2019 (UTC)
I have deleted several sections of text and refs because the only citations were animal studies, hence not WP:MEDRS. Content can be restored if review articles based on human research can be identified. Also looking at content based on individual clinical trials rather than reviews. David notMD ( talk) 13:14, 3 October 2019 (UTC)
You suggest that the front section should read like this and below I make several points as to why the information should be improved:
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by the stomach,[1] and sometimes called a "hunger" hormone because ghrelin increases food intake.[2] Blood levels of ghrelin are highest during hunger.[2] When the stomach is empty, ghrelin is secreted, and when it is stretched, secretion stops.[2] It acts on hypothalamic brain cells both to increase hunger and to increase gastric acid secretion and gastrointestinal motility to prepare the body for food intake.[3] Ghrelin is a neuropeptide in the central nervous system.[2] Besides regulating appetite, it participates in regulating energy homeostasis, learning and memory, circadian rhythms, reward behavior, and taste sensation.[2] The receptor for ghrelin – the ghrelin/growth hormone secretagogue receptor (GHS-R) – is found on the same cells in the brain as the receptor for leptin, the satiety hormone that has opposite effects from ghrelin.[2]
1. Sentence 1 would be more informative if it indicated that the cells secreting ghrelin are the enteroendocrine cells of the stomach. There are ghrelin cells elsewhere in the gastrointestinal tract but 80% of circulating ghrelin comes from the stomach. It is very important that we cite the article of the lab who discovered it in 1999. It should read "Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach [1] [2], and is often called a "hunger" hormone because it increases food intake. [3]"
2. The following sentence should be deleted because it is factually incorrect: "When the stomach is empty, ghrelin is secreted, and when it is stretched, secretion stops.[2]". Ghrelin release has nothing to do with stomach stretching. Actually the correct information is written elsewhere on the page (at least 3 times) and so this sentence is redundant. Even the previous sentence gives the correct information. My suggestion is that these sentences (2 and 3) are combined and that you cite the article that first shows that ghrelin release is highest before mealtimes after which levels decline once again. I am sorry that it is from 2001 - it is just the article that is most important. Their article has been cited 1939 times. It is the first thing we tell students about plasma ghrelin levels. Therefore the new text should now read "Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes". [4]"
3. There are SERIOUS problems with the information in the next sentence: "It acts on hypothalamic brain cells both to increase hunger and to increase gastric acid secretion and gastrointestinal motility to prepare the body for food intake.[3]" The two parts of the sentence have correct information but they should not be combined in this way because it is midleading/wrong. Yes, ghrelin acts on the hypothalamus (as well as many other parts of the feeding circuits) and yes, this is likely important for its effects on food intake. Effects on gastric motility, especially involve effects locally in the gut. How ghrelin controls gastric acid secretion is unclear. The first ever article showing that the hypothalamus is a target for ghrelin agonists was the discovery that peripheral ghrelin injection causes activation of cells in the arcuate nucleus, for which I take credit. I like the idea that it prepares the body for food intake but that is an opinion and not a fact. Thus, my suggestion is: "Ghrelin may help prepare for food intake [5]by increasing gastric motility as well as gastric acid secretion. [6] Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [7] including the orexigenic neuropeptide Y neurones [8] that co-express agouti-related peptide (AgRP). Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A).
PLEASE NOTICE THAT ALL REFERENCES WERE ALREADY LISTED ON THE GHRELIN PAGE, INCLUDING ARTICLES TO WHICH I HAVE CONTRIBUTED.
Thus, putting it all together, my improved suggestion is ...
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach [9] [10], and is often called a "hunger" hormone because it increases food intake. [11] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [12] Ghrelin may help prepare for food intake [13] by increasing gastric motility as well as gastric acid secretion. [14] Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [15] including the orexigenic neuropeptide Y neurones [16] that co-express agouti-related peptide (AgRP). Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [17] whose brain distribution has been extensively mapped. [18]
Suzanne Dickson 07:00, 3 October 2019 (UTC)
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Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach [1] [2], and is often called a "hunger" hormone because it increases food intake. [3] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [4] Ghrelin may help prepare for food intake [5] by increasing gastric motility as well as gastric acid secretion. [6] Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [7] including the orexigenic neuropeptide Y neurones [8] that co-express agouti-related peptide (AgRP). Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [9] whose brain distribution has been extensively mapped. [10] Suzanne Dickson 07:03, 3 October 2019 (UTC)
References
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It is written: The receptor for ghrelin, the ghrelin/growth hormone secretagogue receptor (GHS-R), is found on the same cells in the brain as the receptor for leptin, the satiety hormone that has opposite effects from ghrelin.[10] Ghrelin also plays an important role in regulating reward cognition in dopamine neurons that link the ventral tegmental area to the nucleus accumbens[11][12] (a site that plays a role in processing sexual desire, reward, and reinforcement, and in developing addictions) through its colocalized receptors and interaction with dopamine and acetylcholine.[7][13] Ghrelin is encoded by the GHRL gene and is presumably produced from the cleavage of the prepropeptide ghrelin/obestatin. Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
Unlike the case of many other endogenous peptides, ghrelin is able to cross the blood-brain-barrier, giving exogenously-administered ghrelin unique clinical potential.[14]
———————
My points
1. The first sentence. We have now already mentioned the ghrelin receptor in the earlier section and we also have a whole section on the ghrelin page dedicate to the receptor. The first thing I expect to read about the receptor is not that it colocalises with another receptor. The sentence is also misleading as written because this colocalization is only known to occur on some cells and either unknown or not the case for other brain areas where the receptor is located. It is my suggestion that this information is therefore moved to the section on the receptor and that it is added as an extra piece of information about the receptor.
