Talk:Ghrelin

Merge?

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)

Agreed —Preceding unsigned comment added by 59.101.89.179 (talk) 12:29, 8 June 2008 (UTC)

Contradiction?

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.

Ghrelin levels in the plasma of obese individuals are lower than those in leaner individuals. Ghrelin levels low -> low stimulation of appetite -> individual eats less -> individual tends to be leaner than comparable group... I too must say it seems illogical that persons with low Ghrelin levels tend to be obese. --Abdull 15:52, 25 May 2006 (UTC)

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)

Just a thought; deep sleep is linked to HGH production, and Ghrelin increases HGH production. HGH increases metabolism and reduces fat. --76.175.199.3 (talk) 06:39, 15 January 2008 (UTC)

"What is known is that ghrelin promotes weight gain and fat storage through its metabolic actions, decreasing the breakdown of stored fat for energy as well as curbing energy expenditure itself." - from the source article about an anti-ghrelin vaccine. But ghrelin increases HGH? This seems contradictory. --76.175.199.3 (talk) 08:08, 15 January 2008 (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)

Ghrelin expression in hypothalamus

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)

Can we have the lead paragraph written in normal English?

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 is something wrong with the first sentence

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

Cardiovascular functions?

"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)

"suppresses appetite"

"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)

What triggers production of ghrelin?

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)

Love the complete contradiction found in two nearby sections/

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)

Rewrite introduction

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)

Lead

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)

I agree with Boghog - this article needs to reflect this content in the lead like other peptide articles. MOS:MCB is also relevant/important in determining the layout of the article. Seppi333 (Insert 2¢ | Maintained) 11:51, 4 May 2014 (UTC)

I have submitted the above difference of opinion for dispute resolution. My view is that the Lead show focus on the function and significance of the hormone: the details of its transcription and chemical relationship to compounds which are not the subject of the page are best left in the body of the page, where the details can be expanded. Not a right or wrong issue just a opinion and personal preference. Is it a detail or a theme?

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)

It's a convention in the manual of style. There's wiggle room with the MOS, so if you truly feel it's not lead worthy, I'm okay with not including it so long as there's a rational justification for doing so. MOS:MCB is what indicates stating it there with the following language regarding the lead section:

1. Lead

   The lead section is defined as "the section before the first headline. The table of contents, if displayed, appears between the lead section and the first headline."

   The first sentence of the lead should define what the scope of the article is. For genes/proteins in which a human ortholog exists, "<recommended UniProt name> is a protein that in humans is encoded by the <approved HUGO gene symbol> gene." would be appropriate.

Regards, Seppi333 (Insert 2¢ | Maintained) 22:28, 21 May 2014 (UTC)

Sentence on reward perception in lead

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)

Sounds fine. I added it with a new ref, but it's also discussed lightly in the body. Seppi333 (Insert 2¢ | Maintained) 08:26, 6 May 2014 (UTC)

I've copyedited that material and added a ref per your request. Best, Seppi333 (Insert 2¢ | Maintained) 22:30, 21 May 2014 (UTC)

PTSD ongoing research

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)

Blood levels

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)

New view of ghrelin as fat storage promoter, not appetite promoter

“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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Confusing statement

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)

Inflammation and GI

This section was removed because

• the sources date from 2004-10, so are outdated per WP:MEDDATE
• no source is a WP:MEDRS-quality review
• the sources are from lab research and discuss "animal models" (WP:PRIMARY)
• the content exaggerates interpretations from lab results and is speculative, using such unverified terms as "possibility" and "beneficial", WP:V
• checking the PubMed review literature (we don't use Google as a source), there are no high-quality 2014-19 reviews discussing any effect of ghrelin or its drug agonists specifically on the human GI system or its mechanisms of function

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)

@Zefr: The material that was deleted in this edit is both peer reviewed and secondary (see PMID 19788870). Per WP:MEDANIMAL, it is OK to include this material as long as it is made clear that it is based on animal studies. Boghog (talk) 02:43, 26 March 2019 (UTC)

