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Feel free to drop a note on my talk page if you have any problems. I wish you all the best on your wiki voyages! Zefr ( talk) 17:23, 1 October 2019 (UTC) reply

Hello. Some of your recent genre changes, such as the one you made to Ghrelin, have conflicted with our neutral point of view and verifiability policies. While we invite all users to contribute constructively to Wikipedia, we urge all editors to provide reliable sources for edits made. When others disagree, we recommend you seek consensus for certain edits by discussing the matter on the article's talk page. With respect to your knowledge on this topic, please edit in logical steps, rather than making a mass change. See WP:MOS for general style, and WP:MEDMOS for medical content. Feel free to discuss here on your talk page, as I am following and others may contribute guidance. Zefr ( talk) 17:25, 1 October 2019 (UTC) reply

Suzanne Dickson. I have reviewed your comments below and reverted your inserted text and own sources on the Ghrelin article where you appear to have a substantial conflict of interest and potential copyright violations by using directly copied content. I suggest you seek advice about your editing and use of your own materials at WP:HELPDESK. I reviewed your substantial publication history on PubMed, and can see your expertise and potential value to Wikipedia, but it is a violation of Wikipedia policies to copy directly from your own work, and to rely almost exclusively on your own sources; see WP:SELFPUBLISH. Other editors or Wikipedia admin personnel may contact you. The explanations and sources below are relevant to improving the ghrelin article, but using your own copied content and your own sources is not the way Wikipedia works - a WP:NPOV (neutral) view is preferred from general reviews - not primary research, but major review publications explained in WP:MEDREV - and major content changes like you made yesterday are subject to review first by multiple-editor consensus, WP:CON, from a talk page discussion. Also, changes constructed on scientific jargon like you used are discouraged, WP:NOTJARGON; Wikipedia is a resource for a "general literate user", not a fellow expert in the research discipline; see MEDMOS pitfalls here. More later. -- Zefr ( talk) 14:44, 2 October 2019 (UTC) reply

While reading the ghrelin page, I found much of the information fragmented, repeated and misleading in places. In particular 1. It should be very clear that the evidence base supports the idea that ghrelin increases food intake and that it increases growth hormone secretion. It has some other actions that should not receive the same weight in the text as these effects. 2. The evidence should be presented here that it has gained status as a hunger hormone (based on the fact it increases food intake acutely and the fact ghrelin levels increase prepradially). 3. The historical section is incomplete and should cite the key articles, with an explanation. 4. Information about the ghrelin receptor appears twice and should be condensed. 5. The first thing we learn on this page about the ghrelin receptor is that it is located on neurones expressing leptin. While I doubt this is true over the entire brain, the text needs to be modified to give a more accurate account of the receptor and its distribution. 6. The section on ghrelin and reward is muddled and doesn't provide a full account. 7. I have never heard of “lenomorelin, despite having worked on ghrelin over 25 years. 8. The sentence “When the stomach is empty, ghrelin is secreted. When the stomach is stretched, secretion stops” should be deleted or improved. Actually I refer to David Cummings work in my edited improved text. 9. I think it is important to have the most important articles cited correctly.

To begin the process, I made the some edits that will follow.

Suzanne Dickson 09:37, 2 October 2019 (UTC)

Ghrelin (pronounced /ˈɡrɛlɪn/), the "hunger hormone", also known as lenomorelin (INN), is a peptide hormone produced by ghrelinergic cells in the gastrointestinal tract.[1][2] Ghrelin functions as a neuropeptide in the central nervous system.[3] Besides regulating appetite, it also plays a significant role in regulating energy homeostasis.[4]

When the stomach is empty, ghrelin is secreted. When the stomach is stretched, secretion stops.a 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.[5]

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.[6] Ghrelin also plays an important role in regulating reward cognition in dopamine neurons that link the ventral tegmental area to the nucleus accumbens[7][8] (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.[3][9] 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.[10]

Ghrelin (pronounced /ˈɡrɛlɪn/), is a circulating hormone that is produced by the stomach ^[1]. It is often referred to as a "hunger" hormone, because ghrelin delivery acutely increases food intake ^[2] and feeding behaviours ^{[3] [4] [5]} and also because plasma levels are highest before meals when hungry ^[6]. Daily ghrelin injections increase body weight in rodents by increasing respiratory quotient ^[7].