2. The second sentence is not linked at all to the first sentence. Suddenly we are reading about the reward system. This text can also be moved to a sections discussing the actions of ghrelin. If not, then I suggest you modify it. The term reward cognition is odd. It is over-simplified to write "in dopmine neurones" since an entire reward circuit is engaged. On the ghrelin page are articles to which I contributed showing that ghrelin engages the dopamine system. Again, it was another first from our group and it was published around the same time as Abizaid and colleagues (another important article). If you don't want original articles then there are plenty of reviews. Again, I have written many of them on this topic. So it would be hard to avoid citing this work somehow. I propose rather that lower down the page, we have a whole section dedicated to the actions of ghrelin that are linked to its effects on the reward system - for natural (food, gambling, sex) and artifical rewards (drugs, alcohol).
3. The third sentence is a complete switch in topic again but not entirely irrelevant and could be encorporated here as a separate topic. Since there were no sources for information obestatin, I added one.
4. The last sentence could be inserted into the previous text that I edited. I have done this below and inserted the same reference.
Therefore I propose that this section should now read ...
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by
enteroendocrine cells of the
gastrointestinal tract, especially the stomach
[1]
[2], and is often called a "hunger" hormone because it increases food intake.
[3] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes.
[4] Ghrelin may help prepare for food intake
[5] by increasing gastric motility as well as gastric acid secretion.
[6] Ghrelin can access the brain where it activates cells in the
arcuate nucleus of the hypothalamus,
[7] including the orexigenic
neuropeptide Y neurones
[8] that co-express
agouti-related peptide (AgRP). Because ghrelin, unlike many other endogenous peptides, is able to cross the
blood-brain-barrier, it gives exogenously-administered ghrelin unique clinical potential.
[9]
Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [10] whose brain distribution has been extensively mapped. [11]
Ghrelin also plays an important role in regulating reward processing engaging dopamine neurons that link the ventral tegmental area to the nucleus accumbens [12][11](a site that plays a role in processing reinforcment for natural rewards (food, sexual desire, gambling) and artificial rewards (drugs, alcohol and in developing addictions) through its colocalized receptors and interaction with dopamine and acetylcholine [13] [14]
Ghrelin is encoded by the GHRL gene and is presumably produced from the cleavage of the prepropeptide ghrelin/ obestatin. [15] Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
---
I found it difficult to insert this reference in its original place because it is a book. It was placed after the reference to Naleid et al.
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 10:Neural and Neuroendocrine Control of the Internal Milieu". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 265–66. ISBN 9780071481274.
Suzanne Dickson 07:03, 3 October 2019 (UTC)
OK. I can't devote more time to this page at the moment. I hope you recognise that it is much improved.
Suzanne Dickson 08:00, 3 October 2019 (UTC)
Nestler EJ, Hyman SE, Holtzman DM, Malenka RC (2015). "Neural and Neuroendocrine Control of the Internal Milieu". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. pp. 245–267. ISBN 9780071827690. - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 09:46, 3 October 2019 (UTC)
References
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Thanks for helping to add the reference back. I am trying to do do as little as I can to disturb the references that were there before. Thanks everyone for support and help to improve the page. I just want the hormone that I devote my research to, to have a good page on wikipedia. I refer to wikipedia myself for information and I want to know it is a reliable source of information. I try to make the ghrelin page that. Suzanne Dickson 12:55, 3 October 2019 (UTC) — Preceding unsigned comment added by Suzanne Dickson ( talk • contribs)
--- Perfect Suzanne Dickson 05:02, 4 October 2019 (UTC) Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, [1] [2] [3] and is often called a "hunger hormone" because it increases food intake. [3] [4] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [3] [5] Ghrelin may help prepare for food intake [3] [6] by increasing gastric motility and gastric acid secretion. [2] [3]
Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [3] [7] [8] including the orexigenic neuropeptide Y neurones that co-express agouti-related peptide (AgRP) [3] [9] Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [3] [10] whose brain distribution has been extensively mapped. [3] [11]
References
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Hello @ Markworthen and Zefr: what do you think of the following for the lede? :-) -- Signimu ( talk) 20:48, 6 October 2019 (UTC)
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, [1] [2] [3] and is often called a "hunger hormone" because it increases food intake. [3] [4] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [3] [5] Ghrelin may help prepare for food intake [3] [6] by increasing gastric motility and gastric acid secretion. [2] [3]
Unlike many other endogenous peptides, ghrelin is able to cross the blood-brain-barrier [7] and access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [3] [8] [9] including the orexigenic neuropeptide Y neurones that co-express agouti-related peptide (AgRP) [3] [10] Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [3] [11] whose brain distribution has been extensively mapped. [3] [12]
References
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Are better refs available? Existing are from small human studies. David notMD ( talk) 01:02, 9 October 2019 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 28 August 2023 and 15 December 2023. Further details are available on the course page. Student editor(s): RCC23A ( article contribs). Peer reviewers: Vmt19, Achait2023.