I would ask: is a 2009 short review (really just an op-ed) – based on rodent and in vitro studies dated 1999-2009 – that then speculates on vague mechanisms and comes to a conclusion that a ghrelin effect on inflammation "still remains to be explained", the best we can do? Here is possibly a more complete MEDRS-quality review on ghrelin's putative anti-inflammatory effect. Ghrelin and pro- or anti-inflammatory effects are a complex topic requiring stronger sources and more neutral discussion than the article currently contains. --Zefr (talk) 13:24, 26 March 2019 (UTC)

Zefr (talk · contribs), Boghog (talk · contribs) - I agree with Boghog in general altho in this case I think it's worth asking to raise the bar a bit - the edit did rely upon some pretty old studies cited directly. The question "is this the best" is interesting, but Wikipedia isn't actually about the "best" per se - I don't revert every content addition that isn't an A+, best possible summary of the evidence. And we can always do subpages as things get more and more detailed. "The best" is not really compatible with the encyclopedia anyone can boldly edit. We iterate and improve. I'm also skeptical of the statement that "there are no high-quality 2014-19 reviews discussing any effect of ghrelin or its drug agonists specifically on the human GI system"; a PubMed search on reviews in the last 5 years with ghrelin in the title or MeSH pulls up 255 results, many of which discuss seem to discuss the human physiology and GI tract. Winnowing down to include "inflammation" (MeSH or title) pulls up 11. II | (t - c) 07:45, 20 April 2019 (UTC)

If there are better sources available (i.e., more recent peer-reviewed secondary sources), they we should definitely use those. The review that was questioned above PMID 19788870, could possibly be replaced or supplemented with PMID 29248481 and the one listed below (PMID 26809582). Boghog (talk) 09:55, 20 April 2019 (UTC)

Emerging clinical uses

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):

• metabolic syndrome, Pereira et al.
• immune system regulation, Pereira
• cachexia and respiratory disease, PMID 28652535
• neurodegenerative disorders, PMID 26809582
• drug abuse and addiction, Panagopoulos
• potential ghrelin drugs for treating cancer cachexia, PMID 28751550

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)

Mass edits on Oct 1-2 by a ghrelin research expert

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)

The following is Suzanne Dickson's summary of the edits desired, as provided verbatim from my talk page. The information from her as an expert is valuable, and the article needs considerable change, but there are concerns about bias, possible copyright issues, use of jargon, and use of primary research, among others. --Zefr (talk) 16:48, 2 October 2019 (UTC)

I'm fairly new at editing wikipedia. The ghrelin page that I edited did not give a proper overview of ghrelin. It was full of fragmented information that does not give a correct view regarding the hormone. Having worked on this hormone for over 20 years, I feel qualified to edit it and place correct information there, including the key references for the most important findings. If you want to have correct information and sources on the page on ghrelin, I suggest that you accept my changes. There are 10330 articles published on ghrelin. Do you know the expression "you cannot see the wood for the trees". It is important that the balance of information is correct such that you learn what the hormone does and how it does it. I have referenced all of the main articles. You can also see that most of the references are published in top journals and are considered authority in the field. The breakthrough discoveries - not someone's poorly informed or poorly phrased opinion. Given my expertese, it is surely a good thing that I spend several hours editing the information to improve it. Much that is written is wrong. It is stated that ghrelin increases appetite or hunger (in different places). This idea stems from the fact that it increases food intake - but does it really increase appetite or hunger? It increases food intake. I then provide a logical reasoning why it gained status as a hunger hormone, including reference to the key hormone. It is hunge assumption that something that increases food intake does so by increasing hunger or appetite. You don't need to feel appetite or hunger to eat. Although I have worked with ghrelin for decades (one of the first people in the field), I have NEVER before heard it being called lenomorelin until I read this on wikipedia. The term "ghrelinergic cell" is a made up term. It is better to refer to them as enteroendocrine cells that produce ghrelin. Ghrelin is not made throughout the gastrointestinal tract - mostly in the stomach. The first thing we learn on the web page about the ghrelin receptor is that it is expressed on the same cells as leptin. Arguably, this information is very misleading. If you look up the distribution of the ghrelin receptor and the distribution of the leptin receptor in the brain, you will find there there may be some overlap in the arcuate nucleus but this is absolutely not proven for the rest of the brain. Besides, this fact is not the first thing we should learn about the receptor. I didn't edit it yet but the sentence about reward cognition is odd. Ghrelin receptors are present on some dopamine neurones in the VTA that are involved in reward and motivation. But usually we don't use the term reward cognition. I could easily correct that sentence to make it informative. In the historical section that I expanded considerably, I provide the full history with only key articles cited. Here I added much useful information. There is much repeat between the different sections, which I tried to reduce. There is still a lot of work to do on that page to make the information correct. The sentence "When the stomach is empty, ghrelin is secreted. When the stomach is stretched, secretion stops" is ridiculous and not founded on real science. The correct information is in the reference to David Cummings article from 2000, which I included. I think the top researchers in the world that work on ghrelin would support these changes and would be happy to get their authority on it as well. I am sure they would welcome edits that provide improvement and accuracy. I would be very disappointed in wikipedia if it doesn't listen to reason over what is correct, what is wrong and what is misleading. It shouldn't become a dumping ground for people to get attention to their publications, without taking into account the big picture. Suzanne Dickson (talk) 05:38, 2 October 2019 (UTC)

