Wikipedia

Suzanne Dickson

Joined 1 October 2019
Latest comment: 5 years ago by David notMD in topic 'Signing'

Welcome to Wikipedia from the Medicine WikiProject!

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Latest comment: 5 years ago1 comment1 person in discussion
Welcome to Wikipedia and WikiProject Medicine

Welcome to Wikipedia from WikiProject Medicine (also known as WPMED).

We're a group of editors who strive to improve the quality of medical articles here on Wikipedia. One of our members has noticed that you are interested in editing medical articles; it's great to have a new interested editor on board. In your wiki-voyages, a few things that may be relevant to editing Wikipedia articles are:

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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

October 2019

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Latest comment: 5 years ago2 comments1 person in discussion

  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

This page needs to be organised and made factually correct.

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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)

I suggest a change to the introductory section on ghrelin

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The original text:

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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]

Should be replaced with ...

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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].

Further edits

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

We need a proper section on the History of ghrelin. I have made a suggestion

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A brief history of ghrelin

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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]

A concise description of the ghrelin receptor

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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)

The ghrelin receptor

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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)

Edits to the section on the function of ghrelin

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These need to be gathered and organised, minimizing repeat.

Function and mechanism of action

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Control of food intake

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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

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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

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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)

References

  1. ^ Kojima, M; Hosoda, H; Date, Y; Nakazato, M; Matsuo, H; Kangawa, K (9 December 1999). "Ghrelin is a growth-hormone-releasing acylated peptide from stomach". Nature. 402 (6762): 656–60. doi:10.1038/45230. PMID 10604470.
  2. ^ Wren, AM; Small, CJ; Ward, HL; Murphy, KG; Dakin, CL; Taheri, S; Kennedy, AR; Roberts, GH; Morgan, DG; Ghatei, MA; Bloom, SR (November 2000). "The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion". Endocrinology. 141 (11): 4325–8. doi:10.1210/endo.141.11.7873. PMID 11089570.
  3. ^ Egecioglu, E; Jerlhag, E; Salomé, N; Skibicka, KP; Haage, D; Bohlooly-Y, M; Andersson, D; Bjursell, M; Perrissoud, D; Engel, JA; Dickson, SL (July 2010). "Ghrelin increases intake of rewarding food in rodents". Addiction biology. 15 (3): 304–11. doi:10.1111/j.1369-1600.2010.00216.x. PMID 20477752.