— Assignment last updated by GradStudent4Life ( talk) 23:02, 5 December 2023 (UTC)
Under the section 'Locations of Action' subsection 'Sleep' I read: "A review reported finding strong evidence that sleep restriction affected ghrelin or leptin levels, or energy expenditure." When I follow the link mentioned to the PubMed abstract I read: "Overall, we did not find strong evidence supporting the significant impact of sleep restriction on mean leptin or ghrelin levels or energy expenditure. "
This seems to be the opposite of the line in Wikipedia. I do not know anything about Wikipedia-editing, so I do hope someone with more knowledge of both editing and/or ghrelin might take a look at this. — Preceding unsigned comment added by 2001:1C01:1D0D:4200:69D3:BBC2:D179:F5DA ( talk) 14:30, 7 February 2024 (UTC)
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There is mention on the Obestatin page that Obestatin be merged with Ghrelin. I strongly disagree. It is true that they are both coded on the same gene, but they are distinct in their action. I see nothing that justifies their being merged. —Preceding unsigned comment added by 71.15.92.103 ( talk) 17:22, 6 June 2008 (UTC)
it is my understanding the levels of ghrelin present in the plasma of obese individuals is low ccompared to the amount present in lean individuals.
That section absolutely needs to be improved, there's either something wrong or some complex mechanism is involved which needs to be explained better in the article.-- C39 13:34, 17 June 2007 (UTC)
Explanation: Ghrelin levels are low in obesity (except in Prader Willi snydrome). In fact most people with obesity don't get hungry (the growling stomach hunger caused by ghrelin). However the arcuate nucleus in obesity is oversensitive to ghrelin from chronically low levels of ghrelin and high levels of leptin. As a result the output from the NPY/AGRP cell is increased (more NPY and AGRP) and the output from the POMC cell (alpha MSH) is decreased. The result is increased cravings, decreased metabolic rate in the setting of low "hunger" levels. Ghrelin is also responsible for sleep progression which maybe why obese people have such a high rate of sleep disturbance.
Prader Willi is different. They have a genetic block of ghrelin stimulating the growth hormone releasing hormone receptor and as a result get very high ghrelin levels. These patients are obese because they overeat because they are always hungery ("the growling stomach hunger"). Todd Burstain, MD Associate Professor of Medicine, University of Iowa. todd-burstain@uiowa.edu —Preceding unsigned comment added by 129.255.246.56 ( talk) 18:49, 21 September 2007 (UTC)
"the novel stomach hormone ghrelin ... is an endogenous agonist at the growth hormone secretagogne [sic, s.b. secretagogue -dsws] receptor and is the motilin-related family of regulatory peptides"
Abstract
[1] full text
[2]
dsws 20:02, 29 July 2005 (UTC)
GHRELINWASORIGINALLY isolated from human and
rat stomach as a cognate endogenous ligand for the
GH secretagogue receptor. This 28-aminoacid
peptide has a posttranslational n-octanoyl modification
indispensable for its activity. Ghrelin stimulates GH release
when peripherally or centrally administered to rats and
when applied directly to rat primary pituitary cells. In
addition, ghrelin administration increases food intake and
body weight gain. Whereas ghrelin secretion is upregulated
under negative energy balance conditions, including
starvation, insulin-induced hypoglycemia, cachexia, and
anorexia nervosa, it is down-regulated under conditions of
positive energy balance, such as feeding, hyperglycemia, and
obesity. Gastric ghrelin enters the brain across the
blood-brain barrier . Recently, stomach-derived ghrelin’s
signals for starvation has been reported to be relayed to the
hindbrain via the vagus afferent nerve.Ateeq Muhammed Khaliq
Ghrelin, the endogenous ligand of the GH secretagogue receptor (GHS-R), is a newly identified, ubiquitously expressed molecule that has been involved in a wide array of endocrine and nonendocrine functions, including cell proliferation. In this context, the GHS-R type 1a, in the human ovary and testis as well as several testicular tumors. Ovarian malignancies, however, remain unexplored. Notably, a vast majority of ovarian tumors derive from the surface epithelium, which originates from the celomic epithelium. Considering the proven expression of ghrelin in the human ovary, and its reported effects in the proliferative activity of different cancer cell lines, we aimed at evaluating whether the ovarian