Incorrect evaluation of my edits on the ghrelin page.

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.

Your work and contributions are valued, but keep in mind Wikipedia is an encyclopedia, not a journal for publishing comprehensive review articles and expert interpretations. Please review WP:MEDMOS specifically for a) common pitfalls, b) tangents, c) language, d) writing style, and e) citing sources. As constructive follow up, I suggest - other editors can agree or dispute - that you propose revisions section-by-section as you did on your talk page, i.e., start with the lede and general information (see WP:LEAD), and what changes you recommend while using reviews as sources. After this is reviewed, discussed, and edited, we can move to other revisions and sections. --Zefr (talk) 17:17, 2 October 2019 (UTC)

I wrote the following two days ago:

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."

Let me hasten to say that I do not see Zefr creating a "toxic environment" or launching an "arrogant attack". In fact, Zefr's responses are calm, polite, and they acknowledge Suzanne Dickson's expertise and substantial scientific contributions.

And, at the same time, I understand and empathize with Suzanne Dickson's perspective. She (if that is the appropriate pronoun to use) has clearly done her homework when it comes to learning some of the nitty gritty details of Wikipedia editing. In addition, while acknowledging I am not an expert in this area, I found the majority of her additions & edits to be appropriate, well-sourced (referenced), and certainly well-informed. I do not perceive an attempt to "get my citations on Wikipedia" for some sort of personal gain. I would not have reverted her edits in their entirety, but would have instead reached out to her and offer to provide some "mentoring", edit suggestions or guidance, and most importantly, connect her with other biomedical scientists on Wikipedia for moral support, Wikipedia mentoring, peer review, etc.

@Suzanne Dickson: I highly recommend joining WikiProject Medicine. Reach out for support, advice, & camaraderie on the WikiProject Medicine Talk page.  - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 20:22, 2 October 2019 (UTC)

Markworthen: I welcomed Suzanne Dickson to WP:MED yesterday at her talk page where I raised concerns about mass changes and potential for bias and COI, to which she replied. After the first mass change was reverted yesterday - with request for talk page discussion and editor review - another large edit today was added, containing some of the same formatting errors as in the first. Her editorial value for content is conspicuous, but it would be helpful, in my view, if editors could preview and discuss changes in segments to allow content, sources, and format to be agreed and correctly formatted before going into the article, a process consistent with helping a new editor follow WP style. --Zefr (talk) 20:46, 2 October 2019 (UTC)

I agree with you on a good way to introduce significant additions, deletions, or changes to an article. But I think you're expecting too much from an editor during their first days and weeks on Wikipedia. ¶ My emphasis, as you no doubt discerned, is on recruiting and retaining good editors. In that regard, how we communicate with new editors is crucial. All of us are subject to psychological reactance, but we (including myself) often blame, minimize, or discount the other person (the one who is in reactance mode). The antidote is empathy. ¶ It goes both ways of course, e.g., I should strive to understand why an editor deleted, reverted, or criticized my work on Wikipedia. However, when I communicate with new editors, empathy is much more important than trying to get them to understand why I'm right about the proper procedures. ¶ As Stephen Covey wrote (along with others before him through the ages), "Seek first to understand than be understood." (I think of it as, "Seek first to understand before I seek to be understood" because the saying flummoxed me for many years when I was younger.)   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 04:47, 3 October 2019 (UTC) (edited on 3 Oct 2019 @ 08:56 UTC)