  4. ^ Skibicka, KP; Hansson, C; Alvarez-Crespo, M; Friberg, PA; Dickson, SL (28 April 2011). "Ghrelin directly targets the ventral tegmental area to increase food motivation". Neuroscience. 180: 129–37. doi:10.1016/j.neuroscience.2011.02.016. PMID 21335062.
  5. ^ Perello, M; Sakata, I; Birnbaum, S; Chuang, JC; Osborne-Lawrence, S; Rovinsky, SA; Woloszyn, J; Yanagisawa, M; Lutter, M; Zigman, JM (1 May 2010). "Ghrelin increases the rewarding value of high-fat diet in an orexin-dependent manner". Biological psychiatry. 67 (9): 880–6. doi:10.1016/j.biopsych.2009.10.030. PMID 20034618.
  6. ^ Cummings, DE; Purnell, JQ; Frayo, RS; Schmidova, K; Wisse, BE; Weigle, DS (August 2001). "A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans". Diabetes. 50 (8): 1714–9. doi:10.2337/diabetes.50.8.1714. PMID 11473029.
  7. ^ Tschöp, M; Smiley, DL; Heiman, ML (19 October 2000). "Ghrelin induces adiposity in rodents". Nature. 407 (6806): 908–13. doi:10.1038/35038090. PMID 11057670.
  8. ^ Howard, AD; Feighner, SD; Cully, DF; Arena, JP; Liberator, PA; Rosenblum, CI; Hamelin, M; Hreniuk, DL; Palyha, OC; Anderson, J; Paress, PS; Diaz, C; Chou, M; Liu, KK; McKee, KK; Pong, SS; Chaung, LY; Elbrecht, A; Dashkevicz, M; Heavens, R; Rigby, M; Sirinathsinghji, DJ; Dean, DC; Melillo, DG; Patchett, AA; Nargund, R; Griffin, PR; DeMartino, JA; Gupta, SK; Schaeffer, JM; Smith, RG; Van der Ploeg, LH (16 August 1996). "A receptor in pituitary and hypothalamus that functions in growth hormone release". Science (New York, N.Y.). 273 (5277): 974–7. doi:10.1126/science.273.5277.974. PMID 8688086.
  9. ^ Zigman, JM; Jones, JE; Lee, CE; Saper, CB; Elmquist, JK (20 January 2006). "Expression of ghrelin receptor mRNA in the rat and the mouse brain". The Journal of comparative neurology. 494 (3): 528–48. doi:10.1002/cne.20823. PMID 16320257.
  10. ^ Skibicka, KP; Dickson, SL (November 2011). "Ghrelin and food reward: the story of potential underlying substrates". Peptides. 32 (11): 2265–73. doi:10.1016/j.peptides.2011.05.016. PMID 21621573.
  11. ^ Wren, AM; Small, CJ; Ward, HL; Murphy, KG; Dakin, CL; Taheri, S; Kennedy, AR; Roberts, GH; Morgan, DG; Ghatei, MA; Bloom, SR (November 2000). "The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion". Endocrinology. 141 (11): 4325–8. doi:10.1210/endo.141.11.7873. PMID 11089570.
  12. ^ Wren, AM; Seal, LJ; Cohen, MA; Brynes, AE; Frost, GS; Murphy, KG; Dhillo, WS; Ghatei, MA; Bloom, SR (December 2001). "Ghrelin enhances appetite and increases food intake in humans". The Journal of clinical endocrinology and metabolism. 86 (12): 5992. doi:10.1210/jcem.86.12.8111. PMID 11739476.
  13. ^ Tschöp, M; Smiley, DL; Heiman, ML (19 October 2000). "Ghrelin induces adiposity in rodents". Nature. 407 (6806): 908–13. doi:10.1038/35038090. PMID 11057670.
  14. ^ Faulconbridge, LF; Cummings, DE; Kaplan, JM; Grill, HJ (September 2003). "Hyperphagic effects of brainstem ghrelin administration". Diabetes. 52 (9): 2260–5. doi:10.2337/diabetes.52.9.2260. PMID 12941764.
  15. ^ Cummings, DE; Purnell, JQ; Frayo, RS; Schmidova, K; Wisse, BE; Weigle, DS (August 2001). "A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans". Diabetes. 50 (8): 1714–9. doi:10.2337/diabetes.50.8.1714. PMID 11473029.
  16. ^ Bake, T; Hellgren, KT; Dickson, SL (April 2017). "Acute ghrelin changes food preference from a high-fat diet to chow during binge-like eating in rodents". Journal of neuroendocrinology. 29 (4). doi:10.1111/jne.12463. PMID 28219000.