surface epithelium as well as related reproductive structures and tumors are potential targets of ghrelin. To this end, expression of GHS-R1a was analyzed by immunohistochemistry in a panel of normal, metaplastic, and neoplastic tissues. Uniform GHS-R1a immunostaining was detected throughout the ovarian surface epithelium. Likewise, ciliated cells within the fallopian tube epithelium showed strong GHS-R1a expression. In contrast, other celomic derivatives, such as endometrium and endocervix, were negative for GHS-R1a immunoreactivity. In keeping with data from normal tissues, inclusion cysts from the surface epithelium expressed GHS-R1a. Similarly, benign serous tumors resembling fallopian tube epithelium were also positive, whereas serous cystadenocarcinomas showed GHS-R1a expression only in highly differentiated specimens. In contrast, other neoplasms, such as mucinous cystadenomas and cystadenocarcinomas, endometrioid tumors, clear cell carcinomas, and Brenner tumors, did not express GHS-R1a. In conclusion, our results demonstrate that the ovarian surface epithelium and related tumors are potential targets for systemic or locally produced ghrelin because they express the functional type 1a GHS-R. Considering the relevant role of the ovarian surface epithelium in key physiological events (such as ovulation) and neoplastic transformation of the ovary, the potential actions of ghrelin in those phenomena merit further investigation.--
Ateeq 3:15, 23 of june 2006 (UTC)
"Ghrelin levels increase before meals and decrease after meals" I can understand that it decreases after meals but what specifically prompts the increase? Tremello22 ( talk) 21:13, 22 March 2008 (UTC)
I provided some clarification to the Clinical Significance section wrt bariatric surgeries and ghrelin levels. There are many conflicting studies as to the long term effects on plasma ghrelin from gastric bypass (though it does seem to reduce ghrelin initially during the dramatic weight loss), a fact which I noted. I also added that surgeries which include vertical sleeve gastrectomy result in a 60% reduction in plasma ghrelin the long term. I removed the sentence about cognitive impairments associated with gastric bypass because the referenced research did not note ghrelin as causative and because a number of studies have indicated an absence of long term ghrelin reduction in gastric bypass patients. (The referenced study on cognitive impairments was actually quite interesting. I just don't see how it belonged in this ghrelin article if the cognitive impairments are not specifically linked to ghrelin in a referenced study.) — Preceding unsigned comment added by Bdmwiki ( talk • contribs) 09:47, 3 November 2013 (UTC)
I'm going to remove the mention of ghrelin being expressed in the hypothalamus. I might change it to say something like molecules originating from the ghrelin gene, but not acylated ghrelin, are expressed in the hypothalamus. See http://www.sciencedirect.com/science/article/pii/S030645221100889X. The part in this wiki article where it mentions the ghrelin expressed in the Arc being the one that stimulates the NPY neurons was pretty sketchy even if acyl-ghrelin was expressed there. Also, that paper reports both acyl and desyacyl ghrelin are not expressed in the hypothalamus, so I'm wondering whether any speculated results should even be included in this article, and not wait until we know exactly what ghrelin-like molecules are expressed in the hypothalamus until we include them in this wiki article as it seems they're not ghrelin. -- Africantearoa ( talk) 23:29, 2 October 2011 (UTC)
The lead paragraph is rather too technical. As a mere mortal with normal English as his moher tongue I found this almost impossible to understand. By all means the technical explanation should be in the article, but not in the lead section. In lay language, what it is, and what its functions is/are in simple everyday language would be enough.--
Hauskalainen (
talk) 08:50, 20 June 2009 (UTC)
I agree with this. Scientific articles need a layman's introduction accessible by a non-expert (as in most of us).
Shatuga (
talk) 15:39, 28 February 2012 (UTC)
Yes, can somebody please write a "ghrelin for dummies" article? 09/14/2012 — Preceding unsigned comment added by 12.133.223.254 ( talk) 20:53, 14 September 2012 (UTC)
There's something wrong with the first sentence. It's hard to understand and clumsy. I can't tell what it is supposed to mean. 69.225.15.250 ( talk) 15:58, 23 March 2010 (UTC)
It should also say that it is a peptide hormone, not just hormone.