P.S. I subsequently noticed that you had invited Suzanne Dickson to join WP:MED right from the get-go. Excellent!   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 09:01, 3 October 2019 (UTC)

Lede revision

Suzanne Dickson recommended this edit for the lede on her talk page.

Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone that is produced by the stomach. It is often referred to as a "hunger" hormone, because ghrelin delivery acutely increases food intake and feeding behaviours and also because plasma levels are highest before meals when hungry. Daily ghrelin injections increase body weight in rodents by increasing respiratory quotient.

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)

Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by the stomach, and sometimes called a "hunger" hormone because ghrelin increases food intake. Blood levels of ghrelin are highest during hunger. When the stomach is empty, ghrelin is secreted, and when it is stretched, secretion stops. 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.

Ghrelin is a neuropeptide in the central nervous system. Besides regulating appetite, it participates in regulating energy homeostasis, learning and memory, circadian rhythms, reward behavior, and taste sensation. 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.

References

I'm interested in Suzanne Dickson's perspective, but your (Zefr's) modification makes sense to me. (I'm not a fan of Wikipedia's overemphasis on secondary sources, but I've learned to accept that I'm in the minority on that policy.)   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 04:12, 3 October 2019 (UTC)

Animal research?

Is it appropriate to include animal research? David notMD (talk) 04:27, 3 October 2019 (UTC)

@David notMD: No, it's not for medical articles. Although it would be very interesting, animal studies are too variable and not often translatable to human, and the article should reflect info for the general public (who might not necessarily differenciate between what is of scientific interest but hypothetical, with what is practically applicable for humans). Please thus only use sources about human trials, and foremost reviews on RCT trials, see WP:MEDRS and WP:MEDHOW for more infos. Hope this helps, have a nice day! --Signimu (talk) 04:31, 3 October 2019 (UTC)

I would like to hear from experienced editors who have been actively commenting on this Talk page, as some content in the article rest on animal studies. David notMD (talk) 04:35, 3 October 2019 (UTC)

See above two sections for discussion of primary vs. secondary sources (among other topics). And please don't bite the newcomers. (I'm not saying you were biting anyone. Just adding that reminder b/c we really need to recruit and retain good editors.)   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 05:08, 3 October 2019 (UTC)

I see no problem since there are no newcomers here (I'm contributing since 2006 ;-) ). I have arguably less experience on MED (2 years), but everytime there was animal studies on the articles I worked on, they had to be removed per WP:MEDRS. --Signimu (talk) 06:12, 3 October 2019 (UTC)

Yeah, I guess I am letting my passion for retaining good editors run amok. I'll reign it in. :^)   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 08:50, 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)

I returned to this article today after a 5 1/2 year absence. In May 2014 I contributed 284 edits, and as a result I am the author/editor of about one-fifth of the article. Little had changed in the article since then, until about 5 weeks ago. I was new to WP as of April 2014, and was not aware that animal studies and primary research were discouraged by WP policy. I completely agree with all of the recent deletions by David notMD: those additions of mine do not belong in this article. As time permits, I may contribute to the discussion and revision of the Lead: much has been learned about ghrelin in the last 5 1/2 years, and reasonably current references then are now potentially obsolete. Regards to all who have contributed here over the last 5 weeks, IiKkEe (talk) 10:28, 4 November 2019 (UTC)

Ghrelin: The front section is important

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 , and is often called a "hunger" hormone because it increases food intake."

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"."

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 by increasing gastric motility as well as gastric acid secretion. Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, including the orexigenic neuropeptide Y neurones 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 , and is often called a "hunger" hormone because it increases food intake. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility as well as gastric acid secretion. Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, including the orexigenic neuropeptide Y neurones 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), whose brain distribution has been extensively mapped.