Then I suggest combining the information I removed into headed sections on ghrelin action and the ghrelin receptor, GHSR1A.

Even before ghrelin or its receptor were discovered, a great deal was already known about its effects and mode of action thanks to studies with so-called growth hormone secretagogues, that are now recognised as ghrelin mimetics. The first growth hormone secretagogues were peptides generated by CY Bowers and coworkers (Tulane University), developed to potently stimulate growth hormone release by a direct pituitary action, synnergising with the endogenous growth hormone releasing hormone (GHRH), to obtain a maximal growth hormone response. It soon became apparent that these compounds also act in the brain to activate cells in the arcuate nucleus[8] that include not only GHRH-containing cells but also the orexigenic neuropeptide Y (NPY) cells[9] that coexpress Agouti-Related Peptide (AgRP). Another key advance was the identification, in 1996, of a receptor, the growth hormone secretagogue receptor, by the group of Roy G Smith and colleagues at Merck[10]. In 1999, the first endogenous ligand for this receptor was identified and named "ghrelin"[11] based on its role as a growth hormone-releasing peptide, with reference to the Proto-Indo-European root gʰre-, meaning "to grow".[12]

Here is a starting point for people to add specific information about the receptor, which is separate from the sections about ghrelin's physiological effects.

Suzanne Dickson 09:37, 2 October 2019 (UTC)

Ghrelin exerts its biological effects by binding to GHSR-1A ( growth hormone secretagogue receptor 1A) ^[8]. A second slice variant of this receptor exists in a truncated form (GHSR-1B). The distribution of GHSR1A in rodent brain has been described in detail ^[9]. It is distributed within hypothalamic, brainstem and forebrain areas of relevance for feeding control ^[10]. GHSR-1A is also present in abundance in the pituitary, on the vagus nerve (on both afferent cell bodies and efferent nerve endings) and throughout the gastrointestinal tract[15][40]. Suzanne Dickson 09:36, 2 October 2019 (UTC)

These need to be gathered and organised, minimizing repeat.

Control of food intake

Acute administration of ghrelin causes a feeding response in rodents ^[11] and in humans ^[12]. Typically this feeding response lasts up to 6 hours but does not impact on 24 hour intake ^[13]. However, ghrelin does not increase meal size, only meal number ^[14]. It appears to have a role in meal initiation ^[15] rather than over-eating. Ghrelin also impacts on food choice ^{[16] [17]}. The NPY/AgRP neurones in the arcuate nucleus are widely believed to be the main site at which ghrelin induces a feeding response, although ghrelin can also drive a food intake response when delivered to brain areas that include the ventral tegmental area and nucleus accumbens ^{[18] [19]}, the amygdala ^[20], the hippocampus ^[21], in discrete brainstem areas as well as at several other hypothalamic sites, such as the lateral hypothalamus ^[22] and paraventricular nucleus ^[23].

Control of feeding behaviours

Ghrelin has been shown to promote behaviours that help obtain food. These include food forraging ^[24], food anticipatory ^{[25] [26]} and food motivation ^{[27] [28] [29]}. Ghrelin signalling is required for reward from food ^[30] as well as alcohol ^[31]and other addictive drugs such as cocaine ^[32]. Ghrelin appears to enhance reward by engaging the midbrain dopamine neurones of the ventral tegmental area to the nucleus accumbens ^{[33] [34]}. Thus, addition to its function in energy homeostasis, ghrelin also activates the dopaminergic reward pathway, a circuit that communicates the hedonic and reinforcing aspects of natural rewards such as food and addictive drugs such as ethanol ^[35]. Ghrelin receptors are located on neurones in this circuit ^[36] and ghrelin delivery has been shown to activate this pathways causing an increase in accumbal dopamine release ^[37].