-anon
"Evidence for a cardiovascular function of ghrelin has been found: expression of mRNA encoding both ghrelin and its receptor has been observed in the heart and aortas (89, 169), and intravenous injection of ghrelin into human volunteers induces a decrease in blood pressure (169). In addition, a radiolabeled ghrelin, [125I-His9]ghrelin, was shown to bind to heart and to peripheral vascular tissue." [3]
-- Dan Wylie-Sears 2 ( talk) 04:14, 4 September 2009 (UTC)
"Lack of sleep produces ghrelin, which stimulates appetite and creates less leptin, which, among its many other effects, suppresses appetite." Confusing. Isn't less leptin = increased appetite? —Preceding unsigned comment added by Settledownclown ( talk • contribs) 11:44, 10 November 2010 (UTC)
I guess they were meaning leptin's normal effects are to suppress appetite. Just awkwardly worded phrasing. -- Africantearoa ( talk) 05:21, 8 September 2011 (UTC)
The article says which organs produce it, and what it does, but it does not say what triggers production of the hormone. I'm guessing P/D1 cells produce it upon the stomach being empty and the pancreas produces it upon low blood glucose, but that's just a guess. If science doesn't know, it would make sense to mention it too. Whiterabbit fr31 ( talk) 22:25, 10 January 2012 (UTC)
First sentence:
"Ghrelin is a 28 amino acid hunger-stimulating peptide and hormone that is produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas."
Mechanism of action "It is produced mainly in the small and large intestines, but can also be secreted by the lungs, pancreatic islets, gonads, adrenal cortex, placenta, kidney and brain (Ariyasu, 2001). "
Though, hmm, the article I first find for Ariyasu et al. 2001 has the title "Stomach is a major source of circulating Ghrelin,...."
Also, high Leptin is not thought to cause satiety, even though low Leptin causes hunger. See Leptin article, etc. 172.5.154.148 ( talk) 20:28, 24 September 2013 (UTC)
I am responding to several appeals to have a simpler introduction. No references were deleted, and material I feel could be deleted or merged into the body of the site have been grouped into a last paragraph.
IiKkEe ( talk) 00:22, 2 May 2014 (UTC)
The WP:LEAD of an article should summarize the main points of the article. Furthermore an appropriate length of the lead for an article of this size is probably 2-3 paragraphs. Finally the scope of this article is wider than WP:MED, it also includes WP:MCB. Hence I think the following passage which conveys basic information about where the peptide comes from and what protein family it belongs to is very appropriate to include in the lead and should be restored:
Ghrelin together with obestatin is produced from cleavage of the ghrelin/obestatin prepropeptide (also known as the appetite-regulating hormone or growth hormone secretagogue or motilin-related peptide), which in turn is encoded by the GHRL gene. Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
Boghog ( talk) 09:18, 4 May 2014 (UTC)
IiKkEe ( talk) 07:47, 14 May 2014 (UTC)
Just found out this should be settled at WP:third party, NOT WP: dispute resolution. Will pursue.
IiKkEe ( talk) 19:46, 14 May 2014 (UTC)
To Seppi333 - Thank you for adding this sentence and reference to the lead: I think it's a great addition. Did you move it from the body of the article, or is it a new addition? If it was in there before, I missed it. I have separated it into its own paragraph to emphasize it. I would like to italicize "reward perception" to further emphasize it. Are you OK with that? Thanks.
IiKkEe ( talk) 17:48, 5 May 2014 (UTC)
I think more information should be included on its relationship with ptsd. A good source to include and bad further sourcing would be http://www.foxnews.com/health/2013/12/11/mit-researchers-discover-possible-vaccine-for-post-traumatic-stress-disorder/ Dmatteng ( talk) 15:28, 12 September 2014 (UTC)
Dear all,
Regarding the sentence: "Circulating ghrelin concentrations rise before eating and fall afterward, more strongly in response to protein and carbohydrate than to lipids". It must be taken with caution, the studies are not conclusive. I know one that says the opposite, that is so, ghrelin levels increase with protein-rich meals. This sentence must be revised, with more sources, even proving otherwise. Jorge Pires ( talk) 16:19, 5 June 2015 (UTC)
“Hunger Hormone” No More?: Ghrelin promotes fat storage not feeding, according to a study. by Ruth Williams | The New Scientist, April 20, 2016 MaynardClark ( talk) 14:38, 1 June 2016 (UTC)
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The first sentence of the second paragraph says "When the stomach is empty, ghrelin is absorbed." This seems to contradict the general gist of the rest of the article, that an empty stomach raises the ghrelin level, causing hunger. Maproom ( talk) 12:11, 9 January 2018 (UTC)
I second this. There was an "Undo" edit in November that changed it from "secreted" to "absorbed." I'm almost certain "secreted" is the correct word here. Pdavis68 ( talk)
This section was removed because
There are several sections of this article relying on early-stage lab studies, and are therefore too weak for an encyclopedia. That's why we rely on WP:MEDSCI and WP:MEDASSESS. -- Zefr ( talk) 00:47, 26 March 2019 (UTC)
With most of the article based on old (before 2014) primary literature, there is more that can be covered on evolving clinical uses, beyond the short section here. Emerging clinical topics and reviews (although still based mostly on primary lab research):
These topics and reviews - all published within the last 5 years ( WP:MEDDATE) - provide higher-quality content more relevant to current understanding about ghrelin in physiological mechanisms, diseases, and drug development. -- Zefr ( talk) 15:27, 26 March 2019 (UTC)
New editor Suzanne Dickson, who has a long, distinguished publishing record on ghrelin - PubMed list here - made two mass-change edits on Oct 1-2. The first - which extensively cites her own work - sourced both reviews and outdated lab research, changed lede content, and provided improved sections on history, ghrelin receptor theory, and effects. The second has text and refs in [square brackets] possibly indicating copy from a different source. These edits were reverted as undiscussed here on the talk page, having format errors, having potential for WP:COI, and potential for copyright violations. I indicated to the editor in edit comments and on her talk page that providing rationale for the changes by talk page discussion, and in segments rather than a mass change, would be preferred to allow other editors to comment. The user's talk page shows her responses (which would better be transferred here for all editors to review). -- Zefr ( talk) 16:23, 2 October 2019 (UTC)