  17. ^ Schéle, E; Bake, T; Rabasa, C; Dickson, SL (2016). "Centrally Administered Ghrelin Acutely Influences Food Choice in Rodents". PloS one. 11 (2): e0149456. doi:10.1371/journal.pone.0149456. PMID 26925974.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  18. ^ Skibicka, KP; Hansson, C; Alvarez-Crespo, M; Friberg, PA; Dickson, SL (28 April 2011). "Ghrelin directly targets the ventral tegmental area to increase food motivation". Neuroscience. 180: 129–37. doi:10.1016/j.neuroscience.2011.02.016. PMID 21335062.
  19. ^ Naleid, AM; Grace, MK; Cummings, DE; Levine, AS (November 2005). "Ghrelin induces feeding in the mesolimbic reward pathway between the ventral tegmental area and the nucleus accumbens". Peptides. 26 (11): 2274–9. doi:10.1016/j.peptides.2005.04.025. PMID 16137788.
  20. ^ Hansson, C; Haage, D; Taube, M; Egecioglu, E; Salomé, N; Dickson, SL (28 April 2011). "Central administration of ghrelin alters emotional responses in rats: behavioural, electrophysiological and molecular evidence". Neuroscience. 180: 201–11. doi:10.1016/j.neuroscience.2011.02.002. PMID 21303683.
  21. ^ Carlini, VP; Varas, MM; Cragnolini, AB; Schiöth, HB; Scimonelli, TN; de Barioglio, SR (16 January 2004). "Differential role of the hippocampus, amygdala, and dorsal raphe nucleus in regulating feeding, memory, and anxiety-like behavioral responses to ghrelin". Biochemical and biophysical research communications. 313 (3): 635–41. doi:10.1016/j.bbrc.2003.11.150. PMID 14697239.
  22. ^ Olszewski, PK; Li, D; Grace, MK; Billington, CJ; Kotz, CM; Levine, AS (April 2003). "Neural basis of orexigenic effects of ghrelin acting within lateral hypothalamus". Peptides. 24 (4): 597–602. doi:10.1016/s0196-9781(03)00105-0. PMID 12860204.
  23. ^ Olszewski, PK; Grace, MK; Billington, CJ; Levine, AS (June 2003). "Hypothalamic paraventricular injections of ghrelin: effect on feeding and c-Fos immunoreactivity". Peptides. 24 (6): 919–23. doi:10.1016/s0196-9781(03)00159-1. PMID 12948845.
  24. ^ Keen-Rhinehart, E; Bartness, TJ (March 2005). "Peripheral ghrelin injections stimulate food intake, foraging, and food hoarding in Siberian hamsters". American journal of physiology. Regulatory, integrative and comparative physiology. 288 (3): R716-22. doi:10.1152/ajpregu.00705.2004. PMID 15576659.
  25. ^ Verhagen, LA; Egecioglu, E; Luijendijk, MC; Hillebrand, JJ; Adan, RA; Dickson, SL (May 2011). "Acute and chronic suppression of the central ghrelin signaling system reveals a role in food anticipatory activity". European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 21 (5): 384–92. doi:10.1016/j.euroneuro.2010.06.005. PMID 20620030.
  26. ^ Merkestein, M; Brans, MA; Luijendijk, MC; de Jong, JW; Egecioglu, E; Dickson, SL; Adan, RA (May 2012). "Ghrelin mediates anticipation to a palatable meal in rats". Obesity (Silver Spring, Md.). 20 (5): 963–71. doi:10.1038/oby.2011.389. PMID 22282050.
  27. ^ Skibicka, KP; Hansson, C; Egecioglu, E; Dickson, SL (January 2012). "Role of ghrelin in food reward: impact of ghrelin on sucrose self-administration and mesolimbic dopamine and acetylcholine receptor gene expression". Addiction biology. 17 (1): 95–107. doi:10.1111/j.1369-1600.2010.00294.x. PMID 21309956.
  28. ^ Skibicka, KP; Hansson, C; Alvarez-Crespo, M; Friberg, PA; Dickson, SL (28 April 2011). "Ghrelin directly targets the ventral tegmental area to increase food motivation". Neuroscience. 180: 129–37. doi:10.1016/j.neuroscience.2011.02.016. PMID 21335062.
  29. ^ Perello, M; Sakata, I; Birnbaum, S; Chuang, JC; Osborne-Lawrence, S; Rovinsky, SA; Woloszyn, J; Yanagisawa, M; Lutter, M; Zigman, JM (1 May 2010). "Ghrelin increases the rewarding value of high-fat diet in an orexin-dependent manner". Biological psychiatry. 67 (9): 880–6. doi:10.1016/j.biopsych.2009.10.030. PMID 20034618.