Suzanne Dickson 07:00, 3 October 2019 (UTC)

References

Here is the same text without the other information

Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach , and is often called a "hunger" hormone because it increases food intake. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility as well as gastric acid secretion. Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, including the orexigenic neuropeptide Y neurones 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), whose brain distribution has been extensively mapped. Suzanne Dickson 07:03, 3 October 2019 (UTC)

References

Ghrelin - the next section and some suggestions

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 , and is often called a "hunger" hormone because it increases food intake. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility as well as gastric acid secretion. Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, including the orexigenic neuropeptide Y neurones 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.

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), whose brain distribution has been extensively mapped.

Ghrelin also plays an important role in regulating reward processing engaging dopamine neurons that link the ventral tegmental area to the nucleus accumbens [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

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.

---

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)

@Suzanne Dickson: I edited the Malenka, et al. citation (diff). Does this look okay to you?

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

References

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)

Dear @Suzanne Dickson:, here is my modest contribution to help this discussion progress. Unfortunately, even if you do keep the references as they were, it's not because they are there currently that it's any good, as they can be deleted anytime if they do not fit WP:MEDRS. Thus, ensuring that each claim is backed by a review makes the claim more "future-proof", in the sense that it has less chances to be removed. Since you did a lot of work to provide Wikipedia with more accurate information, it's important we ensure your writing does not get suppressed at a later time just because the references are not deemed adequate. I understand that you used as references the "landmark papers", but they are not enough here as they are not reviews. But, according to WP:MEDRS, it is possible to use both the landmark paper + a review citing it. Thus, I mainly did in the following proposition only 2 things:

1. I used the muller review as suggested above by Zefr as the review paper, in which I tried to confirm that each sentences can indeed be found in some form, if it corresponded then the muller review was added in addition to the landmark paper. I could confirm every sentences and sources except Hill, GM (January 1975). "Simplified technic for jacket crown impressions". I could not find any citation of this paper either, nor could read it, as it appears too old to be digitized online. But the same claim (ghrelin being called "hunger hormone" because it increases food intake) can be found in the muller, so I added it to back up.
2. I fixed the citation formatting (notice that on Wikipedia the citations should be after punctuation, not before), and shortened some easy instances (eg, "as well as" -> "and") without denaturing the meaning.

Having said that, I would humbly recommend to try to vulgarize further the info for the lay person. Not in the sense that it's too complex, but more in the sense that "what would be interesting to know, to take home, for a lay person who wants to learn about ghrelin under 2 minutes?". To give a concrete example, I found that the mention about "ghrelin being able to cross the blood-brain-barrier contrary to many other endogenous peptides", isn't it accurate?

Here is my proposition below. --Signimu (talk) 00:07, 4 October 2019 (UTC)

--- 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, and is often called a "hunger hormone" because it increases food intake. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility and gastric acid secretion.

Ghrelin can access the brain where it activates cells in the arcuate nucleus of the hypothalamus, including the orexigenic neuropeptide Y neurones 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), whose brain distribution has been extensively mapped.

References

---

Lede discussion

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, and is often called a "hunger hormone" because it increases food intake. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility and gastric acid secretion.

Unlike many other endogenous peptides, ghrelin is able to cross the blood-brain-barrier and access the brain where it activates cells in the arcuate nucleus of the hypothalamus, including the orexigenic neuropeptide Y neurones 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), whose brain distribution has been extensively mapped.

References

I don't know enough about the topic. But I appreciate you asking. :0)   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 20:59, 6 October 2019 (UTC)

Thank you Markworthen Well if nobody else has any objection, I think we can try to change the lede, if this goes well we can later continue with the same process to prepare the first section as Suzanne Dickson suggested --Signimu (talk) 20:41, 7 October 2019 (UTC)

Gastric bypass surgery refs

Are better refs available? Existing are from small human studies. David notMD (talk) 01:02, 9 October 2019 (UTC)

Wiki Education assignment: Adv Molecular Bio Bass-FSU-Fa23

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)

Contradictory information ghrelin and sleep

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)