I would like to mention that "extensively" is an over-statement. Outdated means that wikipedia only valued work published recently. The work undertaken by the people in the field is not valued because it is old. I do not agree. I doubt anyone agrees that knows anything about the ghrelin field. In my edits, I included work from the giants who established the field ... CY Bowers, Roy G Smith, Kangawa and Kogima, David Cummings, Tamas Horvath, Matthias Tschöp and Mark Heiman, Jeffrey Zigman, Alfonso Abizaid, Zane Andrews and many more. I DID NOT COPY ANYTHING FROM ANY SOUCE OTHER THAN THIS WEB PAGE ITSELF. Everything in both versions was either written by me de novo over the past 36 hours or was a direct edit on your web page of the text already existing. Some text was simply moved and combined. The same information was repeated over and over, sometimes better than others. It seems like too much work to improve wikipedia. It seems experts especially are not the people you want to edit. I will write to all ghrelin researchers that are senior informing them of what has happened and asking them to read this and other dialogues. I know they also are disappointed with the ghrelin web page. At least I tried.
From my perspective, our biggest problem is attracting and retaining good editors. I loved what MontanaBW wrote: "Wikipedia needs to improve the sometimes hostile and toxic environment for article creators and editors, both new and old." Amen. We routinely drive away potential good editors with unrestrained criticism, which often comes across as an arrogant attack. I frequently encourage friends and colleagues to contribute to Wikipedia. The few that do usually tell me later something like, "Why should I spend time writing on a topic I know in-depth, only to have some jerk delete it all and throw a bunch of rules with colons at me and treat me like I'm an ignoramus?" I try my best to encourage them to "hang tough" and "don't let the rule-bound editors suffering from a superiority complex get in your way." But most have made up their mind and moved on to "volunteer work where my contributions are appreciated."
Suzanne Dickson recommended this edit for the lede on her talk page.
References
The proposed revision contains sources all over 9 years old, several of which are primary lab studies. It also is unformatted for WP:REFPUNCT. Following WP:MEDLEDE, I suggest this paragraph below could be used with the Muller review as the main ref, using some of the current lede. -- Zefr ( talk) 03:38, 3 October 2019 (UTC)
References
Is it appropriate to include animal research? David notMD ( talk) 04:27, 3 October 2019 (UTC)
I have deleted several sections of text and refs because the only citations were animal studies, hence not WP:MEDRS. Content can be restored if review articles based on human research can be identified. Also looking at content based on individual clinical trials rather than reviews. David notMD ( talk) 13:14, 3 October 2019 (UTC)
You suggest that the front section should read like this and below I make several points as to why the information should be improved:
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by the stomach,[1] and sometimes called a "hunger" hormone because ghrelin increases food intake.[2] Blood levels of ghrelin are highest during hunger.[2] When the stomach is empty, ghrelin is secreted, and when it is stretched, secretion stops.[2] It acts on hypothalamic brain cells both to increase hunger and to increase gastric acid secretion and gastrointestinal motility to prepare the body for food intake.[3] Ghrelin is a neuropeptide in the central nervous system.[2] Besides regulating appetite, it participates in regulating energy homeostasis, learning and memory, circadian rhythms, reward behavior, and taste sensation.[2] The receptor for ghrelin – the ghrelin/growth hormone secretagogue receptor (GHS-R) – is found on the same cells in the brain as the receptor for leptin, the satiety hormone that has opposite effects from ghrelin.[2]
1. Sentence 1 would be more informative if it indicated that the cells secreting ghrelin are the enteroendocrine cells of the stomach. There are ghrelin cells elsewhere in the gastrointestinal tract but 80% of circulating ghrelin comes from the stomach. It is very important that we cite the article of the lab who discovered it in 1999. It should read "Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach [1] [2], and is often called a "hunger" hormone because it increases food intake. [3]"
2. The following sentence should be deleted because it is factually incorrect: "When the stomach is empty, ghrelin is secreted, and when it is stretched, secretion stops.[2]". Ghrelin release has nothing to do with stomach stretching. Actually the correct information is written elsewhere on the page (at least 3 times) and so this sentence is redundant. Even the previous sentence gives the correct information. My suggestion is that these sentences (2 and 3) are combined and that you cite the article that first shows that ghrelin release is highest before mealtimes after which levels decline once again. I am sorry that it is from 2001 - it is just the article that is most important. Their article has been cited 1939 times. It is the first thing we tell students about plasma ghrelin levels. Therefore the new text should now read "Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes". [4]"
3. There are SERIOUS problems with the information in the next sentence: "It acts on hypothalamic brain cells both to increase hunger and to increase gastric acid secretion and gastrointestinal motility to prepare the body for food intake.[3]" The two parts of the sentence have correct information but they should not be combined in this way because it is midleading/wrong. Yes, ghrelin acts on the hypothalamus (as well as many other parts of the feeding circuits) and yes, this is likely important for its effects on food intake. Effects on gastric motility, especially involve effects locally in the gut. How ghrelin controls gastric acid secretion is unclear. The first ever article showing that the hypothalamus is a target for ghrelin agonists was the discovery that peripheral ghrelin injection causes activation of cells in the arcuate nucleus, for which I take credit. I like the idea that it prepares the body for food intake but that is an opinion and not a fact. Thus, my suggestion is: "Ghrelin may help prepare for food intake [5]by increasing gastric motility as well as gastric acid secretion. [6] Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [7] including the orexigenic neuropeptide Y neurones [8] that co-express agouti-related peptide (AgRP). Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A).