  30. ^ Egecioglu, E; Jerlhag, E; Salomé, N; Skibicka, KP; Haage, D; Bohlooly-Y, M; Andersson, D; Bjursell, M; Perrissoud, D; Engel, JA; Dickson, SL (July 2010). "Ghrelin increases intake of rewarding food in rodents". Addiction biology. 15 (3): 304–11. doi:10.1111/j.1369-1600.2010.00216.x. PMID 20477752.
  31. ^ Jerlhag, E; Egecioglu, E; Landgren, S; Salomé, N; Heilig, M; Moechars, D; Datta, R; Perrissoud, D; Dickson, SL; Engel, JA (7 July 2009). "Requirement of central ghrelin signaling for alcohol reward". Proceedings of the National Academy of Sciences of the United States of America. 106 (27): 11318–23. doi:10.1073/pnas.0812809106. PMID 19564604.
  32. ^ Clifford, PS; Rodriguez, J; Schul, D; Hughes, S; Kniffin, T; Hart, N; Eitan, S; Brunel, L; Fehrentz, JA; Martinez, J; Wellman, PJ (November 2012). "Attenuation of cocaine-induced locomotor sensitization in rats sustaining genetic or pharmacologic antagonism of ghrelin receptors". Addiction biology. 17 (6): 956–63. doi:10.1111/j.1369-1600.2011.00339.x. PMID 21790898.
  33. ^ Perello, M; Dickson, SL (June 2015). "Ghrelin signalling on food reward: a salient link between the gut and the mesolimbic system". Journal of neuroendocrinology. 27 (6): 424–34. doi:10.1111/jne.12236. PMID 25377898.
  34. ^ Skibicka, KP; Shirazi, RH; Rabasa-Papio, C; Alvarez-Crespo, M; Neuber, C; Vogel, H; Dickson, SL (October 2013). "Divergent circuitry underlying food reward and intake effects of ghrelin: dopaminergic VTA-accumbens projection mediates ghrelin's effect on food reward but not food intake". Neuropharmacology. 73: 274–83. doi:10.1016/j.neuropharm.2013.06.004. PMID 23770258.
  35. ^ Jerlhag, E; Egecioglu, E; Dickson, SL; Andersson, M; Svensson, L; Engel, JA (March 2006). "Ghrelin stimulates locomotor activity and accumbal dopamine-overflow via central cholinergic systems in mice: implications for its involvement in brain reward". Addiction biology. 11 (1): 45–54. doi:10.1111/j.1369-1600.2006.00002.x. PMID 16759336.
  36. ^ Abizaid, A; Liu, ZW; Andrews, ZB; Shanabrough, M; Borok, E; Elsworth, JD; Roth, RH; Sleeman, MW; Picciotto, MR; Tschöp, MH; Gao, XB; Horvath, TL (December 2006). "Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite". The Journal of clinical investigation. 116 (12): 3229–39. doi:10.1172/JCI29867. PMID 17060947.
  37. ^ Jerlhag, E; Egecioglu, E; Dickson, SL; Douhan, A; Svensson, L; Engel, JA (March 2007). "Ghrelin administration into tegmental areas stimulates locomotor activity and increases extracellular concentration of dopamine in the nucleus accumbens". Addiction biology. 12 (1): 6–16. doi:10.1111/j.1369-1600.2006.00041.x. PMID 17407492.
  38. ^ Folgueira, C; Seoane, LM; Casanueva, FF (2014). "The brain-stomach connection". Frontiers of hormone research. 42: 83–92. doi:10.1159/000358316. PMID 24732927.
  39. ^ Lall, S; Tung, LY; Ohlsson, C; Jansson, JO; Dickson, SL (12 January 2001). "Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues". Biochemical and biophysical research communications. 280 (1): 132–8. doi:10.1006/bbrc.2000.4065. PMID 11162489.
  40. ^ Tschöp, M; Smiley, DL; Heiman, ML (19 October 2000). "Ghrelin induces adiposity in rodents". Nature. 407 (6806): 908–13. doi:10.1038/35038090. PMID 11057670.
  41. ^ Chebani, Y; Marion, C; Zizzari, P; Chettab, K; Pastor, M; Korostelev, M; Geny, D; Epelbaum, J; Tolle, V; Morisset-Lopez, S; Pantel, J (19 April 2016). "Enhanced responsiveness of Ghsr Q343X rats to ghrelin results in enhanced adiposity without increased appetite". Science signaling. 9 (424): ra39. doi:10.1126/scisignal.aae0374. PMID 27095593.
  42. ^ Schwartz, MW; Woods, SC; Porte D, Jr; Seeley, RJ; Baskin, DG (6 April 2000). "Central nervous system control of food intake". Nature. 404 (6778): 661–71. doi:10.1038/35007534. PMID 10766253.