Control of energy homeostasis

Ghrelin is a participant in regulating the complex process of energy homeostasis which adjusts both energy input – by adjusting hunger signals – and energy output – by adjusting the proportion of energy going to ATP production, fat storage, glycogen storage, and short-term heat loss. The net result of these processes is reflected in body weight, and is under continuous monitoring and adjustment based on metabolic signals and needs. At any given moment in time, it may be in equilibrium or disequilibrium. Gastric-brain communication is an essential part of energy homeostasis, and several communication pathways are probable, including the gastric intracellular mTOR/S6K1 pathway mediating the interaction among ghrelin, nesfatin and endocannabinoid gastric systems ^[38] and both afferent and efferent vagal signals.

Ghrelin and growth hormone secretagogues increase body weight and fat mass ^{[39] [40] [41]}.

Studies have shown that ghrelin levels are negatively correlated with weight. This data suggests that ghrelin functions as an adiposity signal, a messenger between the body's energy stores and the brain ^[42].

Suzanne Dickson 09:36, 2 October 2019 (UTC)

Hello, Suzanne Dickson. We welcome your contributions, but if you have an external relationship with the people, places or things you have written about in the page Ghrelin, you may have a conflict of interest (COI). Editors with a conflict of interest may be unduly influenced by their connection to the topic. See the conflict of interest guideline and FAQ for organizations for more information. We ask that you:

• avoid editing or creating articles about yourself, your family, friends, company, organization or competitors;
• propose changes on the talk pages of affected articles (you can use the {{ request edit}} template);
• disclose your conflict of interest when discussing affected articles (see Wikipedia:Conflict of interest#How to disclose a COI);
• avoid linking to your organization's website in other articles (see WP:Spam);
• do your best to comply with Wikipedia's content policies.

In addition, you are required by the Wikimedia Foundation's terms of use to disclose your employer, client, and affiliation with respect to any contribution which forms all or part of work for which you receive, or expect to receive, compensation. See Wikipedia:Paid-contribution disclosure.

Also, editing for the purpose of advertising, publicising, or promoting anyone or anything is not permitted. I'll discuss this further on your talk page and the Ghrelin talk page, but you are literally lifting text out of your own publications and copying them into the Ghrelin article. Please read the COI notice and declare that you have a conflict. It is not good to rely so heavily on your own work, then copy it into Wikipedia. Zefr ( talk) 14:21, 2 October 2019 (UTC) reply

Anything I uploaded today was written by me today or yesterday. I spent much time on pubmed retrieving peoples articles. So, there is nothing pasted from things I have published elsewhere.

I do include a few of my own publications on the page. That is because we contributed to the field of research, If those leading the research field cannot contribute to wikipedia, there is something fundamentally wrong.

Of course I can indicate which articles I contributed to. No problem. I guess that is what you mean by conflict of interest.

This is just getting too difficult for me. I invested a lot of time into this web page to get the correct information on your site. It was much better in content. Correct. Less repeat. Cites ket findings (mostly not by my group).

The only issue is the reference to my own articles but I can't figure out how to deal with that from the web pages that you directed me to.

Here I don't reference departments.

I see the problem with citations that look as if they are from an external source. If you look carefully you will see that ALL of those that are incorrect come from this wikipedia page (as that was my source).