PLEASE NOTICE THAT ALL REFERENCES WERE ALREADY LISTED ON THE GHRELIN PAGE, INCLUDING ARTICLES TO WHICH I HAVE CONTRIBUTED.
Thus, putting it all together, my improved suggestion is ...
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach [9] [10], and is often called a "hunger" hormone because it increases food intake. [11] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [12] Ghrelin may help prepare for food intake [13] by increasing gastric motility as well as gastric acid secretion. [14] Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [15] including the orexigenic neuropeptide Y neurones [16] that co-express agouti-related peptide (AgRP). Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [17] whose brain distribution has been extensively mapped. [18]
Suzanne Dickson 07:00, 3 October 2019 (UTC)
References
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Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach [1] [2], and is often called a "hunger" hormone because it increases food intake. [3] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [4] Ghrelin may help prepare for food intake [5] by increasing gastric motility as well as gastric acid secretion. [6] Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [7] including the orexigenic neuropeptide Y neurones [8] that co-express agouti-related peptide (AgRP). Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [9] whose brain distribution has been extensively mapped. [10] Suzanne Dickson 07:03, 3 October 2019 (UTC)
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It is written: The receptor for ghrelin, the ghrelin/growth hormone secretagogue receptor (GHS-R), is found on the same cells in the brain as the receptor for leptin, the satiety hormone that has opposite effects from ghrelin.[10] Ghrelin also plays an important role in regulating reward cognition in dopamine neurons that link the ventral tegmental area to the nucleus accumbens[11][12] (a site that plays a role in processing sexual desire, reward, and reinforcement, and in developing addictions) through its colocalized receptors and interaction with dopamine and acetylcholine.[7][13] Ghrelin is encoded by the GHRL gene and is presumably produced from the cleavage of the prepropeptide ghrelin/obestatin. Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
Unlike the case of many other endogenous peptides, ghrelin is able to cross the blood-brain-barrier, giving exogenously-administered ghrelin unique clinical potential.[14]
———————
My points
1. The first sentence. We have now already mentioned the ghrelin receptor in the earlier section and we also have a whole section on the ghrelin page dedicate to the receptor. The first thing I expect to read about the receptor is not that it colocalises with another receptor. The sentence is also misleading as written because this colocalization is only known to occur on some cells and either unknown or not the case for other brain areas where the receptor is located. It is my suggestion that this information is therefore moved to the section on the receptor and that it is added as an extra piece of information about the receptor.
2. The second sentence is not linked at all to the first sentence. Suddenly we are reading about the reward system. This text can also be moved to a sections discussing the actions of ghrelin. If not, then I suggest you modify it. The term reward cognition is odd. It is over-simplified to write "in dopmine neurones" since an entire reward circuit is engaged. On the ghrelin page are articles to which I contributed showing that ghrelin engages the dopamine system. Again, it was another first from our group and it was published around the same time as Abizaid and colleagues (another important article). If you don't want original articles then there are plenty of reviews. Again, I have written many of them on this topic. So it would be hard to avoid citing this work somehow. I propose rather that lower down the page, we have a whole section dedicated to the actions of ghrelin that are linked to its effects on the reward system - for natural (food, gambling, sex) and artifical rewards (drugs, alcohol).
3. The third sentence is a complete switch in topic again but not entirely irrelevant and could be encorporated here as a separate topic. Since there were no sources for information obestatin, I added one.
4. The last sentence could be inserted into the previous text that I edited. I have done this below and inserted the same reference.
Therefore I propose that this section should now read ...