Managing a conflict of interest

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Latest comment: 5 years ago1 comment1 person in discussion

  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

In reply

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Latest comment: 5 years ago2 comments2 people in discussion

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

Suzanne Dickson, you are invited to the Teahouse!

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Hi Suzanne Dickson! Thanks for contributing to Wikipedia.
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16:04, 2 October 2019 (UTC)

Welcome from Markworthen

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Latest comment: 5 years ago2 comments1 person in discussion

  Welcome, Suzanne Dickson!

Hello, Suzanne Dickson, and welcome to Wikipedia! I'm Markworthen, one of the thousands of editors here at Wikipedia. Here are a few good links for newcomers:

Introduction
The Five Pillars of Wikipedia
How to edit a page
Help
How to write a great article
Simplified Manual of Style

Thank you for your contributions to Wikipedia, users like you are what makes Wikipedia such a great encyclopedia!

I hope you enjoy editing here and being a Wikipedian! Please sign your name on talk pages using four tildes (~~~~); this will automatically produce your username and the date. If you need help, check out Wikipedia:Where to ask a question, ask me on my talk page, or type {{helpme}} here on your talk page and someone will show up shortly to answer your questions. Again, welcome!

  - Mark D Worthen PsyD (talk) (I am a man. The traditional male pronouns are fine.) 20:36, 2 October 2019 (UTC)Reply


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

Ghrelin page

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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)

User page

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Latest comment: 5 years ago4 comments2 people in discussion

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 https://en.wiki.x.io/wiki/User:Suzanne_Dickson in the URL bar and then add /NameOfThePageYouWantToCreate. Here, this will create the https://en.wiki.x.io/wiki/User:Suzanne_Dickson/Curriculum_Vitae page, where you can copy-paste what is currently on your https://en.wiki.x.io/wiki/User:Suzanne_Dickson page. Likewise, you can create a https://en.wiki.x.io/wiki/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)

WikiJournals

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Latest comment: 5 years ago1 comment1 person in discussion

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

Suggested Edits to the section on the history and name of ghrelin on the ghrelin page

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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)~

History and name

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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)~

Edits to the section on Ghrelin-producing cells

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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)~

Ghrelin page

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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)

Function and mechanism of action

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Growth hormone release

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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?

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Food anticipatory and food motivated behaviours

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Energy balance and energy expenditure

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Glucose homeostasis

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Locomotor activity

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Consumption of alcohol and drugs of abuse

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Other functions

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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)

'Signing'

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Latest comment: 5 years ago1 comment1 person in discussion