Suzanne Dickson 14:36, 2 October 2019 (UTC) Suzanne Dickson 17:36, 2 October 2019 (UTC)

After a brief review of the article in question, I do not see evidence of biased editing for personal gain. Instead, I see well-informed contributions from an expert in the field. Please, please let us not drive away another smart, generous, expert editor.   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 20:32, 2 October 2019 (UTC) reply

For what it's worth, you also have my support. I am convinced that content (and foremost correct content) is far more important for an encyclopedia than its form. I hope this will resolve peacefully and that you will start enjoying the good sides of Wikipedia :-D Thank you for your contributions! -- Signimu ( talk) 04:24, 3 October 2019 (UTC) reply

Hi Suzanne Dickson! Thanks for contributing to Wikipedia. Be our guest at the Teahouse! The Teahouse is a friendly space where new editors can ask questions about contributing to Wikipedia and get help from experienced editors like Doctree ( talk). Visit the Teahouse We hope to see you there! Delivered by HostBot on behalf of the Teahouse hosts 16:04, 2 October 2019 (UTC)

P.S. I added my perspective to the discussion on the Ghrelin Talk page.   - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 20:41, 2 October 2019 (UTC) reply

I saw that there was an earlier discussion about ghrelin levels being low in obesity despite it causing an increase in food intake. This is correct. Not my work but it has been reporduced by many groups. It is not very confusing actually. It just tells us that obesity is not causes by high ghrelin levels. What ghrelin does is to organise food intake into meals. It does not necessarily increase 24 hour food intake. So, yes it is orexigenic (increases food intake), yes levels are a little lower in obese patients.

The only exception is Prader Willi patients who are hyperphagic and obese. They have high circulating ghrelin levels and in these patients ghrelin may have a role in their over-eating.

At the other end of the spectrum, malnutrition (eh anorexia or cachexia) increases plasma ghrelin levels. They have a high drive to eat, which gets even higher when they do not eat.

Suzanne Dickson 13:53, 3 October 2019 (UTC)

Your User page is intended to briefly describe your background and intentions toward being a Wikipedia editor. It is not intended to be a third-person written version of your CV. See Wikipedia:User pages. Many editors have advanced degrees in their areas of interest, and academic careers, but the User pages are not intended as displays for all that. The content you have could be move to your Sandbox, or to a draft of an article to be submitted to Wikipedia, but people are strongly advised against crafting an article about themselves. See WP:Autobiography. David notMD ( talk) 15:21, 3 October 2019 (UTC) reply

So, this is not the place for it? I saw the wikipedia entry of a colleague Martien Kas. How do I have a page like that on wikipedia myself?

Suzanne Dickson 15:26, 3 October 2019 (UTC)

@ Suzanne Dickson: I would not worry about it, WP:Autobiography is about guidelines for creating main Wikipedia articles, but here this is your userspace, you can write whatever you want as long as there is no profanity, no diffamation, no harassment, etc. However, most users are not indeed interested in your real-life CV but your "Wikipedian CV", but your real-life CV does matter to comply with WP:COI. In practice, I would propose that you write: when you joined, why you joined, and a brief description of your real-life job and affiliation with a link to a more extensive CV (you can copy-paste your current page there for example). Concrete example:

"Hello, I am Suzanne Dickson, I joined Wikipedia on ..., I intend to enhance articles pertaining to my expertise, eg Ghrelin. I am a Professor in Neuroendocrinology, at the Institute of Neuroscience and Physiology at the Sahlgrenska Academy at the University of Gothenburg in Sweden, leading the Neurobiology of Appetite group focusing on ghrelin. For more details, see my User_talk:Suzanne_Dickson/Curriculum_Vitae."

If you click on the last link, this will lead you to a new subpage of your userspace (you can create any page under your userspace, meaning you write /info/en/?search=User:Suzanne_Dickson in the URL bar and then add /NameOfThePageYouWantToCreate. Here, this will create the /info/en/?search=User:Suzanne_Dickson/Curriculum_Vitae page, where you can copy-paste what is currently on your /info/en/?search=User:Suzanne_Dickson page. Likewise, you can create a /info/en/?search=User:Suzanne_Dickson/Draft page to draft anything you want on it (so that you can test formatting, sentence phrasing, etc.) before modifying an article. It's up to you, your userspace is yours :-)

I hope this clarifies the somewhat implicit expectations and inner workings of Wikipedia userspaces :-) Have a great day! -- Signimu ( talk) 18:22, 3 October 2019 (UTC) reply