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by
enteroendocrine cells of the
gastrointestinal tract, especially the stomach
[1]
[2], and is often called a "hunger" hormone because it increases food intake.
[3] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes.
[4] Ghrelin may help prepare for food intake
[5] by increasing gastric motility as well as gastric acid secretion.
[6] Ghrelin can access the brain where it activates cells in the
arcuate nucleus of the hypothalamus,
[7] including the orexigenic
neuropeptide Y neurones
[8] that co-express
agouti-related peptide (AgRP). Because ghrelin, unlike many other endogenous peptides, is able to cross the
blood-brain-barrier, it gives exogenously-administered ghrelin unique clinical potential.
[9]
Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [10] whose brain distribution has been extensively mapped. [11]
Ghrelin also plays an important role in regulating reward processing engaging dopamine neurons that link the ventral tegmental area to the nucleus accumbens [12][11](a site that plays a role in processing reinforcment for natural rewards (food, sexual desire, gambling) and artificial rewards (drugs, alcohol and in developing addictions) through its colocalized receptors and interaction with dopamine and acetylcholine [13] [14]
Ghrelin is encoded by the GHRL gene and is presumably produced from the cleavage of the prepropeptide ghrelin/ obestatin. [15] Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
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I found it difficult to insert this reference in its original place because it is a book. It was placed after the reference to Naleid et al.
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 10:Neural and Neuroendocrine Control of the Internal Milieu". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 265–66. ISBN 9780071481274.
Suzanne Dickson 07:03, 3 October 2019 (UTC)
OK. I can't devote more time to this page at the moment. I hope you recognise that it is much improved.
Suzanne Dickson 08:00, 3 October 2019 (UTC)
Nestler EJ, Hyman SE, Holtzman DM, Malenka RC (2015). "Neural and Neuroendocrine Control of the Internal Milieu". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. pp. 245–267. ISBN 9780071827690. - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 09:46, 3 October 2019 (UTC)
References
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Thanks for helping to add the reference back. I am trying to do do as little as I can to disturb the references that were there before. Thanks everyone for support and help to improve the page. I just want the hormone that I devote my research to, to have a good page on wikipedia. I refer to wikipedia myself for information and I want to know it is a reliable source of information. I try to make the ghrelin page that. Suzanne Dickson 12:55, 3 October 2019 (UTC) — Preceding unsigned comment added by Suzanne Dickson ( talk • contribs)
--- Perfect Suzanne Dickson 05:02, 4 October 2019 (UTC) Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, [1] [2] [3] and is often called a "hunger hormone" because it increases food intake. [3] [4] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [3] [5] Ghrelin may help prepare for food intake [3] [6] by increasing gastric motility and gastric acid secretion. [2] [3]
Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [3] [7] [8] including the orexigenic neuropeptide Y neurones that co-express agouti-related peptide (AgRP) [3] [9] Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [3] [10] whose brain distribution has been extensively mapped. [3] [11]
References
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
Hello @ Markworthen and Zefr: what do you think of the following for the lede? :-) -- Signimu ( talk) 20:48, 6 October 2019 (UTC)
Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, [1] [2] [3] and is often called a "hunger hormone" because it increases food intake. [3] [4] Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. [3] [5] Ghrelin may help prepare for food intake [3] [6] by increasing gastric motility and gastric acid secretion. [2] [3]
Unlike many other endogenous peptides, ghrelin is able to cross the blood-brain-barrier [7] and access the brain where it activates cells in the arcuate nucleus of the hypothalamus, [3] [8] [9] including the orexigenic neuropeptide Y neurones that co-express agouti-related peptide (AgRP) [3] [10] Ghrelin's effects on food intake involve direct effects on hypothalamic, brainstem and forebrain areas and involve a dedicate receptor, the growth hormone secretagogue receptor 1A (GHSR-1A), [3] [11] whose brain distribution has been extensively mapped. [3] [12]
References
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
Are better refs available? Existing are from small human studies. David notMD ( talk) 01:02, 9 October 2019 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 28 August 2023 and 15 December 2023. Further details are available on the course page. Student editor(s): RCC23A ( article contribs). Peer reviewers: Vmt19, Achait2023.
— Assignment last updated by GradStudent4Life ( talk) 23:02, 5 December 2023 (UTC)
Under the section 'Locations of Action' subsection 'Sleep' I read: "A review reported finding strong evidence that sleep restriction affected ghrelin or leptin levels, or energy expenditure." When I follow the link mentioned to the PubMed abstract I read: "Overall, we did not find strong evidence supporting the significant impact of sleep restriction on mean leptin or ghrelin levels or energy expenditure. "
This seems to be the opposite of the line in Wikipedia. I do not know anything about Wikipedia-editing, so I do hope someone with more knowledge of both editing and/or ghrelin might take a look at this. — Preceding unsigned comment added by 2001:1C01:1D0D:4200:69D3:BBC2:D179:F5DA ( talk) 14:30, 7 February 2024 (UTC)