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

Some refs

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  1. ^ Kojima, M; Hosoda, H; Date, Y; Nakazato, M; Matsuo, H; Kangawa, K (9 December 1999). "Ghrelin is a growth-hormone-releasing acylated peptide from stomach". Nature. 402 (6762): 656–60. doi:10.1038/45230. PMID 10604470.
  2. ^ Inui, A; Asakawa, A; Bowers, CY; Mantovani, G; Laviano, A; Meguid, MM; Fujimiya, M (March 2004). "Ghrelin, appetite, and gastric motility: the emerging role of the stomach as an endocrine organ". FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 18 (3): 439–56. doi:10.1096/fj.03-0641rev. PMID 15003990.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Veldhuis, JD; Bowers, CY (2010). "Integrating GHS into the Ghrelin System". International journal of peptides. 2010. doi:10.1155/2010/879503. PMID 20798846.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Howard, AD; Feighner, SD; Cully, DF; Arena, JP; Liberator, PA; Rosenblum, CI; Hamelin, M; Hreniuk, DL; Palyha, OC; Anderson, J; Paress, PS; Diaz, C; Chou, M; Liu, KK; McKee, KK; Pong, SS; Chaung, LY; Elbrecht, A; Dashkevicz, M; Heavens, R; Rigby, M; Sirinathsinghji, DJ; Dean, DC; Melillo, DG; Patchett, AA; Nargund, R; Griffin, PR; DeMartino, JA; Gupta, SK; Schaeffer, JM; Smith, RG; Van der Ploeg, LH (16 August 1996). "A receptor in pituitary and hypothalamus that functions in growth hormone release". Science (New York, N.Y.). 273 (5277): 974–7. doi:10.1126/science.273.5277.974. PMID 8688086.
  5. ^ Smith, RG (May 2005). "Development of growth hormone secretagogues". Endocrine reviews. 26 (3): 346–60. doi:10.1210/er.2004-0019. PMID 15814848.
  6. ^ Ariyasu, H; Takaya, K; Tagami, T; Ogawa, Y; Hosoda, K; Akamizu, T; Suda, M; Koh, T; Natsui, K; Toyooka, S; Shirakami, G; Usui, T; Shimatsu, A; Doi, K; Hosoda, H; Kojima, M; Kangawa, K; Nakao, K (October 2001). "Stomach is a major source of circulating ghrelin, and feeding state determines plasma ghrelin-like immunoreactivity levels in humans". The Journal of clinical endocrinology and metabolism. 86 (10): 4753–8. doi:10.1210/jcem.86.10.7885. PMID 11600536.
  7. ^ Suckale, J; Solimena, M (1 May 2008). "Pancreas islets in metabolic signaling--focus on the beta-cell". Frontiers in bioscience : a journal and virtual library. 13: 7156–71. doi:10.2741/3218. PMID 18508724.
  8. ^ Müller, TD; Nogueiras, R; Andermann, ML; Andrews, ZB; Anker, SD; Argente, J; Batterham, RL; Benoit, SC; Bowers, CY; Broglio, F; Casanueva, FF; D'Alessio, D; Depoortere, I; Geliebter, A; Ghigo, E; Cole, PA; Cowley, M; Cummings, DE; Dagher, A; Diano, S; Dickson, SL; Diéguez, C; Granata, R; Grill, HJ; Grove, K; Habegger, KM; Heppner, K; Heiman, ML; Holsen, L; Holst, B; Inui, A; Jansson, JO; Kirchner, H; Korbonits, M; Laferrère, B; LeRoux, CW; Lopez, M; Morin, S; Nakazato, M; Nass, R; Perez-Tilve, D; Pfluger, PT; Schwartz, TW; Seeley, RJ; Sleeman, M; Sun, Y; Sussel, L; Tong, J; Thorner, MO; van der Lely, AJ; van der Ploeg, LH; Zigman, JM; Kojima, M; Kangawa, K; Smith, RG; Horvath, T; Tschöp, MH (June 2015). "Ghrelin". Molecular metabolism. 4 (6): 437–60. doi:10.1016/j.molmet.2015.03.005. PMID 26042199.
  9. ^ Cabral, A; López Soto, EJ; Epelbaum, J; Perelló, M (15 March 2017). "Is Ghrelin Synthesized in the Central Nervous System?". International journal of molecular sciences. 18 (3). doi:10.3390/ijms18030638. PMID 28294994.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  10. ^ Ferrini, F; Salio, C; Lossi, L; Merighi, A (March 2009). "Ghrelin in central neurons". Current neuropharmacology. 7 (1): 37–49. doi:10.2174/157015909787602779. PMID 19721816.
  11. ^ Momany, FA; Bowers, CY; Reynolds, GA; Chang, D; Hong, A; Newlander, K (January 1981). "Design, synthesis, and biological activity of peptides which release growth hormone in vitro". Endocrinology. 108 (1): 31–9. doi:10.1210/endo-108-1-31. PMID 6109621.
  12. ^ Kojima, M; Hosoda, H; Date, Y; Nakazato, M; Matsuo, H; Kangawa, K (9 December 1999). "Ghrelin is a growth-hormone-releasing acylated peptide from stomach". Nature. 402 (6762): 656–60. doi:10.1038/45230. PMID 10604470.
  13. ^ Dickson, SL; Leng, G; Robinson, IC (March 1993). "Systemic administration of growth hormone-releasing peptide activates hypothalamic arcuate neurons". Neuroscience. 53 (2): 303–6. doi:10.1016/0306-4522(93)90197-n. PMID 8492908.
  14. ^ Bowers, CY; Reynolds, GA; Durham, D; Barrera, CM; Pezzoli, SS; Thorner, MO (April 1990). "Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone". The Journal of clinical endocrinology and metabolism. 70 (4): 975–82. doi:10.1210/jcem-70-4-975. PMID 2108187.
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