The Martien Kas article is a Wikipedia article about Martein Kas, not written by Kas. If your academic career is noteworthy to the point that people have published articles about you, then you might be an appropriate topic that in time someone will write. Again, Wikipedia strongly advises people not to create an article about themselves, as difficult to achieve a neutral point of view. In passing, the article about Kas is so weakly referenced (mostly content from his CV) that it probably should not have been accepted as an article, and is a plausible candidate for Articles for Deletion. Minimally, it needs more references. And that probably applies to every other article the creator created. David notMD ( talk) 18:28, 3 October 2019 (UTC) reply

Useful Thanks Suzanne Dickson 19:26, 3 October 2019 (UTC)

Lastly, indent comments to differentiate from the previous one by adding one or more : at beginning of comment. And 'sign' by typing four of ~ at end. David notMD ( talk) 21:16, 3 October 2019 (UTC) reply

I provided a new page Suzanne Dickson 12:23, 7 October 2019 (UTC)

This is an aside—something to check out when you can. ... You might be interested in reading or contributing to the WikiJournal of Medicine and the WikiJournal of Science. From the WikiJMed home page:

WikiJournal of Medicine is an ISSN-registered, peer reviewed, open access journal in medicine and biomedicine published free of charge. The journal is hosted by the Wikimedia Foundation, the same organization that runs Wikipedia. Articles that pass peer-review are published as a citeable, indexed PDF, and suitable text and images are integrated into Wikipedia and related projects (with a link to the indexed PDF). The vast readership of Wikipedia results in a high effective impact of included works.

The journal publishes both review articles and original research in various formats. WikiJournals enable academic and medical professionals to contribute expert knowledge to the Wikimedia movement in the academic publishing format that directly rewards them with citable publications. Included works are assigned DOI codes (permanent links to each work via Crossref) and are indexed by Scholar, DOAJ and others.

The journal targets a broad population spanning from advanced researchers and clinicians to students and laypersons, wherein the latter can get quick explanations of advanced terms by in-line links to Wikipedia.

  - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 19:58, 3 October 2019 (UTC) reply

Comment: The history of ghrelin is interesting and explains why the receptor for ghrelin has the name "growth hormone secretagogue receptor". First there were synthetic ligands, then the receptor for those synthetic ligands was discovered and then the endogenous ligand for the receptor was discovered. As we say in English, it is a classic case of putting the cart before the horse. I think this information is useful.

The text currently reads:

History and name Ghrelin was discovered after the ghrelin receptor (called growth hormone secretagogue type 1A receptor or GHSR-1A) was discovered in 1996[15] and was reported in 1999.[16] The hormone name is based on its role as a growth hormone-releasing peptide, with reference to the Proto-Indo-European root gʰre-, meaning "to grow".[17]

List of suggested changes

1. Swapping these 2 sentences around

2. The term growth hormone releasing peptide is misleading here because means that ghrelin could get confused with a different peptide, growth hormone-releasing hormone (GHRH) which is also known "growth hormone-releasing peptide". Therefore I corrected this.

3. Adding text that helps people understand the relationship between the word "ghrelin" and the term "growth hormone secretagogue".

Suggested new text

Suzanne Dickson 05:57, 8 October 2019 (UTC)

06:52, 8 October 2019 (UTC)06:52, 8 October 2019 (UTC)06:52, 8 October 2019 (UTC)~

The name "ghrelin" is based on its first known role as a hormone that releases growth hormone from the pituitary gland, with reference to the Proto-Indo-European root ghre-, meaning "to grow" ^{[1] [2]}. It was shown to amplify the growth hormone-releasing effects of growth hormone-release hormone from the hypothalamus ^[3]. Unusually, the receptor for ghrelin was discovered before ghrelin ^[4]. The receptor was named the " growth hormone secretagogue receptor" because it is activated by synthetic peptide and non-peptide compounds with potent growth hormone-secreting activity, namely the growth hormone secretagogues (GHS) ^[5].

Suzanne Dickson 07:20, 4 October 2019 (UTC) Suzanne Dickson 09:44, 4 October 2019 (UTC)

Comment: If I was reading this page, I would really want to understand the relation between ghrelin and the word growth hormone secretagogue. That is why the last sentence was also included here. Ghrelin itself is a growth hormone secretagogue since it releases growth hormone by binding to the growth hormone secretagogue receptor.

06:58, 8 October 2019 (UTC)06:58, 8 October 2019 (UTC)06:58, 8 October 2019 (UTC)~

It is written on the web page ...

Location[edit source]

Ghrelin cells are found mainly in the stomach[27] and duodenum, but also in the jejunum, lungs, pancreatic islets,[28] gonads, adrenal cortex, placenta, and kidney. It has recently been shown that ghrelin is produced locally in the brain[29]

The issue: There is much much more ghrelin produced by the stomach than by the duodenum and jejunum. If the stomach is removed then circulating ghrelin levels fall by 80% or so. Therefore I made an edit to include this. This also means that I had to divide the first sentence into 2 sentences.

There are two problems with the second sentence. 2009 is not recent. In addition, this is much disputed. Most people in the ghrelin field do not believe it is produced in the brain. There are 2 options you can either delete the sentence or add additional information indicating that this is disputed. I direct you to an excellent review by Cabral S et al PMID: 28294994. Perhaps this should replace the current reference since it discusses the issue - the evidence for and against - and it is a review.

Suggested edit:

Ghrelin-producing cells are found in the gastrointestinal tract, mainly in the stomach ^[6] but also the duodenum and jejunum. They are also found in the lungs, pancreatic islets ^[7], gonads, adrenal cortex, placenta, and kidney ^[8]. It remains debated whether ghrelin is produced locally in the brain ^{[9] [10]}.

Suzanne Dickson 09:40, 4 October 2019 (UTC)

06:53, 8 October 2019 (UTC)06:53, 8 October 2019 (UTC)06:53, 8 October 2019 (UTC)~

The section on the function and mechanism of action of ghrelin could be improved. First, I suggest breaking it up into different subsections. This will help readers to easily get information about specific effects that they are interested in. It will also be important to used words that help the reader know what the main functions are versus what the additional functions are. If we build a strong core here, people will want to add information to it because the base for building information is secure and correct. I suggest these sub-headings and I will deal with each one separately:

Suzanne Dickson 05:46, 8 October 2019 (UTC)

Growth hormone release

Ghrelin and synthetic growth hormone secretagogues (GHS; ghrelin mimetics) increases circulating levels of growth hormone involving a direct pituitary action ^{[11] [12]}, and also by activating growth hormone-releasing hormone neurones in the hypothalamic arcuate nucleus ^[13]. Ghrelin/GHS amplify the effects of GHRH to release growth hormone ^[14].

Note: Potential COI: The reference Dickson et al (ie my work) was already cited on the ghrelin page. It is a key reference because it was first to show that these compounds act in the brain and also first to show that the activated cells include the GHRH cells.

Suzanne Dickson 06:50, 8 October 2019 (UTC)

06:53, 8 October 2019 (UTC)06:53, 8 October 2019 (UTC)06:53, 8 October 2019 (UTC)~

Food intake: how much, when and what?

Food anticipatory and food motivated behaviours

Energy balance and energy expenditure

Glucose homeostasis

Locomotor activity

Consumption of alcohol and drugs of abuse

Other functions

It is my plan to help each of these sections develop using the existing text and references on the web page as a starting point.

Suzanne Dickson 16:29, 4 October 2019 (UTC)

On your own Talk page and Talk pages of articles, the proper way to 'sign' is to type four of ~ at the end. This creates a 'signature' with your User name, and a date. You, typing that information, is not the same thing. David notMD ( talk) 21:26, 7 October 2019 (UTC) reply